Interstitial nephritis is clinically manifested. Causes and treatment of interstitial nephritis

Diet

1. limit the amount of food you eat;
2. since protein digestibility is impaired during the period of illness, try to take no more than 50 g of the nutrient per day;
3. To improve kidney function, you should include dairy products in your diet. An exception is hard cheese;
4. include fruits and vegetables in your diet. Particular attention should be paid to greens;
5. During the treatment period, it is recommended to avoid eating legumes;
6. In addition to fast food, hot and spicy sauces, you must avoid eating onions and garlic. Canned and smoked food and pickles are also prohibited.

Prevention

Like any other disease, interstitial nephritis is easier to prevent than to cure.

1. don't take it serious medical supplies(for example, antibiotics) without agreeing on a treatment regimen with a doctor. The same applies to diuretics;
2. try to eat right. Avoid eating fatty and fried foods;
3. if you have a genetic predisposition to the disease or suffer from other kidney diseases, it is recommended to test your urine for each disease;
4. for normal kidney function it is very important to adhere to drinking regime. Drink 1.5 to 2 liters of water daily. You can determine the required volume of liquid using the following form: 30 ml of water for every 10 kg of weight;
5. If possible, try to avoid taking antibiotics and pain medications;
6. the functioning of the kidneys is closely related to the functioning of the entire genitourinary system. Therefore, you should not expose your body to additional risk in the form of hypothermia. It has been proven that one of the complications that arose against the background of untreated cystitis is precisely the development of such an ailment as nephritis;
7. try to avoid stress and increased fatigue.

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Lecture on tubulointerstitial nephritis by Associate Professor of Medical Sciences:

Now you know what interstitial nephritis is and how to recognize it. Don't forget that this pathology non-infectious nature cannot be self-medicated. Therefore, in order to get rid of the disease and prevent its transition to a chronic form, it is necessary to consult a competent doctor as soon as possible. He will conduct a series of examinations and diagnostics, based on which he will be able to select medications that are suitable for your case.

• Causes of the disease
  • Characteristic symptoms
  • Diagnostic methods
  • Preventive measures

Interstitial nephritis is a disease that occurs inflammatory nature and affects the renal tubules and interstitial tissues. With interstitial nephritis, the kidney tissue does not change, the disease does not affect the area of ​​the calyces and pelvis. The disease has no age limit and can be diagnosed even in newborns.

Most often, pathological processes in the kidneys appear in people between 20 and 50 years old. Chronic interstitial nephritis is considered a serious form of the disease, since if treatment measures are not taken, the disease can transform into nephrosclerosis - shrinkage of the kidney, which can lead to sad outcome.

Impairment of proper kidney function under the influence of inflammatory process may occur due to a number of reasons such as:

1. Uncontrolled use of medications. Many medications, especially antibiotics, diuretics, and non-steroidal drugs antiseptic action, can provoke disturbances in the functioning of the kidney.
2. Intoxication with heavy metals and toxins of plant or animal origin.
3. Infectious diseases, such as diphtheria or streptococcus.
4. Disorders of metabolic processes in the body.
5. Obstruction of the urinary tract, which is caused by diseases such as tumors, kidney stones, etc.
6. Effect of ionizing radiation.
7. Scleroderma.
8. Systemic lupus erythematosus.

If the diagnosis of the disease has not been able to establish the cause of its occurrence, then it is customary to call this form of nephritis idiopathic.

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Characteristic symptoms

The manifestation of symptoms depends on the degree of pathological processes in the kidneys and intoxication of the body.

There are two forms of the disease: acute and chronic interstitial nephritis.

Each form has its own symptoms. But the danger of this disease is that it for a long time may not manifest itself in any way and imperceptibly go into chronic type.

Acute interstitial nephritis manifests itself with symptoms such as:

1. General weakness, loss of appetite, drowsiness, headache, pale skin.
2. Fatigue, fever, aching joints, muscle pain, allergic skin rashes.
3. Promotion blood pressure and body temperature.
4. The presence of protein and red blood cells in the urine.

