Bilateral renal nephrosclerosis. Nephrosclerosis: symptoms, treatment and types

A disease such as nephrosclerosis has remained unattended by doctors for a long time. Until the 19th century, there was no complete description of it. It began to be considered an independent disease only three decades later, when information about the etiology appeared. The disease was associated with damage to arterial vessels due to their damage by cholesterol. His prognosis is not always favorable. After a course of therapy, many patients have to deal with complications such as blindness and ventricular dysfunction. To maintain the vitality of the body, in such cases, urgent blood purification is required artificially.

Anatomical information: renal nephrosclerosis

If you suspect an illness, you should seek help from such a center or a local physician. The latter, after studying the clinical picture, can give a referral to a specialist.

Diagnosis of the disease begins with a study of the patient’s complaints, his medical history and physical examination. During the consultation, the nephrologist may also palpate the abdominal cavity. The listed manipulations allow us to suggest a preliminary diagnosis and outline further examination tactics.

At the next stage, the patient is prescribed laboratory tests. For example, blood biochemistry may indicate the following symptoms of kidney dysfunction:

• increase in performance;
• reduction in quantitative protein content;
• a decrease in potassium levels, and an increase in phosphorus and magnesium.

A urine test reveals protein and red blood cells, but its density is significantly reduced. When examining a blood test, it turns out that the level of platelets and hemoglobin falls, and the quantitative content of leukocytes increases.

To more accurately assess the functioning of organs, instrumental methods are used to examine patients diagnosed with nephrosclerosis. Ultrasound of the kidneys, for example, allows you to assess their size and the condition of the cortex. Urography is mandatory. Angiography gives a complete picture of the condition of the vessels in the affected organ.

Based on the examination results, the doctor confirms or refutes the preliminary diagnosis and makes recommendations for further treatment.

Use of medications

This disease is treated in specialized nephrology centers. It comes down to eliminating the main provoking factor. Attempts to restore lost kidney function without the first step are usually unsuccessful.

Treatment is always comprehensive and long-term. Depending on the clinical picture and general condition of the patient, the following medications may be required:

1. Anticoagulants (Heparin) to prevent blood clots.
2. Medicines to lower blood pressure.
3. ACE inhibitors(“Diroton”, “Berlipril”) to dilate the blood vessels of the kidneys.
4. Diuretics, which remove excess fluid from the body.
5. Calcium antagonists that promote dilation of arteries (Falipamil).
6. Multivitamin complexes.

For other disorders caused by kidney dysfunction, medications are selected individually.

Surgery

At the 3-4th stage pathological process Drug treatment is usually ineffective. In such cases, the patient is indicated for hemodialysis or a transplant. The essence of the first procedure is to cleanse the blood of toxic substances. A special filter is used for this. artificial kidney. The frequency of hemodialysis is determined by the patient’s condition and the severity of the pathological process. The procedure must be accompanied by drug therapy.

Surgical treatment involves transplantation of a donor kidney. This is one of the few types of operations where an organ can be removed from both a living person and a corpse. During the recovery period, the patient is prescribed serious medication support and complete rest.

Nutritional Features

An excellent addition to the course of treatment is to follow a fairly strict diet. Nutrition for kidney nephrosclerosis is selected by the doctor individually for each patient. Typically, the following principles are followed:

1. Limit protein intake. However, you cannot completely abandon it. When choosing protein foods, preference should be given to poultry, fish and dairy products. It is important to completely exclude potatoes, cereals and bread from the diet.
2. The diet must necessarily include seafood, but you should not abuse them for the following reason: high content phosphorus.
3. Limiting table salt consumption. At any consultation, the nephrologist will say that at stages 1-2, up to 15 g of salt per day is allowed, and at stages 3-4 this amount is halved. You cannot completely abandon this spice, as the likelihood of dehydration increases.
4. Be sure to include potassium-rich foods in your diet. For example, bananas, dried apricots, raisins.
5. Nutrition should be as balanced as possible, containing the required amount of calories and vitamins.

Most patients are forced to adhere to this diet for the rest of their lives.

Forecast

Renal nephrosclerosis is chronic disease. In the initial stages of its development, it is possible to maintain organ functions, but for this it is necessary to follow the doctor’s recommendations and adhere to certain restrictions. For example, for patients with this diagnosis, it is important to minimize the consumption of table salt and constantly monitor calcium and phosphorus levels in the blood. With each exacerbation of the pathology, it is necessary to seek medical help and undergo a course of therapy each time.

A “wrinkled kidney” identified at stages 3-4 requires a slightly different approach. In this case, all restrictions are much stricter. It is no longer possible to restore lost organ tissue. Therefore, in such situations, therapy comes down to ensuring the functionality of the remaining nephrons. Sometimes this is not enough.

The term “renal nephrosclerosis” refers to a pathology that occurs due to the replacement of the kidney parenchyma with connective tissues. There are several types of disease that occur for various reasons. Symptoms increase as the disease progresses. This affects the methods of treating pathology. There are no special preventive measures. Predicting the course depends on many factors, the main one of which is the benignity or malignancy of the disease.

A pathological phenomenon is the process of overgrowth of the kidney parenchyma connective tissue.

The disease was first diagnosed in the early 20th century. The cause of the development of nephrosclerosis is the replacement of the organ parenchyma with connective tissue, causing the kidney to become denser and become wrinkled. Another name for the disease is “shrunken kidney.” This leads to deterioration in the functioning of the organ. Previously, it was believed that the disease was provoked by glomerulonephritis; now experts are inclined to believe that the main causes of the development of kidney nephrosclerosis are diabetes mellitus and arterial hypertension. Statistics say that the disease is diagnosed in every 6 people out of 10 thousand.

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Types and forms

Due to its formation, a wrinkled kidney is classified into 2 types:

• primary wrinkled kidney (the blood supply to the organ deteriorates due to atherosclerosis, hypertension, or age-related changes that develop in older people);
• secondary wrinkled kidney (results from organ trauma, radiation or other kidney pathologies, for example, pyelonephritis or tuberculosis).

Primary renal sclerosis occurs:

• hypertensive;
• involutive;
• diabetic;
• atherosclerotic.

Hypertensive nephrosclerosis is characterized by a frequent increase in pressure in the vessels when the lumen narrows. The kidney cells do not receive enough oxygen, and the parenchyma of the organ is replaced by connective tissues. Hypertensive nephroangiosclerosis is a disease that affects the small vessels of the kidney. Nephroangiosclerosis of the arteries develops against the background of arterial hypertension. Atherosclerotic nephrosclerosis occurs against the background of arterial stricture, the cause of which is a sclerotic plaque. The disease usually does not lead to large-scale damage to the kidney, and its functions are preserved.

In diabetic nephrosclerosis, microangiopathy develops, which leads to complete defeat organ. Pathology develops in 4 stages:

• 1st - not accompanied by pronounced symptoms;
• 2nd (prenephrotic) - characterized a little high blood pressure and changes in blood formulas, which are reflected in the results of general and biochemical tests;
• 3rd (nephrotic) - swelling appears and blood pressure increases greatly;
• The 4th stage of diabetic nephrosclerosis is accompanied by renal failure and develops over several years.

The course of the disease allows us to distinguish the following types of nephrosclerosis:

• benign;
• malignant.

Benign nephrosclerosis takes a long time to develop. It takes a long time for the function of the artery to be impaired. First, a thickening of the inner layer occurs, which over time spreads to the entire thickness of the organ wall, causing blockage of the vessel. The development of the pathological process leads to deterioration of blood flow in the kidney, resulting in impaired renal function. Malignant nephrosclerosis is characterized by a more rapid development of processes, so timely diagnosis is important, which will help prevent changes in the kidney. The prognosis for benign sclerosis is much better.

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Causes of sclerotic kidney

Structural abnormalities of the kidneys may be a consequence of complications of diabetes, tuberculosis, or other inflammations internal organs.

• thromboembolism;
• atherosclerosis;
• hypertension.

The wrinkled organ in which the secondary lesion occurred is a consequence of other kidney pathologies:

• tuberculosis;
• nephropathy in pregnant women;
• pyelonephritis;
• amyloidosis;
• glomerulonephritis;
• injuries;
• diabetes mellitus

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Pathological anatomy

Sclerotic pathology develops in 2 phases. At the first stage, it is important to determine the disease, which is the cause of sclerotic processes in the organ. At this point, the relationship is quite easy to find. At the second stage, this is much more difficult to do, sometimes unrealistic. Wrinkling occurs very quickly, covering more and more kidney tissue. In this case, the organ increases slightly, its surface becomes granular, many irregularities form, and tissue scarring begins. Sometimes the organ shrinks evenly, sometimes not.

The disease can develop in benign and malignant forms. With benign sclerosis of the kidney, individual groups of nephrons shrink, the process develops slowly. Connective tissues first replace the intermediate space, and then the atrophied zones. With malignant wrinkling, pathological changes occur faster, which worsens the prognosis. Necrosis of arterioles and capillary glomeruli develops, and many complications arise. Death due to late diagnosis is common.

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Symptoms of the disease

Wrinkling of the kidneys is manifested by swelling, pressure surges, frequent urges to the toilet.

In the initial stages, shriveled organs do not make themselves felt at all or the symptoms are mild. The problem can only be diagnosed by blood and urine tests, which show small changes in the functioning of the organ. The main symptoms appear at a late stage. The first symptoms are:

• increased urination;
• frequent urination;
• the presence of protein in the urine;
• high blood pressure;
• swelling.

In addition, there are:

• symptoms of damage to the heart and blood vessels;
• iron deficiency anemia.

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Risk of kidney nephrosclerosis in a child

Sclerotic kidney damage in a child cannot be diagnosed. The development of pathological changes that lead to wrinkling is facilitated by prolonged exposure to unfavorable factors. If a baby has congenital pathologies of the kidneys and genitourinary system, the risk of developing nephrosclerosis increases, so it is important to carefully examine such children.

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Diagnostic methods

When a patient visits a doctor, the doctor first takes a history and visually examines the patient. After analyzing the symptoms of the disease, the specialist performs palpation abdominal cavity patient. All these methods make it possible to suggest a certain diagnosis and understand in what perspective to continue research.

Laboratory diagnostic methods:

• blood biochemistry (there is an increase in the level of urea, creatine, a decrease in protein by late stages sodium, magnesium, potassium, phosphorus may be increased);
• complete blood count (hemoglobin and platelet levels are low);
• general urinalysis (the protein in the urine is increased, the density of the substance decreases, red blood cells and casts are visualized, which should not be in the urine).

The diagnosis cannot be made without instrumental research methods:

• Ultrasound (on the monitor during an ultrasound it can be seen that the size of the organ is less than normal, atrophy of the cortical substance is observed);
• angiography of the vessels of the organ (the places of narrowing and deformation that occurred in the small vessels, the cortex becomes thinner, the contour of the organ changes);
• excretory urography (iodine-containing substances are administered, so it is clear that the organ and its cortex are smaller than normal);
• vascular Doppler (blood flow in nephrons and vessels is slower);
• scintigraphy (it is clear that the isotope is not distributed evenly);
• computed tomography;
• radionuclide renography;
• biopsy and histological analysis of the biopsy sample (a macropreparation is used).

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Treatment options

Sclerotic changes begin to be treated only after diagnosis. If signs have not yet appeared and the disease is at an early stage, the patient may be prescribed treatment with the following medications:

Early deformations of the kidney structure can be stopped with pills, and later ones can only be stopped with surgery.

• anticoagulants (for example, Heparin);
• potassium preparations to normalize salt balance (for example, Asparkam);
• antiplatelet agents that improve blood flow (for example, Trental);
• multivitamins;
• vitamin D;
• iron supplements;
• sorbents.

Medications are also used that help reduce blood pressure, but their use at a later stage, when the kidney has shriveled, is extremely undesirable:

• calcium antagonists (for example, Verapimil);
• diuretics (for example, Furosemide);
• adrenergic receptor blockers (for example, Propranolol).

If renal sclerosis is diagnosed in the last stages, drug treatment is ineffective. The patient needs hemodialysis or surgical treatment. The essence of hemodialysis is that the blood of a patient whose kidneys have shriveled is passed through a special filter for an artificial kidney. This cleanses the blood of toxic substances and normalizes salt balance. The frequency of hemodialysis is determined by the patient’s condition and the degree of renal dysfunction. The procedure is accompanied by treatment with pharmaceuticals.

Surgical treatment for patients with kidney shrinkage is carried out through kidney transplantation. This is one of the few types of transplantation when an organ can be removed not only from a corpse, but also from a living person. At the same time, this is an extremely difficult operation. During the recovery period, the patient is recommended to rest completely and take medications that inhibit the defense mechanisms immune system. Signs of glomerulonephritis or kidney failure can sometimes be treated with hirudotherapy (leeches). Leeches are placed in the lumbar region in quantities of up to 8 pieces. The duration of the course of treatment is 7−12 times (5 procedures every other day, and the rest - once a week).

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Nutritional Features

A change in the parenchyma of the right or left kidney requires an indispensable change in nutrition. Need to eat in small portions many times a day. The presence of protein should be limited. Among protein products, it is better to choose meat, dairy, fermented milk products, egg white. It is not recommended to eat cereals, potatoes or bread. The diet should include fish, as it is rich in phosphorus.

To prevent such a sign as edema, it is necessary to limit the amount of salt, but not completely abandon it. Nutrition should be rational. It should contain a lot of vitamins. The diet encourages the consumption of seaweed, buckwheat, nuts and mineral waters, which contain a lot of magnesium. If the patient has a secondary disease, it is necessary to drink up to 3 liters of water per day, which cannot be done if there are signs of problems with the heart or blood vessels.

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Traditional treatment

You can help your kidneys recover from nephrosclerosis with infusions and decoctions of natural ingredients.

Treatment with folk remedies cannot be the only type of therapy used. It is prohibited to use folk remedies without first consulting a doctor. Healers say that the symptoms of the disease can be smoothed out using the following medications:

• birch sap;
• infusion of lingonberry fruits;
• infusion of alcohol from aspen buds;
• a decoction of flaxseed (5 spoons), strawberry leaves (1 spoon), birch (2 spoons) and nettle (2 spoons) leaves;
• licorice root in infusion.

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Prognosis for recovery

The diagnosis of nephrosclerosis implies different outcomes. Since this is a chronic pathology, in which remissions and exacerbations constantly occur, while compensating for the pathology of one kidney, dietary nutrition and following the recommendations of your doctor, you can reduce the number of attacks. In this case, the patient will lead a normal lifestyle and will not lose his ability to work. The prognosis for the outcome of malignant shrinkage of the kidney is not so favorable, since the nephrons die and renal failure develops. Usually the patient awaits permanent hemodialysis or transplantation. Failure to do this leads to death.

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Disease prevention

There are no special preventive measures that can prevent the kidney from shrinking. Doctors recommend sticking to proper nutrition, not overexerting yourself, and resting. It's good to get enough sleep. An important point is to maintain an active lifestyle. You should monitor your blood pressure and consult a doctor promptly if you feel unwell.

Most people over forty suffer from a benign form of nephrosclerosis, which means that the blood vessels in the kidneys gradually change, but these changes do not occur as quickly and do not require treatment. For patients with benign nephrosclerosis, all that is required is to monitor their condition and take measures to prevent the progression of the disease. Other patients have a malignant form of nephrosclerosis, in which case damage to the renal vessels occurs so quickly that drug treatment or even surgery is necessary.

Definition

Nephrosclerosis is the process of replacement of the renal parenchyma with connective tissue, which leads to thickening of the walls of arteries and arterioles in the kidneys. Such arteries cannot normally supply blood to the kidney, a disruption in the nutrition of the glomeruli and tubules occurs, and subsequently their death and replacement with connective tissue. The kidney decreases in volume (primarily shriveled kidney) and begins to lose its functions.

Pain in the lower back indicates possible kidney problems

Types of disease

Depending on the cause, there are two types of kidney nephrosclerosis:

• primary, which occurs as a result of impaired blood supply to the kidneys due to diseases and conditions such as atherosclerosis, hypertension, kidney infarction, venous congestion in the kidneys, etc. Primary nephrosclerosis also often occurs due to senile changes in the body;
• secondary, which develops against the background of existing kidney diseases (glomerulo- and pyelonephritis, kidney stones, tuberculosis, syphilis, renal amyloidosis, diabetes mellitus), as well as as a result of their injury, or exposure to ionizing radiation on the body.

Primary nephrosclerosis, in turn, is further divided into the following forms:

• atherosclerotic;
• involutive;
• hypertensive.

Also, depending on the course of the process, there are:

• benign nephrosclerosis, in which there is a gradual and long-term deterioration of function renal arteries. First, the inner layer of the walls of smaller vessels thickens and gradually this thickening spreads to the entire wall, sometimes blocking the central channel of the vessel. Fat is then deposited in the degenerated wall tissue. Large arteries have excess elastic tissue, which can block their channels. Both of these conditions cause disruption of blood flow to vital areas in the kidneys, which in turn leads to poor functioning of the kidney tissue;
• malignant nephrosclerosis, in which the above-described changes develop much faster.

Reasons

The cause of nephrosclerosis is a violation of the blood supply to the kidneys, which is the result of a narrowing of the lumen of its vessels. Hypoxia occurs, as a result of which atrophy and degeneration of the renal parenchyma and proliferation of connective tissue develop. Such processes are most often observed in the kidneys during atherosclerosis and hypertension. Also, nephrosclerosis can develop due to the development of inflammatory and dystrophic processes in the kidneys in diseases such as glomerulo- and pyelonephritis, diabetes mellitus, tuberculosis, syphilis, kidney stones, systemic lupus erythematosus, and renal amyloidosis.

Sometimes nephrosclerosis can be associated with age-related changes vascular system kidney

Symptoms

In the initial stages of nephrosclerosis, there are often no symptoms. The first signs of kidney damage can be observed in urine tests, which will be characterized by poly- and nocturia, the presence of protein in the urine, microhematuria, decreased renal clearance, and hyposthenuria. Patients complain of increased blood pressure(diastolic blood pressure exceeds 120 mmHg).

The main symptoms of kidney nephrosclerosis include:

• visual impairment ;
• blood in urine;
• weight loss;
• uremia (accumulation of urea and other nitrogenous compounds in the blood);
• attacks of angina.

Diagnostic methods

First you need to correctly collect anamnesis and analyze the clinical picture. Laboratory methods are also used for diagnosis, including:

• biochemical blood test, which reveals elevated levels of urea, creatinine and uric acid, decrease total protein, at the final stages, an increase in potassium, magnesium, phosphorus and sodium;
• a general urinalysis, which reveals an increased amount of protein, a decrease in the relative density of urine, as well as the presence of red blood cells and casts that are absent normally;
• a general blood test, which shows a decrease in hemoglobin and platelet levels.

Among the instrumental research methods that are effective are:

• ultrasound examination, which reveals a decrease in the size and function (atrophy) of the renal cortex, as well as the presence of calcifications in the renal parenchyma;
• excretory urography of the kidneys, which allows you to identify a decrease in the volume of the kidney and its cortex;
• angiography of the renal vessels, which determines the narrowing and deformation of small renal arteries, uneven contour of the kidney, thinning of the renal cortex;
• kidney scintigraphy, which reveals uneven distribution of the radioisotope in nephrosclerosis;
• renal vascular Doppler, which detects slowing of blood flow in the renal vessels and nephrons;
• radionuclide renography, which detects delayed accumulation and excretion of a radiopharmaceutical drug by the kidneys;
• computed tomography of the kidneys;
• kidney biopsy.

Treatment options

First you need to determine the cause and begin treatment of the causative disease. Therapy in the early stages involves drugs such as anticoagulants (heparin, warfarin), antiplatelet agents (pentoxifylline, trental, dipyridamole), which help improve renal blood supply. Drugs are also used to lower blood pressure, but in the later stages of nephrosclerosis they should be used with caution. These include ACE inhibitors (captopril, enalapril), calcium antagonists (verapamil, nifedepine), β-adrenergic receptor blockers (atenolol, propranolol), diuretics (furosemide, hypothiazide). Potassium preparations (asparkam, panangin) are also prescribed in order to eliminate salt imbalances. No less important are multivitamin preparations, iron supplements, and sorbents.

With the development of stage III-IV chronic renal failure, when drug treatment It is impossible to restore kidney function; hemodialysis or kidney transplantation are used. During hemodialysis, the blood of a patient with nephrosclerosis is passed through a special membrane in an artificial kidney apparatus, which cleanses the body of toxins and metabolic end products and normalizes the water-salt balance.

The frequency of hemodialysis procedures depends on the patient’s condition and the degree of functional activity of the kidneys. During hemodialysis, the patient is prescribed antihypertensive drugs, vitamins, potassium supplements and other medications.

Carrying out hemodialysis procedures for nephrosclerosis

A kidney transplant is a radical method that allows the patient to lead his usual lifestyle. A donor organ can be taken from a corpse or from a living donor (for example, from relatives with their consent). After kidney transplant surgery, patients are prescribed special medications that suppress the activity of the immune system to prevent rejection of the donor organ.

Doctor's note: you need to remember that a kidney transplant operation is extremely dangerous, since it can entail many complications such as bleeding, rejection of the transplanted kidney, and urological complications. Therefore, resorting to this method of treatment should only be used as a last resort.

If the patient has glomerulonephritis or chronic renal failure, they also resort to hirudotherapy (treatment medical leeches). In this case, leeches are placed in the lumbar zone, sacral zone, lower abdominal and hepatic zones. Advantage is given to the lumbar area. During one session of hirudotherapy, from 2 to 8 leeches are used, depending on the severity of the patient’s condition. The course of treatment includes from 7 to 12 procedures, with the first 5 procedures performed at intervals of a day, and the next 2 times a week.

Also used in the treatment of renal nephrosclerosis traditional medicine, preparing infusions from different medicinal herbs, For example:

• It is recommended to drink birch sap, which cleanses the kidneys; alcohol infusion from aspen buds, take 30 drops diluted in a tablespoon of water before meals;
• lingonberry infusion, for the preparation of which take 1 tablespoon of lingonberry fruits, 200 ml of boiled water, take 1 spoon 4 times a day;
• infusion of strawberry leaves (10 g), birch (20 g), nettle (20 g) and flax seed (50 g). Take 100 ml 4 times a day before meals;
• licorice infusion, which is prepared from 2 tsp. licorice and one and a half glasses hot water. The infusion should be drunk in several doses throughout the day.

Features of nutrition in nephrosclerosis

To achieve maximum effects from treatment, you need to eat properly and rationally. When creating your diet, you must adhere to some rules, namely:

• limit protein because it is a substrate for the production of urea. Among protein foods, preference should be given to poultry, rabbit, lean beef, fish, dairy and fermented milk products, and egg whites. You should exclude bread, cereals, and potatoes from your diet;
• for patients with nephrosclerosis, the diet must include dairy and fish products, but you should not abuse them, as they contain a lot of phosphorus;
• Limit salt as it increases swelling. In the early stages, up to 10-15 g of salt per day is allowed, in the later stages up to 3-7 g. But salt should not be completely abandoned, as this can lead to dehydration of patients; include foods rich in calcium and potassium in your diet; calcium is found in peas, beans, green vegetables, and whole grain flour. Foods such as raisins, dried apricots, bananas, and chocolate are rich in potassium. But in the later stages of nephrosclerosis, foods containing potassium should be limited;
• nutrition should provide a sufficient amount of calories and vitamins;
• You need to eat 4-5 times a day in small portions.

Doctor's opinion: in the initial stages of nephrosclerosis, when blood pressure is not elevated and there is no swelling yet, water may not be limited. But in the later stages, the volume of liquid should be no more than 800-900 ml per day.

An approximate menu for a patient with nephrosclerosis is as follows:

First breakfast: low-fat boiled fish, sourdough bread, butter, weak tea with lemon.

Second breakfast: buckwheat porridge with milk, compote.

Lunch: vegetable soup, boiled lean meat (chicken, rabbit, turkey), baked potatoes, fruit juice.

Dinner: rice porridge with dried apricots, dried fruit compote. An hour before bedtime: crackers, jelly.

Forecast

Nephrosclerosis is a chronic disease that lasts a long time with alternating periods of exacerbations and remissions. Therefore, with good compensation for the underlying disease, following the diet and doctor’s prescriptions, the patient will be able to reduce the number of periods of exacerbations and lead an active life. But a malignant course of nephrosclerosis is also possible, in which kidney function quickly deteriorates, nephrons die and chronic renal failure sets in, which in the future can only be compensated with the help of hemodialysis or kidney transplantation.

Prevention

There is no specific prevention of renal nephrosclerosis. The main methods to prevent the progression of the disease are to follow a diet, avoid physical and mental stress, get enough rest, constantly monitor blood pressure, and maintain an active lifestyle.

Kidneys are vital organs, without them our body would not be able to function. Therefore, you need to remember that when you take care of them, the frequency of exacerbations of the underlying disease that caused nephrosclerosis is reduced.

Renal nephrosclerosis is a pathology accompanied by the death of nephrons and replacement of parenchyma with connective tissue. Due to such pathological changes, the kidneys are not able to function successfully, clearing the blood of toxins and waste products.

Also, due to such pathological processes, the renal organ is significantly reduced, wrinkled, and subsequently provokes the occurrence of renal failure.

Nephrosclerosis of the kidney is a disease that, by medical standards, is quite “young”, since it was discovered at the beginning of the last century.

At the same time, a close connection between two pathological processes was monitored and scientifically proven, one of which is hypertension, and the second is renal vascular sclerosis.

Causes and classification of pathology

Depending on what causes the pathology, nephrosclerosis is classified into primary and secondary.

The primary form of kidney nephrosclerosis occurs against the background of impaired blood supply to the parenchyma, which is typical for those patients who are characterized by frequent increases in blood pressure, as well as those who have been diagnosed with atherosclerosis.

Nephrosclerosis of the kidneys

Also, the primary type of nephrosclerosis develops if the patency of the renal arteries is impaired; thrombosis and thromboembolism act as the cause of such disorders.

Blockage of the renal veins can be caused by renal infarction, as well as venous stasis. Poor circulation and, accordingly, the occurrence of nephrosclerosis are quite often diagnosed in older people.

Secondary nephrosclerosis occurs after damage to the renal organs by some other pathological processes. Most often, pathologies such as pyelonephritis, glomerulonephritis, amyloidosis, and diabetes mellitus act as provocateurs of nephrosclerosis.

Secondary nephrosclerosis can be provoked by the negative effects of ionizing radiation.

If for some reason the kidneys are injured, the patient after a short period of time may discover signs of nephrosclerosis.

Doctors classify primary nephrosclerosis of the kidney into three separate forms: involutive, hypertensive, atherosclerotic.

This disease is classified into two more types depending on the course of the pathological process.

Ultrasound angiography

If the functions of the renal veins are accompanied by persistent deterioration, but only gradual and rather slow, doctors point to a benign form of nephrosclerosis.

With benign nephrosclerosis, the walls of the renal arteries thicken, after which fat begins to accumulate near them, as a result of which the lumen of the renal veins decreases, the blood flow is practically blocked.

In this regard, the blood circulation of the kidneys is disrupted, as a result of which their functioning is seriously impaired. Malignant form Kidney nephrosclerosis develops rapidly, so the patient quickly begins to feel the corresponding symptoms and just as quickly needs emergency treatment.

Symptoms

With nephrosclerosis, symptoms, unfortunately, do not appear immediately, but only in the last stages of the pathological process. In this regard, patients often seek help from a doctor only when the disease has already become irreversible.

Nephrosclerosis can be detected during laboratory tests. A large amount of protein and signs of hematuria are found in the urine. The density of the urinary fluid is noticeably reduced. Also during the diagnostic process, polyuria and nocturia are detected.

Urine protein test

The process of polyuria is characterized by an excessive increase in the total volume of urine excreted; in most cases, the amount of daily urine exceeds two liters.

Nocturia is characterized by an increase in the number of urinary processes at night; a third of the daily urine excreted occurs during this period.

Patients are faced with the appearance of swelling, which at the very beginning appears only on the face, but later spreads to the entire body. The patient's condition begins to deteriorate, and due to renal ischemia, patients are additionally seriously worried about arterial hypertension.

Due to the fact that arterial hypertension is accompanied by a malignant nature, it is very difficult to respond to any medical therapy. For this reason, patients face some additional complications that pose health risks.

In particular, coronary insufficiency may occur due to the fact that the left ventricle of the heart takes on increased loads.

Patients often become hostages to such dangerous concomitant pathologies as strokes.

Nephrosclerosis can cause vision problems. The pathology provokes retinal detachment, as well as swelling of the optic nerve papilla, and subsequently its complete atrophy, which leads to blindness.

Of course, another symptom of nephrosclerosis is pain concentrated in the lumbar region, which is characteristic of many kidney pathologies.

Diagnostics

In order to identify pathological processes, stage correct diagnosis Doctors refer the patient for a kidney diagnostic test.

When implementing diagnostic measures Laboratory tests of urine and blood are required.

Blood test

Nephrosclerosis is indicated by an increase in protein in the urinary fluid, the detection of red blood cells, and a decrease in urine density. When conducting a biochemical blood test, a decrease in the amount of protein in the blood is revealed, on the contrary.

An increase in the amount of urea and creatinine is also detected in the blood. If laboratory diagnostics are carried out when the pathology has reached its final stages, an increase in the growth of magnesium is detected in the blood, as well as potassium, which is not excreted in the urine during urination.

When conducting a general blood test, the patient may notice a decrease in hemoglobin levels, along with an increase in the number of leukocytes, which is the main sign of poisoning of the body.

However, doctors are not limited to results only laboratory research. The patient is also referred for instrumental diagnostics.

Ultrasound examination creates conditions so that the doctor can analyze the size of the renal cortex, examine salt deposits in the parenchyma, and also evaluate the functioning of the renal organs.

The patient may be referred for urography, during which images of the organ are taken, on the basis of which it is possible to identify changes in the size of the kidneys due to nephrosclerosis, as well as detect salt deposits.

Angiography

Angiography is another type of kidney diagnostics that focuses on assessing the renal veins and arteries. During its implementation, fractured arterial branches are revealed, which indicates the development of nephrosclerosis of the kidney.

To assess blood flow, Doppler of the renal vessels is used. X-rays demonstrate the functionality of the renal glomeruli and urinary tubules.

Computed tomography is accompanied by high information content, since thanks to its capabilities it is possible to obtain a holistic picture of pathological changes in the organ. When it is carried out, it is possible to identify changes in the size of the kidneys, their contour, structure and condition of blood vessels.

To clarify the malignant or benign form of nephrosclerosis, the patient is recommended to undergo a kidney biopsy, which involves taking kidney tissue for analysis.

Medical assistance

In case of kidney nephrosclerosis, treatment is primarily aimed at eliminating the pathology or cause that triggered the onset of the disease.

If the root cause is not eliminated, it is impossible to hope for a cure for nephrosclerosis in the future. It is very important to develop a treatment plan that will help restore kidney function.

Diuretics

The patient must be prepared for a fairly long-term treatment, since a short course will not eliminate all the problems that have arisen.

Doctors prescribe medications, the action of which is aimed at preventing the occurrence of blood clots. Medicines that promote vasodilation are also indicated.

Patients are prescribed diuretics to get rid of swelling. Due to the fact that nephrosclerosis is accompanied by arterial hypertension, doctors prescribe drugs that help lower blood pressure.

However, such drugs are prescribed very carefully. The urologist carefully calculates exact dosage, because sharp decline blood pressure can, on the contrary, negatively affect the patient’s health.

The issues of regulating the water-salt balance in the body must be considered. To maintain immunity, doctors recommend taking multivitamin complexes.

With nephrosclerosis, a wrinkled kidney is not able to function properly, as a result of which chronic renal failure occurs at the 3-4 stage of the pathology.

This dangerous kidney disease is characterized by the fact that breakdown products cannot be eliminated from the body naturally. For this reason, the patient needs artificial blood filtration.

Such patients are prescribed hemodialysis with a frequency depending on individual characteristics human body.

The only option to avoid hemodialysis is kidney transplantation.

In order to improve efficiency conservative treatment the patient is recommended to adhere to a special diet, as well as to maintain a correct daily routine, which should include sufficient time for rest.

Patients whose kidney function has been compromised should not engage in heavy physical labor.

So, nephrosclerosis is dangerous disease, if the patient ignores his treatment in the first stages of the development of the pathology. Only with strict adherence to all doctors’ instructions can it be possible to reduce the number of exacerbations that occur, increase the performance of the kidneys, restore their functioning, and, accordingly, avoid the occurrence of renal failure.

Not a single kidney disease goes away without a trace; any pathological process in the kidney leads to damage and death of its structural and functional units - nephrons. The loss of single nephrons does not affect the function of the organ in any way. With the massive death of renal structures, they are replaced by connective tissue, and the function of the kidney is lost.

The process of replacing functioning nephrons with connective tissue is nephrosclerosis. This is not independent disease, A possible outcome any pathological processes in the kidney. The outcome of nephrosclerosis is complete loss of function, reduction in size and ultimately shrinkage of the kidney. Sometimes doctors even replace the term “nephrosclerosis” with the concept of “wrinkled kidney”; in essence, they are the same thing.

Causes of nephrosclerosis

Atherosclerosis of the renal arteries will sooner or later lead to nephrosclerosis.

There are two forms of this pathology: primary and secondary wrinkled kidney.

• Primary nephrosclerosis is caused by vascular damage and impaired blood supply to the renal tissue as a result of hypertension, atherosclerosis of the renal vessels and renal infarctions, and impaired venous outflow. The structure of the kidneys undergoes sclerotic changes with age; by the age of 70, the number of active renal structural units in the kidneys decreases by 30-40%.
• The secondary form of the disease occurs as a result of damage to the kidney parenchyma during prolonged glomerulonephritis, chronic pyelonephritis, urolithiasis, autoimmune processes, diabetes mellitus, amyloidosis, syphilis, kidney tuberculosis; severe nephropathy in pregnant women and organ trauma can lead to nephrosclerosis.

IN last decades The main causes of this pathology are considered to be hypertension and diabetes mellitus, although literally 20 years ago glomerulonephritis was in the lead.

Main symptoms of nephrosclerosis

The disease can last for decades, with the deterioration of kidney function occurring gradually, and the symptoms initially do not bother patients much. A doctor is often consulted when edema appears, urination problems and signs of arterial hypertension appear. With such symptoms, changes in the kidneys are often irreversible, and the function of the organ is already significantly reduced.

Urinary dysfunction

This symptom includes polyuria (excessive urination - 2 liters per day or more) and nocturia (increased number and volume of urination at night).

In severe forms of nephrosclerosis, polyuria gives way to oliguria, when the amount of urine, on the contrary, sharply decreases. Anuria (complete absence of urine may indicate end-stage renal failure).

Also, an admixture of blood appears in the urine, and it turns the color of meat slop - this symptom is called gross hematuria.

Arterial hypertension

When the blood supply to the kidneys is disrupted, a protective mechanism is activated aimed at increasing the pressure in the renal vessels, as a result of which substances are released into the blood that increase the pressure throughout the bloodstream. With nephrosclerosis, arterial hypertension reaches very high values, possible hypertensive crises with an increase in systolic pressure to 250-300 mm Hg. Art., and it is very difficult to reduce the pressure.

Edema

Fluid retention in the body leads to edema. They first appear on the face in the morning and go away after a while. Then they gradually go down, the fingers on the hands swell (patients note that they cannot take off the rings in the morning) and shins (can’t put on shoes, can’t fasten boots). As the disease progresses, swelling spreads throughout the body, and anasarca occurs - generalized swelling of subcutaneous fat, soft tissues, and in the worst case, internal organs.

Pulmonary edema (cardiac asthma) occurs as a result of overload of the heart due to the increased amount of fluid in the body. The result is heart failure and blood stagnation in the pulmonary capillaries. The patient experiences shortness of breath, cough, sweating, cyanosis (blue discoloration) is observed during the attack. skin), increased heart rate and breathing rate. Cardiac asthma is a serious complication that can be fatal if left untreated.

Stages of nephrosclerosis

There are 2 periods in the development of this pathology:

1. In the first phase, there are no manifestations of nephrosclerosis, however, the patient has and may progress one or more diseases leading to the replacement of normal renal parenchyma with connective tissue. During this period, changes characteristic of kidney damage already appear in urine and blood tests.
2. Symptoms characteristic of nephrosclerosis, and, accordingly, renal failure, appear in the second stage of the process, when changes in the structure of the kidneys can be detected using ultrasound and other instrumental research methods.

Also, depending on the course of the pathological process, malignant and benign forms of nephrosclerosis are distinguished.

Fortunately, the vast majority of patients experience a second form of the disease, in which the process progresses slowly, with successful treatment underlying disease, the progression of nephrosclerosis can be slowed down.

In a malignant course, nephrosclerosis progresses quickly and within a few years can lead to complete loss of kidney function, severe renal failure and doom the patient to lifelong hemodialysis. Such an unfavorable outcome can be observed with malignant arterial hypertension and eclampsia in pregnant women.

Diagnosis of nephrosclerosis

With nephrosclerosis, corresponding changes will be detected in a general urinalysis.

Since the symptoms of a shriveled kidney appear in the later stages, it is very important to identify this pathology as early as possible through examination, since the effectiveness of treatment in this case will be much higher. Taking the patient's medical history plays an important role.

• General urine analysis. Any kidney examination, of course, begins with a urine test, with initial nephrosclerosis the following deviations from the norm can be detected: a decrease in the relative density of urine, the appearance of protein, single red blood cells and cylinders.
• Blood tests. In a clinical blood test, a decrease in the level of hemoglobin and platelets is possible. In biochemical – a decrease in the amount of total protein, an increase in the level of urea, creatinine, uric acid and sodium. An increase in glucose and cholesterol levels should alert you.

Such changes in urine and blood tests are very nonspecific and can be observed not only in kidney diseases. However, the combination of such deviations in laboratory test results, in the presence of a history of factors that can lead to kidney damage, forces the doctor to think about further diagnosis.

For examination, many instrumental methods are used, such as ultrasound, excretory urography (x-ray of the kidneys with contrast agent), angiography, computed tomography, radioisotope studies, etc. All of them reveal a decrease in the size of the kidney, the presence of calcium deposits, impaired blood flow in the renal vessels and other changes indicating the proliferation of connective tissue. A biopsy can give an accurate answer about the condition of the renal parenchyma.

Treatment of nephrosclerosis

There is no specific therapy aimed at treating nephrosclerosis. It is necessary to treat the disease, which has led to kidney damage and death of nephrons, followed by their replacement with connective tissue. That is why not only a nephrologist, but also a specialized specialist treats patients with nephrosclerosis.

In addition to therapy aimed at treating the underlying disease, patients must follow a diet. It is recommended to limit the amount of protein and table salt; the diet should have enough vitamins and mineral salts. In the absence of arterial hypertension and edema, fluid and protein restriction is not required.

In end-stage renal failure, when both kidneys have lost their functions, patients are advised to undergo hemodialysis. The only way out in this situation is kidney transplantation; in recent years, this operation has been successfully carried out in Russia, and for citizens of our country it is free.

Which doctor should I contact?

A nephrologist treats kidney diseases and their complications, in particular nephrosclerosis and renal failure. If necessary, consultations with other specialists are prescribed: a cardiologist (if high blood pressure), endocrinologist (for diabetes), vascular surgeon(for atherosclerosis of the renal artery), a urologist (for urolithiasis), an infectious disease specialist (for suspected kidney tuberculosis). You can get a referral for a kidney examination by contacting your general practitioner with relevant complaints.

Nephrosclerosis- chronic kidney disease, in which functional kidney cells (nephrons) gradually die, and connective tissue grows in their place (not responsible for the functioning of the organ).

As a result, the kidneys become denser, wrinkle, decrease in size and cease to perform their functions - chronic renal failure develops ( international name - chronic disease kidney).

Nephrosclerosis is not an independent disease. A large number of severe illnesses lead to its formation: diabetes mellitus, arterial hypertension and others.

Statistics

In the last century, the “palm” for the reason leading to the development of nephrosclerosis resulting in chronic renal failure (CRF) belonged to glomerulonephritis. Whereas now the first place is occupied by diabetes mellitus and arterial hypertension.

In Europe, according to statistics, chronic renal failure occurs in 600 cases per 1,000,000 inhabitants.

The number of patients with nephrosclerosis who are on hemodialysis (artificial kidney) with chronic renal failure ranges from 10 to 20%. Moreover, the mortality rate among patients with chronic renal failure reaches 22% per year.

Story

Nephrosclerosis is a relatively “young” disease. For the first time, the idea that nephrosclerosis affects the vessels of the kidneys was expressed by Gall and Sutton only in 1872.

Then in 1914, Volgard and Fahr proved that arteriosclerotic changes (deposition of “harmful” fats) occur in the vessels of the kidneys, linking them with high blood pressure. They also identified nephrosclerosis in separate disease, proposing to divide it into simple and malignant forms.

A doctor by training and a writer by vocation, Mikhail Bulgakov, passed away from nephrosclerosis. He authored famous works that have not lost their relevance even today: “The Master and Margarita”, “Notes of a Young Doctor” and others.

In a letter sent to his friend a few months before his death, Bulgakov wrote: “Dying is painful, boring and vulgar. As you know, there is one decent type of death - from firearms, but, unfortunately, I don’t have that.”

Anatomy and function of the kidneys

The kidney is a paired, bean-shaped organ located on the sides of the spine in the lumbar region.

The kidney contains renal tissue (parenchyma) and the pyelocaliceal system.

Kidney tissue consists of a cortex (contains nephrons, the smallest units of the kidney) and a medulla (contains urinary tubules). Urine is produced in the kidney tissue.

Pyelocalyceal system consists of calyces and pelvis, in which urine accumulates and is then excreted.

The outside of each kidney is covered with a capsule.

Nephron structure

It consists of a vascular glomerulus (closely intertwined small blood vessels) - a renal corpuscle, which is surrounded by a spherical capsule (Shumlyansky-Bowman).

The structure of the glomerulus

The renal artery, having reached the renal tissue, decreases in diameter and branches, forming the afferent atreriole (a small-caliber artery).

Having entered the capsule, the afferent arteriole branches into the smallest vessels - a glomerulus is formed, which has about 50 loops. When leaving the nephron capsule, the vascular loops unite and form the efferent arteriole.

The walls of the glomerular vessels have complex structure, due to which “windows” are formed.

Capsule structure

Consists of outer and inner leaves, and between them there is a cavity into which it penetrates liquid part blood from the glomerulus with substances dissolved in it.

The urinary tubules of the nephron begin from the glomerular capsule, which flow into the collecting urinary tubules. Then they unite with each other and open into the renal cups of the pyelocaliceal system.

Mechanism of blood filtration and urine formation

First, arterial blood enters choroidal glomerulus. Here, through the “windows” in the walls of the glomerular capillaries, the liquid part of the blood, together with the substances dissolved in it, seeps into the lumen of the nephron capsule.

Moreover, the “windows” let through both useful substances(for example, amino acids) and harmful (toxins, drugs). However, with such filtration, blood elements (erythrocytes, leukocytes), blood proteins and large molecules are retained. This is how primary urine is formed (150-180 liters per day).

Next, primary urine enters the urinary tubules, in which beneficial substances (vitamins, fats, glucose) and water are reabsorbed, and harmful substances, on the contrary, accumulate. This is how primary urine turns into secondary urine (about 1.5-2.0 liters per day).

Then secondary urine enters the collecting ducts, then into the pyelocaliceal system of the kidney, then into the ureter and bladder. During the act of urination, secondary urine is removed from the body.

Kidney functions

• Removal from the body excess fluid, toxins, end products of metabolism of certain substances (urea, creatinine, bilirubin), allergens, medications and others.
• Hormone production:
  • Renin, which is involved in the regulation of vascular tone and blood pressure (the conversion of angiotensin I into angiotensin II), the content of sodium and potassium salts in the body, as well as the reabsorption of water in the urinary tubules,
  • Erythropoietin, which stimulates the formation of red blood cells (erythrocytes) in the bone marrow.
• Maintaining blood acidity(normal blood pH is from 7.37-7.44).
• Synthesis of a substance (urokinase), which regulates blood clotting.
• Converting vitamin D to its active form, improving the absorption of calcium and phosphorus in the small intestine.

Causes and classification of nephrosclerosis

Depending on the underlying disease, nephrosclerosis can be primary (caused by impaired blood supply to the kidneys) and secondary (develops when the kidney parenchyma is damaged). As a result, the nephrons do not receive enough nutrition and oxygen, so they atrophy (reduce in volume and lose viability), and connective tissue grows in their place.

Causes of primary nephrosclerosis (primary shriveled kidney)

Hypertension

A prolonged increase in blood pressure (BP) causes spasm and constriction of the blood vessels of the kidneys, they lose their elasticity, their pressure and resistance to blood flow increase.

Hypertensive nephrosclerosis occurs in two variants:

• Benign nephrosclerosis(arteriolosclerotic nephrosclerosis) - when connective tissue grows in the walls of the arteries of the kidneys, which leads to a decrease in their elasticity. The disease develops over 10 years or more. Often this form is combined with atherosclerosis (vascular disease).
• Malignant nephrosclerosis(arteriolonecrotic nephrosclerosis, Farah nephrosclerosis) develops over a short time (several years) with severe course arterial hypertension (AH). In this disease, the arterioles and capillaries of the glomeruli die. Hemorrhages also occur in the wall of the urinary tubules, leading to atrophy of the cells of their inner layer (they decrease in size and lose viability).

Kidney infarction

Partial or complete blockage of the lumen of the renal artery occurs with a detached blood clot(thrombosis) or embolus (for example, a cluster of microbes in pyelonephritis). As a result, the lumen of the arteries narrows. Therefore, the flow of blood to the kidney or its individual zones decreases - heart attacks develop (areas of living tissue die).

In single and small heart attacks, the work of the kidney is compensated. Whereas with repeated and extensive heart attacks dies larger number nephrons, leading to the development of nephrosclerosis.

Atherosclerosis

Fat-like substances - “harmful” fats (atherosclerotic plaques) - are deposited on the inner wall of the arteries throughout the body. Therefore, the lumen of the arteries narrows, and their walls thicken and become less elastic. As a result, the cells of organs and tissues are insufficiently supplied with blood, dying over time. The smaller the caliber of the arteries, the faster changes occur in them.

The most “favorite” areas of atherosclerotic plaques in the kidneys are the places where the renal artery enters the kidney, or where it divides into smaller branches.

Age-related changes

Starting from 40-50 years, the walls of the arteries thicken, and their lumens narrow. The reason is the deposition of calcium on the inner lining of the artery wall, the accumulation of smooth muscle fibers and connective tissue.

Age-related changes in the kidneys lead to thinning of the cortex and atrophy of the cells of the inner layer of the urinary tubules (lose function and viability).

By age 70, the number of nephrons in the kidneys decreases by about 40%.

Chronic venous congestion of the kidneys

It leads to disruption of the outflow of venous blood from the kidneys, creating conditions for excessive growth of collagen (the protein that is the basis of connective tissue) in the wall of the kidney vessels. Therefore, their elasticity decreases.

Changes develop over a long period of time (10 years or more) with nephroptosis (prolapse of the kidneys), narrowing of the renal vein and chronic venous thrombosis.

Causes of secondary nephrosclerosis (secondary wrinkled kidney)

Diabetes mellitus

Against the background of increased blood sugar levels, complex compounds are formed that are deposited on the inner wall of blood vessels (primarily small ones), damaging them. As a result, the vascular wall swells and thickens, and its permeability increases. Therefore, protein gets into the urine (diabetic nephropathy develops).

Also, when the cells of the inner wall of blood vessels are damaged, clotting factors are released into the blood. Therefore, the formation of blood clots in the lumen of the kidney vessels increases.

The changes lead to a slowdown in blood flow in capillaries (small vessels) and a decrease in the supply of oxygen to cells in almost all organs and tissues. That is, not only the kidneys are affected, but also other organs (eyes, heart).

Nephropathy of pregnancy (late toxicosis)

Against the background of hormonal changes in the body during pregnancy, the work of the brain changes, which sends “wrong commands” to all capillaries, leading to their spasm.

Therefore, resistance to blood flow in the vessels increases, and blood pressure rises. As a result, the blood supply to the kidneys deteriorates and nephrons die.

The permeability of the glomerular capillary wall also increases, so salts are retained in the body, and protein is lost in the urine. Such changes contribute to the formation of edema (the release of liquid into the surrounding tissues) and maintain blood pressure at high levels.

In response to an infection (sore throat, pharyngitis), the body produces antibodies (immune system proteins that fight “foreigners”), which, interacting with an antigen (bacterial protein or toxin), form circulating immune complexes(TsIKi) - a protective reaction of the body. Normally, CECs are destroyed by the liver and phagocytes (cells of the immune system). However, if there are disturbances in the functioning of the immune system, this does not happen.

With the blood flow, CECs enter the kidneys and damage the inner lining of the glomerular vessels. At the same time, substances are released into the blood that enhance the formation of blood clots in the lumen of the glomerular vessels, and hyaline (a protein substance of dense consistency) is deposited in their walls. As a result, the elasticity decreases and the permeability of the glomerular vessel wall increases, which leads to impaired blood flow.

Chronic pyelonephritis

Microbes with blood flow or reverse reflux of urine from bladder enter the renal glomeruli and the lumen of the urinary tubules, settling in them. White blood cells accumulate around bacterial clots. During recovery, scars form in their place; if recovery does not occur, ulcers form. When the disease lasts for a long time, the number of scars increases, leading to the death of a large number of nephrons.

Urolithiasis, narrowing or compression of the ureter

In the pyelocaliceal system and ureters, the outflow of urine is disrupted. Therefore, it stagnates, creating conditions for the proliferation of bacteria in it (normally urine is sterile, but during inflammatory processes it contains bacteria). Then the microbes enter the urinary tubules and glomerular vessels with the reverse reflux of urine, damaging their inner wall.

Kidney tuberculosis

With the flow of blood from the lesion (for example, easily), tuberculosis bacilli enter the kidneys, settling on the inner wall of the glomerular vessels. Leukocytes gather around the accumulation of bacteria, forming foci of inflammation. As a result, blood flow slows down and blood vessels narrow, disrupting the flow of blood to the glomeruli.

Systemic lupus erythematosus

With this disease, the immune system “does not recognize” its own tissues, mistaking them for “foreign” ones. Therefore, it tries to destroy normal cells of the body, damaging them. As a result, circulating immune complexes (CICs) are formed in the blood, which consist of an antibody (a protein of the immune system designed to fight “strangers”) and an antigen (particles from the surface of normal cells of the body).

CECs with the bloodstream reach the renal tissue and damage the inner wall of the glomerular vessels. Therefore, inflammation develops, which leads to the death of nephrons.

Kidney amyloidosis

There is a violation of protein metabolism: an abnormal protein is formed - amyloid, which becomes a “stranger” (antigen) for the body. Therefore, the immune system fights it by producing antibodies. The antibody and antigen, interacting, form CECs, which reach the kidneys through the bloodstream and damage the inner wall of the glomerular vessels. As a result, nephrons die. Simultaneously with kidney damage, the lungs, heart and other organs are involved in the process.

Kidney injury or surgery

Particles of kidney tissue can clog the lumen of the arteries and arterioles of the kidney. Therefore, the blood supply to a separate area of ​​the kidney is sharply disrupted, leading to the death of nephrons.

Ionizing radiation

Causes the development of disease years or months after exposure to the body. Moreover, changes occur in all vessels of organs and tissues. The degree of their severity depends on the dose and type of ionizing radiation.

What's happening? The walls of the kidney vessels gradually thicken, and their lumen narrows, therefore the blood flow in the nephrons decreases.

Symptoms

With nephrosclerosis, nephrons gradually die, and the kidneys cease to perform their functions. As a result, the functioning of the entire organism is disrupted, which is manifested by certain symptoms, the severity of which depends on the number of dead nephrons.

Signs of nephrosclerosis

Symptom	Mechanism of occurrence	External manifestations	Changes in ongoing research
Polyuria	The reabsorption of fluid in the urinary tubules from primary urine decreases.	During the day, the patient produces more urine than he drank water - more than 1800-2000 ml.	In a general urinalysis (UCA) or during the Zemnitsky test, the specific gravity (relative density) of urine decreases - an indicator characterizing the concentration of substances dissolved in the urine (urea, uric acid salts).
Oliguria - decreased volume of daily urine	A large number of nephrons die (70-75%), so blood filtration and urine formation are impaired.	The volume of daily urine decreases to 500-800 ml per day (the norm is 1200-1500 ml). Patients have swelling, thirst, dry mouth, nausea, and vomiting.	During the day, urine is collected in a separate container. If its volume is less than 1/3 - ¼ of the norm, we are talking about oliguria.
Nocturia - more urine is produced at night than during the day	Under resting conditions, blood vessels relax and blood flow in the kidneys increases.	Increased volume and frequency of urination at night. Normally, 2/3 of the daily urine volume is excreted during the day, and 1/3 at night.	The Zemnitsky test determines the volume of urine excreted in different portions day and night, as well as the density of urine.
Anuria - lack of urine	It develops when about 90% of nephrons die, so urine is not formed.	There is dry mouth, thirst, nausea and vomiting, severe swelling, headache, drowsiness and lethargy, muscle pain. If help is not provided, the patient dies from self-poisoning 10-12 days from the onset of anuria.	A catheter is used to penetrate the bladder. If it contains less than 50 ml of urine, we are talking about anuria. The biochemical blood test showed increased levels of creatinine, urea and sodium.
Proteinuria- excretion of proteins in urine	Due to damage to the wall of the glomerular vessels, proteins from the blood enter the primary urine, but do not return to the bloodstream in the urinary tubules.	Swelling may appear, the severity of which depends on the volume of dead kidney tissue.	Protein is detected in the TAM, but in a biochemical blood test it decreases.
Hematuria- excretion of blood in the urine	The damaged wall of the glomerulus allows red blood cells to pass into the primary urine, and in the urinary tubules they do not return to the bloodstream.	The urine may turn red, which resembles “meat slop.”	Red blood cells are detected in the TAM.
Cylindruria	In the lumen of the urinary tubules, cylinders are formed, which are casts of blood proteins or altered cells of the mucous membrane of the urinary tubules.	The symptom is unexpressed and inconsistent.	Cylinders are detected in the OAM.
Iron deficiency anemia - decrease in blood hemoglobin	The production of erythropoietin, which stimulates the formation of red blood cells in the bone marrow - hemoglobin carriers, is disrupted.	There is weakness and fatigue, dizziness, fainting, shortness of breath, palpitations.	In the CBC (general blood test), the level of hemoglobin and red blood cells decreases.
Azotemia	It develops when 65-70% of nephrons die, so the end products of protein metabolism (urea, creatinine) are not excreted from the body.	Patients complain of nausea, vomiting, weakness, rapid heartbeat, thirst, weakness and drowsiness or agitation. There is a sour ammonia odor from the mouth and painful itching of the skin. The skin takes on a yellowish tint. Daily urine volume is reduced.	The level of urea and creatinine in the blood is increased.
Uremia - urine in the blood	Develops when 90% of nephrons die. As a result, the kidneys do not excrete the end products of protein metabolism, toxins, medications, and others. harmful substances. Therefore, they accumulate and lead to self-poisoning of the body, and also have a toxic effect on the brain.	Symptoms of azotemia are accompanied by severe nerve damage with impaired sensitivity, decreased strength and volume of muscles (atrophy). “Uraemic frost” appears on the skin - the deposition of urea crystals. There is no urine or its volume is sharply reduced. The patient smells of urine.	There is a persistent increase in urea and creatinine levels in the blood.
Edema	The body retains sodium and water. Sodium attracts water, increasing fluid retention. The body loses proteins in urine. The permeability of all capillaries is increased. Such changes lead to the fact that the liquid part of the blood easily penetrates into the surrounding tissues, but does not return back to the bloodstream.	The swelling is warm. They appear first on the face. Then they fall down, distributed evenly throughout the body. The severity of edema varies: from a slight swelling (pasty) of the face and legs to a feeling that the whole body is soaked in water. Sometimes 2-7 liters of fluid are retained in the body, forming “hidden edema”, which cannot be detected by the eye.	The patient's weight increases - from 0.5 to 1 kg per day. Therefore, it is advisable to weigh yourself daily, as well as measure the amount of fluid you drink and excrete.
High blood pressure (BP)	In the kidneys, the production of renin is increased, which contributes to an increase in blood pressure - compensatory mechanism, which temporarily improves blood circulation in the kidneys. Whereas with a prolonged increase in blood pressure, the blood supply to the kidney tissue deteriorates. Renin also promotes sodium and water retention in the body, which helps maintain blood pressure at high levels.	In the initial stages of the disease, the patient quickly gets tired, complains of headaches and dizziness, memory loss, and numbness in the fingers. At the moment of a sharp increase in blood pressure to high numbers (crisis), severe headache appears (usually in the back of the head), nausea or vomiting, difficulty breathing, spots before the eyes, agitation, irritability or squeezing pain in the region of the heart.	With nephrosclerosis, blood pressure remains at high levels, and it is much more difficult to reduce it to normal levels. Hypertensive crises often develop with an increase in blood pressure to 250/130 - 300/140 mmHg.
Visual impairment	Retinal detachment Fluid accumulates under the retina, which gradually peels it off. Papilledema The outflow of fluid from the part of the optic nerve located in the orbital cavity is disrupted (normally it flows into the cranial cavity). This leads to the development of swelling of the optic nerve papilla, as well as compression of its fibers.	With retinal detachment At the beginning of the disease, a veil appears before the eyes or flashes in the form of lightning and sparks. As the disease progresses, the letters and objects in question become distorted. Areas of vision fall out (appear dark spots), the size of which gradually increases, leading to blindness. With swelling of the optic nerve papilla symptoms develop gradually. First, headaches appear, then there is a veil before the eyes. Further, a certain part of vision falls out from time to time, then vision sharply deteriorates or disappears.	The examination is carried out by an ophthalmologist using a special instrument. With retinal detachment zones of its rupture or detachment are detected. Also, when the eye is illuminated with bright light, the patient can see his own retinal vessels in the form of “cracks” or “convolutions”. For papilledema changes are visible that depend on the stage of the disease. The disc may become swollen, red, or bluish color. At the last stage there is optic nerve atrophy
Tendency to bleed	In the kidneys, the production of urokinase, a substance that regulates blood clotting, decreases.	Bleeding from the gums, nasal cavity and intestines; subcutaneous hematomas (“bruises”) easily appear on the skin from the slightest injury.	Blood clotting time and bleeding duration increase. The level of platelets in the blood decreases - cells involved in blood clotting processes.
Attacks of angina	Increased output Renin causes vasospasm, which leads to a sharp lack of blood supply to a certain area of ​​the heart - ischemia develops. Ischemia can also occur if there is an atherosclerotic plaque in the lumen of the artery that supplies the heart muscle.	Due to physical activity or stress, the patient experiences pain (sharp, squeezing or pressing), as well as discomfort in the heart area or behind the sternum. Sometimes the pain radiates to left side torso: shoulder blade, arm, neck or jaw. During an attack, fear, dizziness, difficulty breathing, nausea or vomiting, and palpitations may occur. The attack usually lasts 1-5 minutes (less often 15-20 minutes).	Changes are visible on the ECG taken during the attack itself.
Cardiac asthma	A prolonged increase in blood pressure, vasoconstriction and fluid retention in the body leads to an increase in the load on the heart muscle of the left ventricle. Therefore, working with greater force, it increases in size. As a result, failure of the left ventricle develops, which can no longer cope with its work. Therefore, blood stagnates in the pulmonary vessels and pulmonary edema develops.	The first to appear is shortness of breath (difficulty breathing) when physical activity or excitement during the day. Then night attacks occur (usually in the first half of the night): the patient wakes up from a feeling of lack of air. He develops severe shortness of breath, a cough with small quantity mucous sputum, fear of death, profuse cold sweat, pulse quickens, skin turns blue. During an attack, it is easier for the patient to sit with his legs down from the bed.	When listening to the lungs during an attack, moist rales are heard (more in lower sections lungs).
Headaches	The production of renin in large quantities causes a narrowing of the capillaries and leads to an increase in blood pressure to high numbers. As a result, the correspondence between the receipt arterial blood to the brain and the outflow of venous blood from it (stagnation develops). In addition, due to vascular spasm, the brain is not sufficiently supplied with blood (ischemia occurs), so it lacks oxygen and nutrients.	They can be located in any area, but most often in the back of the head. As a rule, the pain is throbbing: patients complain of “dull blows to the head,” pulsation in the temples, or “pounding in the head.” However, the pain can be pressing or dull - with chronic cerebral ischemia.	An ophthalmologist examines the fundus of the eye using special equipment, assessing the condition of the fundus vessels (veins and arteries): they can be narrowed or dilated and full of blood.
Increased bone fragility	The conversion of vitamin D by the kidneys is disrupted, which reduces the absorption of calcium in the intestine. In response, according to the feedback principle, the production of parathyroid hormone by the parathyroid glands increases, which “washes out” magnesium and phosphorus from the bones. As a result, bone tissue is discharged and osteoporosis develops.	Tendency to pathological fractures with minimal trauma or falling from one's own height.	The level of calcium in the blood decreases, and the level of phosphorus increases. Densitometry (bone testing) shows a decrease in bone density.
Tendency to frequent viral and bacterial diseases	Caused by the underlying disease and medications taken medicines(hormones, cytostatics and others) that impair the functioning of the immune system.	Severe frequent viral and bacterial infections: ARVI, stomatitis, gingivitis, furunculosis and others.	Changes in TAM, CBC and biochemical analysis, indicating a worsening of nephrosclerosis and the presence inflammatory process in the body.

With nephrosclerosis, nephrons die gradually, affecting individual areas of the kidney tissue. Therefore, the disease goes through several stages in its development, the duration of which depends on the treatment, diet, the primary cause of the disease and other factors. Therefore, before pronounced symptoms of nephrosclerosis appear, years pass, sometimes decades, less often months or weeks.

Periods of nephrosclerosis

First period is caused by manifestations of a disease that leads to disruption of the blood supply to the kidneys in certain sections.

Second period characterized by the gradual death of nephrons and replacement of the renal parenchyma with connective tissue - chronic renal failure (CRF) develops. Depending on the volume of dead kidney tissue, CRF goes through several stages in its formation.

Stages of chronic renal failure

First stage

Patients get tired quickly during physical activity or in the evening. They have decreased ability to work, have slight dry mouth, thirst, polyuria, and nocturia. But in general the patients feel good. In a biochemical blood test, the content of sodium, phosphorus and calcium sometimes changes. Protein may be detected in the TAM, and the relative density of urine may decrease.

Second stage

Symptoms of azotemia appear: decreased appetite, lethargy, itchy skin, nausea and vomiting. Vision is impaired, headaches occur, heart rate increases, heart rate. Blood pressure rises to high levels and is difficult to reduce. The volume of daily urine decreases. In a biochemical blood test, the level of urea and creatinine increases.

At this stage, as the course of the underlying disease improves, tests and the volume of daily urine are normalized, and the well-being of patients improves.

Third stage

Kidney function deteriorates sharply, the volume of daily urine decreases. Patients are weakened, get tired quickly, eat poorly, and are constantly thirsty. They are prone to frequent and severe bacterial or viral infections(ARVI, stomatitis, pustular infections on the skin). The skin is dry, acquires a yellowish tint - due to the accumulation of bile pigment derivatives in the body (normally excreted in the urine, coloring it yellow). The level of creatinine and urea in the blood is increased.

Fourth stage

There is no urine, or its daily volume is sharply reduced, so symptoms of self-poisoning (uremia) increase. Sleep is disturbed, memory is reduced, pulmonary edema develops, there are blood clotting disorders, blood pressure remains high, and so on. There is a persistent increase in creatinine, uric acid and urea in the blood, and total protein is reduced.

All changes that occur at the fourth stage are irreversible.

Diagnosis of nephrosclerosis

Manifestations of nephrosclerosis are most striking in the later stages of the disease. Therefore, it is necessary to recognize the disease as early as possible so that the patient receives timely treatment.

Laboratory research

The goal is to detect changes in kidney function at an early stage.

Biochemical blood test

Indicators indicating renal dysfunction:

• Urea levels increase(2.5-8.3 mmol/l), creatinine(in women - 50-100 µmol/l, in men - 60-115 µmol/l) and uric acid(210 - 420 µmol/l).
• Total protein decreases(65-85 g/l).
• Potassium(3.5-5.5 mmol/l) in the initial stages remains normal or decreases, since it is excreted along with the fluid that the body loses in large volumes. On final stage Potassium levels increase because they are not excreted in the urine, accumulating in the body.
• In the final stages, magnesium levels increase(0.8-1.2 mmol/l) and phosphorus(0.81-1.45 mmol/l). While the calcium content (2.15-2.65 mmol/l) decreases.
• Sodium rises(123-140 mmol/l). However, it may also decrease if the patient sharply limits the consumption of table salt.

General urine test

(standards for adults are given in parentheses in the text)

• Increased protein content(absent or present up to 0.033 g/l)
• Red blood cells appear(0-2-3 red blood cells in the field of view of the microscope) and cylinders (normally absent).
• Relative density of urine decreases (1.010 – 1.022 g/l)

General blood test

(standards for adults are given in parentheses in the text)

Hemoglobin levels decrease(in men - 130-160 g/l, in women -120-150 g/l), red blood cells (3.5 * 10 12

/l – 5.0*10 12 /l). While the level of leukocytes (4-9x10 9) due to self-poisoning, on the contrary, increases.

Platelet levels decrease(180 - 320 *10 9 /l). At the same time, the blood clotting time increases (the beginning of coagulation is from 30 seconds to 2 minutes, the end of coagulation is from 3 to 5 minutes) and the duration of bleeding (2-3 minutes).

Instrumental research methods

They include both the study of blood vessels and the structure of the kidneys.

Ultrasound examination (ultrasound)

For nephrosclerosis there is atrophy (reduction in size and cessation of function) of the renal cortex in relation to the medulla. There is sometimes no separation (differentiation) between the two layers. Deposits of calcium salts in the kidney parenchyma (nephrocalcinosis) are also visible, which indicate the death of kidney tissue.

Excretory urography of the kidneys

The method is based on the fact that the kidneys are capable of secreting certain radiopaque iodine-containing substances introduced into the body intravenously. As a result, X-rays taken at regular intervals provide images of the kidneys and urinary tract.

For nephrosclerosis the volume of the kidney and the size of the cortex are reduced. Deposits of calcium salts (nephrocalcinosis) are often detected.

Angiography of renal vessels

A contrast agent is given intravenously. Then a series of pictures are taken, in which the doctor then assesses the degree of narrowing of the kidney vessels, the presence of an obstruction to blood flow, and so on.

For nephrosclerosis there is deformation and narrowing of small arterial vessels, there is an uneven outer contour of the kidneys and thinning of the cortex. In addition, the symptom of “burnt wood” is visible - when the branches of the renal artery are narrowed and broken, and there is no fine pattern of the arteries.

Renal scintigraphy

A special radioisotope substance is injected intravenously, which is excreted by the kidneys, emitting radiation. This radiation is captured by special equipment and then transmits the image to a computer.

For nephrosclerosis The radioisotope substance is distributed unevenly. Sometimes only isolated areas of kidney tissue are preserved, and sometimes the kidney is not visible at all.

Doppler of renal vessels

Special equipment emits and directs ultrasonic waves, which, upon reaching the organ, are reflected and captured by special equipment. The information is then transferred to a computer where the data is processed.

For nephrosclerosis the method reveals a slowdown in blood flow in the renal vessels and nephrons.

Radionuclide renography

It is considered the most sensitive method in the early stages of kidney disease. Since it allows you to evaluate the function of each kidney, the state of blood flow in the glomeruli, as well as the excretion of urine by the tubules.

A radiopharmaceutical is injected intravenously, which is filtered by the glomeruli and excreted from the body. The drug emits radiation, which is detected by special equipment.

For nephrosclerosis the special drug accumulates and is excreted more slowly by the kidneys.

Computed tomography

To diagnose nephrosclerosis, CT and angiography are combined (administration of a contrast agent intravenously before examination). This allows you to evaluate the structure, structure and position of the kidney, as well as the condition and function of the kidney vessels.

For nephrosclerosis small arterial vessels are narrowed and deformed, the cortex is thinned, and the kidney itself may be reduced in size. There are changes in the vessels: narrowed and broken.

Kidney biopsy

Using a special needle inserted through the skin into the kidney, the doctor obtains a small area of ​​kidney tissue. Then he sends it for research.

Treatment of nephrosclerosis

First of all, the underlying disease is treated. Without this condition, all other methods are ineffective.

Regarding the treatment of nephrosclerosis, drugs are prescribed comprehensively and for a long time (for years and months), courses of treatment are often repeated, but with short breaks between them.

Drug groups	Representatives	Mechanism of action	Directions for use
Improves renal blood flow They are prescribed in the early stages of nephrosclerosis, since in the later stages they increase bleeding.
Anticoagulants	Heparin, Hirudin. Warfarin, Angioflux	Prevents the formation and growth of blood clots in the vascular cavity, improving blood flow (especially capillaries).	Most often at the beginning of treatment they are prescribed in the form of injections, then in tablets. The course is at least 1-1.5 months.
Antiplatelet agents	Xanthinol nicotinate, Trental, Pentoxifyline, Dipyridamole	Prevent platelets (blood cells involved in blood clotting) from sticking together, improving blood flow.	At the beginning of treatment, it is recommended to use medications in injections, then in tablets. The course of treatment is about 1-1.5 months.
Drugs that lower blood pressure Prescribed with caution in the final stages, since a sharp decrease in blood pressure worsens blood flow in the kidneys.
ACE inhibitors	Captopril, Berlipril, Blockordil, Vasopren, Enalapril, Diroton	Blocks the conversion of angiotensin I to angiotensin II (constricts blood vessels) Promotes the accumulation of vasodilating hormones in tissues Due to this, the blood vessels dilate, blood flow in the kidneys improves, and the level of creatinine in the body decreases.	They are used internally for a long time - months and years. The dosage and regimen depends on the blood pressure numbers, the age of the patient, individual tolerance and other factors.
Calcium antagonists	Verapamil, Diltiazem, Amlodipine, Falipamil, Nifedipine	Expand everything small arteries and reduce resistance to blood flow. The kidneys increase blood flow and help remove excess sodium from the body.	They are used internally for a long time (years, months). The dosage and regimen depends on the blood pressure numbers, the patient’s age and other factors.
β-adrenergic receptor blockers	Betaxolol, Atenolol, Metoprolol, Propranolol.	They inhibit the production of renin by the kidneys, reduce the flow of venous blood to the heart and the total blood volume.	Use internally for a long time. The dosage regimen and dosage depend on blood pressure numbers, whether the patient is on hemodialysis, age and other factors.
Diuretics	Indapamide, Tertenstf, Ravel, Furosemide.	They remove water and sodium from the body, reducing the volume of blood in the bloodstream.	Used in the morning, orally, regardless of food intake. The dosage depends on the drug.
Alpha blockers	Prazosin, Doxazosin.	Improves blood flow in the kidneys and the rate of blood passage through the glomeruli (glomerular filtration rate).	They are prescribed orally, as a rule, starting with a smaller dose, gradually increasing it until the desired result is achieved.
Elimination of salt imbalance
Potassium preparations(prescribed with caution depending on the level of potassium in the blood and the stage of nephrosclerosis)	Panangin, Asparkam, Potassium-normine.	Normalizes heart rate, maintains normal acid-base balance blood, improves the functioning of all cells in the body.	It is used both internally and in injections. First, a therapeutic dose is prescribed for a month, then a maintenance dose for 1-2 months. Course - 2-3 months.
Replenishing the body with vitamins
Multivitamin preparations	Multivitamin complexes: Duovit, Vitrum, Ostemag, B vitamin complexes (Beneuron, Milgama) and others.	Speed ​​up and improve everything metabolic processes in the body, improving the metabolism of fats, proteins, carbohydrates, the functioning of the immune system and more.	They are used both as injections and internally in courses of 2-3 months.
Fighting osteoporosis
Calcium supplements + vitamin D	Calcium preparations in combination with vitamin D - Vitrum osteomag, Calcium D3 nikomed, Kalcemin, Complivit® Calcium D3. Vitamin D preparations (colecalciferol): Aqueous solution of vitamin D3, VIGANTOL®, AQUADETRIM® Oksidevit - predecessor active form vitamin D	Calcium preparations replenish the deficiency of this mineral, which is necessary for the synthesis bone tissue. Vitamin D improves calcium absorption in the intestines and dissolves “bad” cholesterol.	Calcium preparations prescribed orally after meals. Course - 2-3 months. Daily dose 3-5 grams. Vitamin D preparations taken orally in drops, regardless of food intake. Course - 2-3 months.
Regulators calcium metabolism- bisphosphonates	Bonviva, Xidofon, Ostalon, Aklasta, Rezorba, Osteochin	Accelerate bone tissue recovery Slows down the destruction of bone tissue	They can be administered orally, intramuscularly or intravenously. The general principle of treatment is long-term use of drugs in courses (on average 8-9 weeks). There are two dosage regimens: constantly and with breaks for several weeks.
Treatment of anemia
Erythropoietin preparations	Recormon, Ertrostim	Stimulates the formation of erythrocytes (red blood cells) in the bone marrow.	It is administered intravenously or subcutaneously. The frequency of use and dose depend on the patient’s well-being, the level of hemoglobin and red blood cells. It is used both in patients undergoing hemodialysis and at the beginning of it.
Iron supplements	Ferroplex, Ferroceron, Tardiferon, Ferrum Lek	Iron is used by the body to synthesize hemoglobin, a blood protein that carries oxygen to tissues.	For I-II degree of anemia, the drugs are taken orally, 1 tablet 3 times a day or 1-2 times (extended-release drugs). When hemoglobin is less than 70 g/l (III degree of anemia), Ferrum Lek is sometimes administered intramuscularly. However, the drug is difficult to tolerate, and patients with nephrosclerosis are already weakened. Therefore, it is not used often.
Reducing the retention of end products of protein metabolism and toxins in the body
Sorbents	Polysorb, Enterosgel Carbolen, Chitosan, Sorbex	Absorb the end products of protein metabolism, bacteria, poisons and toxins in the intestines, and then remove them from the body naturally with feces.	Taken orally three times a day 1-2 hours after or before meals. Course - 3-5 weeks.
Herbal preparations	Hofitol, Lespenefril	They increase the excretion of urea from the body and enhance renal blood flow.	Hofitol administered intravenously or intramuscularly. Course - 12 procedures. Lespenefril prescribed orally before meals, 2-4 teaspoons per day, intravenously or intramuscularly - 3-4 ampoules per day. Course - 3-4 weeks.

The use of drugs for the treatment of nephrosclerosis, as an independent method, is effective on Stages I-II diseases.

Treatment of nephrosclerosis: hemodialysis and kidney transplant

They are used in the development of stages III-IV of chronic renal failure - when kidney function cannot be restored.

During hemodialysis The patient's blood is passed through a special membrane in an artificial kidney machine. Due to this, the body is cleansed of toxins and end products of metabolism, and the balance of water and salts is normalized.
The frequency of the procedure depends on the degree of renal dysfunction and the model of the device used.

A patient undergoing hemodialysis is prescribed medications to lower blood pressure, vitamins, potassium and other medications.

Kidney transplant - a radical method that allows patients to lead an active lifestyle. The donor organ is taken either from a corpse (subject to all conditions) or from a living donor (for example, a brother or sister - with their consent).

After a transplant, patients take special medications that suppress the activity of the immune system so that it does not reject the donor organ.

Is hospitalization necessary for nephrosclerosis?

If the patient receives treatment, his condition is stable and hospitalization is not required.

However, if the condition worsens, there is a need treatment in a hospital setting:

• Increased loss of fluid (polyuria) and salts
• The acid-base balance in the body is disturbed (blood acidification) - when the pH is lower than 7.2
• Self-poisoning with metabolic products
• High urea and creatinine levels
• Increased bleeding
• Severe anemia (hemoglobin below 40-50 g/l)

What is being done?

Lost fluid is replenished with intravenous solutions solutions of glucose, isotonic sodium solution and others.

When salts are lost solutions are used for intravenous administration or oral medications containing sodium and potassium.

To reduce creatinine and urea levels A glucose solution is administered as a drink or intravenously in combination with insulin.

Acid-base balance restored with sodium bicarbonate solution administered intravenously.

For the treatment of anemia red blood cells (the component of blood containing red blood cells) are transfused blood cells- red blood cells).

In case of self-poisoning Solutions (glucose, rheopolyglucin and others) and hemodez are administered intravenously.

Note

A patient undergoing hemodialysis must carry with him a card (memo) indicating the diagnosis and frequency of procedures, telephone numbers and address of the dialysis center. Since in in case of emergency(poisoning, accident, loss of consciousness on the street) doctors must know what kind of patient they are dealing with in order to create conditions for the timely implementation of the hemodialysis procedure.

Nutrition for nephrosclerosis (diet)

Proper and balanced nutrition for nephrosclerosis is an important component of successful treatment of the disease.

Nephrosclerosis: diet and drinking regimen

Nutrition principles include creating conditions to reduce the load on the nephrons, but taking into account the stage of nephrosclerosis.

Protein restriction

Justified, since 100 grams of protein produces 30 grams of urea. Also, a protein-restricted diet encourages the body to reuse urea for protein synthesis.

In the absence of renal protein deficiency is practically unlimited.

However if chronic renal failure has developed, it should be limited. In the early stages of the disease, protein is limited to 50-60 grams per day, in the later stages - to 30-40. Moreover, 2/3 of the protein should be high-value: poultry, low-fat varieties beef, egg white, fish, dairy products. Whereas only 1/3 of the protein should come from potatoes, bread, cereals and other products containing protein. However, you should not abuse dairy products and fish, as they contain phosphorus.

Limiting salt intake

Justified, since sodium attracts water, increasing swelling. However Depending on the stage of chronic renal failure and symptoms, the approach is different:

• In the absence of edema and normal blood pressure numbers salt is not limited.
• In the initial stages of chronic renal failure salt is limited to 10-15 grams per day , in later- up to 3-7.

Long-term and sharp restriction of salt intake is inappropriate, since it leads to dehydration of patients and deterioration of kidney function.

Maintaining potassium, calcium and phosphorus levels close to normal

Traditionally, lactic acid products are rich in calcium. However, in case of nephrosclerosis, they should be limited because they contain phosphorus. Whereas its level in the body is already increased in nephrosclerosis. Therefore, it is necessary to consume more other foods in which contains calcium: legumes (peas, beans), green vegetables, whole grain flour.

Products containing potassium are consumed if there is not enough potassium in the body (in the initial stages). Whereas if potassium is in excess (late stages), products containing it are limited. Lots of potassium in raisins, dried apricots, bananas, chocolate, baked potatoes.

Ensuring you get enough calories and vitamins

Because if there are not enough calories, the body uses its own resources to work - its own proteins. Whereas, by breaking down, proteins increase the level of urea.

Therefore, the patient should receive food rich in carbohydrates, fats and vitamins: rice, potatoes, sweets, fresh vegetables and fruits, butter and vegetable oil, honey.

However, the patient should plan his diet taking into account the underlying disease. For example, if you have diabetes, you should limit your carbohydrate intake.

Drinking regime

In the initial stages When there is no edema and blood pressure does not rise to high levels, water restriction is not required. Moreover, with sufficient water intake (2-2.5 liters per day), blood passes through the kidneys faster, creating conditions for better removal of toxins from the body.

In later stages(in the presence of edema and high blood pressure), the patient is recommended to take 500 ml of fluid more than he excreted in the previous day.

Consequences of nephrosclerosis

Nephrosclerosis is a chronic disease that lasts a long time with alternating periods of exacerbations and remissions (disease signs). Therefore, with good compensation for the underlying disease, it is possible to improve kidney function and restore blood flow in the nephrons. And then the patient feels good for many years, leading an active lifestyle.

However, with an unfavorable course of the underlying disease, kidney function deteriorates, so a large number of nephrons die. As a result, chronic renal failure develops over time, and after several years the patient often needs hemodialysis or a kidney transplant.

This pathological condition, caused by the death of nephrons, their replacement by connective tissue with an increase in renal failure. It manifests itself as polyuria, nocturia, hypertension, swelling, discomfort in the lower back, and in the later stages - oliguria, hematuria, intoxication. Diagnosed using laboratory tests, ultrasound, CT, MSCT of the kidneys, nephroscintigraphy, angiography of the renal vessels, urography, biopsy. For treatment, etiopathogenetic therapy of the underlying disease, anticoagulants, antiplatelet agents, antianemic, detoxification, vitamin and mineral agents, replacement therapy, and kidney allotransplantation are used.

General information

Nephrosclerosis is a secondary clinical and anatomical condition, manifested by compaction, wrinkling of the kidneys and a decrease in their functional capacity due to the replacement of parenchyma with fibers and interstitial substance of connective tissue. The shriveled kidney was first described in 1914 by the German clinician F. Volhard and pathologist K.T. Farom.

Typically, nephrosclerosis complicates the course of urological and other somatic pathologies. In the twentieth century, its leading cause was considered to be glomerulonephritis, currently - arterial hypertension and diabetes mellitus (more than 60% of all diagnosed cases). The prevalence of nephrosclerosis in European countries is 0.06%. At the same time, 10-20% of patients require regular hemodialysis, and mortality from chronic renal failure reaches 22%.

Causes of nephrosclerosis

Kidney shrinkage is a polyetiological process that complicates various vascular disorders and urological diseases. Depending on the type of nephrosclerosis, experts in the field of urology and nephrology identify two groups of causes that cause primary or secondary replacement of the renal parenchyma with fibrous structural elements of connective tissue. A primarily wrinkled kidney is formed against the background of damage to the renal vessels caused by diseases such as:

• Arterial hypertension. In patients with essential hypertension and symptomatic hypertensive conditions, the renal vessels persistently spasm and narrow, and the nutrition of the parenchyma is disrupted. Connective tissue compaction of the vascular wall or death of arterioles and glomerular capillaries ends, respectively, with the formation of slowly progressive arteriosclerotic nephrosclerosis or malignant arteriolenecrotic glomerulosclerosis of Farah.
• Atherosclerosis of the renal arteries. The deposition of atherosclerotic plaques on the inner lining makes the vascular wall less elastic and narrows the lumen of the vessels feeding the renal parenchyma. A decrease in tissue perfusion provokes the destruction of nephrons and tissue hypoxia, which promotes excessive formation of connective tissue. As a result, as a result of atherosclerosis, the cortical substance becomes thinner, the cells of the urinary tubules atrophy, which reduces the functional capacity of the kidney.
• Chronic venous congestion. Against the background of stagnation caused by nephroptosis, narrowing or chronic thrombosis renal veins, parenchymal vessels dilate paretically, the influx of oxygenated arterial blood decreases, ischemia increases in the tissues. The situation is aggravated by compaction of the vascular walls, which further disrupts tissue metabolism. Under hypoxic conditions, partial cell death occurs, and nephrosclerosis occurs within 10-15 years.

In some patients, angiogenic renal destruction occurs acutely with partial or complete thromboembolism of the renal artery. A sharp disruption of blood circulation causes a kidney infarction - massive death of nephrons as a result of acute ischemia. Subsequently, the necrotic area is gradually replaced by connective tissue, and nephrosclerosis develops.

A secondarily wrinkled kidney is spoken of in cases where the patient initially suffers urological disease, in which the renal parenchyma is destroyed under the influence of infectious agents, autoimmune complexes, mechanical factors (stretching, trauma by stones), etc. The main causes of secondary (nephrogenic) nephrosclerosis are:

• Kidney diseases. Hardening of the parenchyma can result in pyelonephritis, kidney tuberculosis, glomerulonephritis, urolithiasis, and polycystic disease. A separate group The causes of nephrosclerosis are secondary nephropathy, which complicates the course of other pathological processes - diabetes mellitus, systemic lupus erythematosus, malignant neoplasia, preeclampsia.
• Diseases of the lower urinary tract. Nephrosclerosis can develop against the background of hydronephrosis, caused by obstructive stagnation of urine during sclerosis of the bladder neck, the formation of uretero-vaginal fistulas, and compression by pelvic tumors. Atrophic processes are observed in 30-60% of patients suffering from vesicoureteral reflux.

Pathogenesis

Despite the variety of causes that cause nephrosclerosis, the mechanism of development of the disease as a whole is common. Initially, under the influence of various damaging factors (hypoxia, inflammatory and dystrophic processes caused by pathogenic factors of microorganisms, autoimmune complexes, direct traumatic effects, etc.), destruction of the glomerular and tubular epithelium occurs with the exclusion of some nephrons from the general blood supply.

Because kidney cells are not capable of regeneration, after phagocytosis of destroyed cellular elements, nephrosclerosis begins - the damaged area is replaced by connective fibers, and the kidneys themselves become denser. In the remaining glomeruli, blood circulation and filtration increase, resulting in an increase in the volume of urine excreted and a decrease in its relative density. Against the background of blood flow disturbances, the synthesis of renin, which regulates glomerular filtration, which contributes to the occurrence or worsening of arterial hypertension.

Due to the high compensatory capabilities of the renal tissue, clinical signs of renal failure appear only with severe nephrosclerosis with the loss of 70% of the nephrons of both kidneys or 85% of one. When 5% of cells or less are retained, functional failure of the organ occurs, requiring replacement therapy.

Symptoms of nephrosclerosis

The clinical picture of the disease at an early stage is characterized by an increase in the amount of daily urine (more than 2 liters), increased frequency of urination at night (more than 3 times per night), constant nagging pain in the lumbar region, and an increase in blood pressure. As nephrosclerosis progresses, swelling appears: first on the face, then it spreads evenly throughout the body. Swelling is most pronounced in the morning.

At a later stage, the symptoms worsen: the volume of daily urine decreases to 0.5–0.8 l, an admixture of blood may appear in the urine, the patient is bothered by dry mouth and constant thirst. General symptoms of intoxication arise and increase: headache, nausea and vomiting, weakness, muscle pain.

Complications

Serious disturbances in the processes of filtration and reabsorption, which occur with the destruction of more than 70-75% of the initial number of nephrons, lead to the formation of chronic renal failure. Because the shriveled kidney stops producing erythropoietin, which is necessary for the maturation of red blood cells in the bone marrow, iron deficiency anemia often develops. Patients with nephrosclerosis have an increased risk of nephrogenic hypertension due to excess renin production. When vitamin D metabolism is disrupted, osteoporosis occurs with increased bone fragility and a tendency to form pathological fractures.

Diagnostics

Patients with suspected nephrosclerosis are prescribed a comprehensive examination to determine the features of the morphological structure of the kidneys, identify signs of parenchymal atrophy, and assess the functional viability of the organ. The most informative laboratory and instrumental methods for diagnosing a wrinkled kidney are:

• General urine test. For nephrosclerosis, a significant decrease in the relative density of urine (up to 1.005-1.015 g/l) is indicative. With increasing signs of chronic renal failure, erythrocyturia (up to 2-3 red blood cells in the field of view), cylindruria, proteinuria (up to 0.033 g/l) are possible.
• General blood test. In patients with a shriveled kidney, the content of hemoglobin and red blood cells decreases, moderate thrombocytopenia, and an increase in the duration of bleeding and blood clotting time are noted. Slight leukocytosis often occurs.
• Blood biochemistry. Assessment of functional capacity according to biochemical parameters detects renal failure. With nephrosclerosis, the content of uric acid, creatinine, urea, magnesium, phosphorus, and sodium may be increased. The level of protein and potassium decreases.
• Sonography. Characteristic echographic signs of nephrosclerosis are a decrease in the size of the affected organ, thinning of the parenchyma, atrophy of the cortex, and its unclear differentiation with the medulla. Often, kidney ultrasound reveals nephrocalcinosis.
• X-ray methods. With survey and excretory urography, the size of the kidneys and the cortical layer are reduced, and calcifications are detected in the parenchyma. Impaired filling of the pyelocaliceal system with a contrast agent may indicate the development of chronic renal failure.
• Angiography. On renal angiograms, the arteries are usually narrowed and deformed. In some patients, the fine arterial pattern may be absent (the “burnt wood” symptom). The cortex is thinned. Irregularity of the outer contour of the kidneys is typical.
• Dynamic nephroscintigraphy. When the kidney shrinks, it accumulates and excretes nephrotropic radionuclide more slowly. The study is complemented by static nephroscintigraphy, which reveals parenchymal defects by the uneven distribution of the radiopharmaceutical.
• Renal tomography. Three-dimensional models and layer-by-layer images obtained during CT and MSCT reveal thinning of the cortical layer and a decrease in the size of the organ. Signs of nephrosclerosis are narrowing and deformation of small arterial vessels.
• Needle biopsy of the kidneys. Histological analysis of a kidney biopsy reveals a significant decrease in the number of nephrons and a large number of connective tissue fibers. During the study, the condition of arterioles and capillaries is assessed.

Differential diagnosis of nephrosclerosis is carried out with sugar and diabetes insipidus, acute renal failure, rapidly progressive glomerulonephritis, hepatorenal syndrome, hypochloremic azotemia. If necessary, the patient, in addition to a nephrologist and urologist, is consulted by a therapist, cardiologist, phthisiatrician, rheumatologist, endocrinologist, oncologist, and oncohematologist.

Treatment of nephrosclerosis

Conservative therapy for the initial stages of kidney shrinkage is aimed at correcting the underlying disease that provoked the sclerotic process and increasing renal failure. Taking into account the pathology that caused nephrosclerosis, the patient is prescribed antibiotics, antihypertensive drugs, statins, glucocorticosteroids, antiglycemic, diuretic, non-steroidal anti-inflammatory and other etiopathogenetic drugs. To relieve disorders caused by functional renal failure, the following can be used:

• Anticoagulants and antiplatelet agents. By influencing the rheological properties of blood, they improve blood flow in the renal arterioles and capillaries and, by restoring tissue perfusion, slow down nephrosclerosis. Prescribed with caution when chronic renal failure increases.
• Vitamin and mineral complexes. To correct changes in the biochemical composition of the blood caused by impaired filtration, potassium, calcium, vitamin D, multivitamin formulations, and bisphosphonates are used. Taking them improves metabolism and prevents osteoporosis.
• Antianemic drugs. If anemia is detected, erythropoietin preparations are prescribed, which stimulate the formation of red blood cells, and iron, necessary for the synthesis of hemoglobin. Reducing hemic hypoxia makes it possible to slow down sclerotic processes in the kidney tissues.
• Detoxification therapy. To speed up the elimination of toxic metabolites that accumulate in the body during nephrosclerosis, enterosorbents are used, which bind metabolic products in the intestine. Herbal remedies based on artichoke can be prescribed to reduce urea levels.

If kidney shrinkage is combined with stage III-IV chronic renal failure, replacement therapy is indicated. renal therapy- peritoneal dialysis, hemodialysis, hemodiafiltration, hemofiltration. A radical treatment method recommended for nephrosclerosis with a decrease in the number of viable nephrons to 5% or less is kidney transplantation after abdominal or laparoscopic nephrectomy.

Prognosis and prevention

With timely detection of the disease, the prognosis is relatively favorable; the appointment of adequate therapy allows one to achieve a long-term state of compensation for nephrosclerosis. Over time, the functioning of the nephrons deteriorates, and chronic renal failure develops: such patients require an organ transplant or regular hemodialysis.

To prevent nephrosclerosis, it is necessary to follow the recommendations of a specialist in the treatment of nephrological diseases (especially of an inflammatory nature), monitor the level of blood pressure, blood glucose, avoid hypothermia, and do not abuse salt and meat foods. Plays an important role in preventing the development of a wrinkled kidney. regular visit family doctor for early detection and correction of somatic pathology.

Not a single kidney disease goes away without a trace; any pathological process in the kidney leads to damage and death of its structural and functional units - nephrons. The loss of single nephrons does not affect the function of the organ in any way. With the massive death of renal structures, they are replaced by connective tissue, and the function of the kidney is lost.

The process of replacing functioning nephrons with connective tissue is nephrosclerosis. This is not an independent disease, but a possible outcome of any pathological processes in the kidney. The outcome of nephrosclerosis is complete loss of function, reduction in size and ultimately shrinkage of the kidney. Sometimes doctors even replace the term “nephrosclerosis” with the concept of “wrinkled kidney”; in essence, they are the same thing.

Causes of nephrosclerosis

Atherosclerosis of the renal arteries will sooner or later lead to nephrosclerosis.

There are two forms of this pathology: primary and secondary wrinkled kidney.

• Primary nephrosclerosis is caused by vascular damage and impaired blood supply to the renal tissue as a result of renal vessels and kidney infarctions, impaired venous outflow. The structure of the kidneys undergoes sclerotic changes with age; by the age of 70, the number of active renal structural units in the kidneys decreases by 30-40%.
• The secondary form of the disease occurs as a result of damage to the kidney parenchyma during long-term autoimmune processes, kidney tuberculosis; severe nephropathy in pregnant women and organ trauma can lead to nephrosclerosis.

In recent decades, the main causes of this pathology are considered to be hypertension and diabetes mellitus, although literally 20 years ago glomerulonephritis was in the lead.

Main symptoms of nephrosclerosis

The disease can last for decades, with the deterioration of kidney function occurring gradually, and the symptoms initially do not bother patients much. A doctor is often consulted when edema appears, urination problems and signs of arterial hypertension appear. With such symptoms, changes in the kidneys are often irreversible, and the function of the organ is already significantly reduced.

Urinary dysfunction

This symptom includes polyuria (excessive urination - 2 liters per day or more) and nocturia (increased number and volume of urination at night).

In severe forms of nephrosclerosis, polyuria gives way when the amount of urine, on the contrary, sharply decreases. Anuria (complete absence of urine may indicate end-stage renal failure).

Also, an admixture of blood appears in the urine, and it turns the color of meat slop - this symptom is called gross hematuria.

Arterial hypertension

When the blood supply to the kidneys is disrupted, a protective mechanism is activated aimed at increasing the pressure in the renal vessels, as a result of which substances are released into the blood that increase the pressure throughout the bloodstream. With nephrosclerosis, arterial hypertension reaches very high values, hypertensive crises are possible with an increase in systolic pressure to 250-300 mm Hg. Art., and it is very difficult to reduce the pressure.

Edema

Fluid retention in the body leads to the appearance. They first appear on the face in the morning and go away after a while. Then they gradually go down, the fingers on the hands swell (patients note that they cannot take off the rings in the morning) and shins (can’t put on shoes, can’t fasten boots). As the disease progresses, swelling spreads throughout the body, and anasarca occurs - generalized swelling of subcutaneous fat, soft tissues, and in the worst case, internal organs.

(cardiac asthma) occurs as a result of overload of the heart due to the increased amount of fluid in the body. As a result, blood stagnation occurs in the pulmonary capillaries. The patient experiences shortness of breath, cough, and during an attack there is sweating, cyanosis (blue discoloration of the skin), increased heart rate and respiratory rate. Cardiac asthma is a serious complication that can be fatal if left untreated.

Stages of nephrosclerosis

There are 2 periods in the development of this pathology:

1. In the first phase, there are no manifestations of nephrosclerosis, however, the patient has and may progress one or more diseases leading to the replacement of normal renal parenchyma with connective tissue. During this period, changes characteristic of kidney damage already appear in urine and blood tests.
2. Symptoms characteristic of nephrosclerosis, and, accordingly, renal failure, appear in the second stage of the process, when changes in the structure of the kidneys can be detected using ultrasound and other instrumental research methods.

Also, depending on the course of the pathological process, malignant and benign forms of nephrosclerosis are distinguished.

Fortunately, in the vast majority of patients, the second form of the disease occurs, in which the process progresses slowly; with successful treatment of the underlying disease, the progression of nephrosclerosis can be slowed down.

In a malignant course, nephrosclerosis progresses quickly and in a few years can lead to a complete loss of kidney function, severe and doom the patient to lifelong renal failure. Such an unfavorable outcome can be observed with malignant arterial hypertension and eclampsia in pregnant women.

Diagnosis of nephrosclerosis

With nephrosclerosis, corresponding changes will be detected in a general urinalysis.

Since the symptoms of a shriveled kidney appear in the later stages, it is very important to identify this pathology as early as possible through examination, since the effectiveness of treatment in this case will be much higher. Taking the patient's medical history plays an important role.

• General urine analysis. Any examination of the kidneys, of course, begins with a urine test; with initial nephrosclerosis, the following abnormalities can be detected: a decrease in the relative density of urine, the appearance of protein, single red blood cells and casts.
• Blood tests. In a clinical blood test, a decrease in the level of hemoglobin and platelets is possible. In biochemical – a decrease in the amount of total protein, an increase in the level of urea, creatinine, uric acid and sodium. An increase in glucose and cholesterol levels should alert you.

Such changes in urine and blood tests are very nonspecific and can be observed not only in kidney diseases. However, the combination of such deviations in laboratory test results, in the presence of a history of factors that can lead to kidney damage, forces the doctor to think about further diagnosis.

For examination, many instrumental methods are used, such as ultrasound, (x-ray of the kidneys with a contrast agent), angiography, radioisotope studies, etc. All of them reveal a decrease in the size of the kidney, the presence of calcium deposits, impaired blood flow in the renal vessels and other changes indicating proliferation connective tissue. A biopsy can give an accurate answer about the condition of the renal parenchyma.

Treatment of nephrosclerosis

There is no specific therapy aimed at treating nephrosclerosis. It is necessary to treat the disease, which has led to kidney damage and death of nephrons, followed by their replacement with connective tissue. That is why not only a nephrologist, but also a specialized specialist treats patients with nephrosclerosis.

In addition to therapy aimed at treating the underlying disease, patients must follow a diet. It is recommended to limit the amount of protein and table salt; the diet should have enough vitamins and mineral salts. In the absence of arterial hypertension and edema, fluid and protein restriction is not required.

In end-stage renal failure, when both kidneys have lost their functions, patients are advised to undergo hemodialysis. The only way out in this situation is kidney transplantation; in recent years, this operation has been successfully carried out in Russia, and for citizens of our country it is free.