Symptoms appear within a few days after the organ is damaged. Kidney failure occurs, the severity of which can progress quickly, so it is very important to begin treatment. If everything is done in a timely manner necessary measures, then after 2-3 days the patient’s condition will become stable. Restoration of the functionality of the urinary system organs will occur no earlier than after 3 months of intensive therapeutic therapy.

Chronic interstitial nephritis at the beginning of its development shows practically no signs of itself. Its symptoms boil down to:

• pain in the lower back and abdomen;
• fatigue;
• an increase in the average daily amount of urine excreted, more than 1800 ml per day.

A clear sign chronic forms Symptoms of the disease are a moderate loss of protein, which is excreted in the urine, moderate proteinuria, as well as a loss of white blood cells and red blood cells, which are excreted from the body in the same way. In chronic interstitial nephritis, crystals of various salts form in the urine. Next, there is a disruption in the regulation of canal secretion of the kidneys and a decrease in urine density. Last stage chronic form of kidney nephrosis is characterized by renal failure, developing fibrosis and nephrosclerosis.

From total number 6% of newborns are diagnosed with interstitial nephritis. Most of these babies are premature. The disease develops against the background of:

• hypoxia;
• toxic effects environment;
• renal tissue dysplasia;
• taking medications;
• metabolic disorders.

Kidney disease may be aggravated by disturbances in the activity of the central nervous or immune systems.

Interstitial nephritis in children is accompanied by edema and increased level urea in a blood test.

Sometimes symptoms of kidney failure are present. Acute interstitial nephritis usually manifests itself clearly, which allows doctors to begin treatment as quickly as possible. But there are cases when the symptoms of the disease do not indicate the presence of pathological processes in the kidneys, and then interstitial nephritis becomes chronic.

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Diagnostic methods

Since the disease may have unexpressed symptoms, at the first complaints and suspicions of nephritis, the doctor prescribes a number of laboratory and instrumental studies. Special attention pay attention to the level of y-glutamyltransferase and alkaline phosphates in the urine analysis. If their content exceeds the norm, this confirms the diagnosis. The echogenicity of the renal parenchyma also increases.

An ultrasound is considered mandatory.

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Treatment of interstitial nephritis

When making this diagnosis, the first thing that is recommended to do is to stop taking all medications that could cause the disease. The patient is hospitalized. After stopping the medications, a repeat blood test is taken to determine the level of urea and creatine in the plasma. If the disease continues to progress, then the main stage of treatment is to find out the cause of interstitial nephritis and find ways to eliminate it.

A diet is prescribed that should fully replenish the required amount of proteins, fats, carbohydrates and vitamins washed out in the urine. You can make up for the missing amount of proteins with vegetable fats and dairy products.

If your blood pressure is high, you should minimize your intake. table salt. When the disease is supported by polyuria, it is recommended to use fruit drinks, jelly, teas and compotes instead of water.

A restriction is introduced on products with increased content proteins of animal origin. It is not recommended to consume marinades, smoked meats and spices. At frequent urination the sodium and potassium levels in the patient’s body are adjusted with medication.

Steroid hormones are prescribed only if it is not possible to quickly determine the cause of interstitial nephritis and prescribe effective treatment, and also when severe course diseases. Prescribed drugs whose action is aimed at improving microcirculation processes.

Treatment is prescribed individually for each patient and involves the restoration and strengthening of all renal functions.

Interstitial nephritis causes acute or chronic damage to the renal interstitium.

The changes are irreversible. At long term the disease leads to kidney failure.

The cause of the condition has not been fully elucidated, but the main etiological factor of the disease is considered to be an immune hypersensitivity reaction that occurs in response to the penetration of beta-hemolytic streptococcus into the body.

The pathology occurs against the background of other nosological forms (gout, urolithiasis), therefore the true etiological factor of its appearance is difficult to establish.

The main causes of damage to the interstitial tissue of the kidneys:

• Hypersensitivity reaction;
• Beta-lactam antibiotics;
• Diuretics (thiazide).

Sulfonamide drugs and their side effects

Based on etiological factors, the following nosological types of the disease are distinguished:

1. Uratnaya;
2. Chronic tubulointerstitial;
3. Acute uric acid;
4. Bacterial;
5. Idiopathic.

Urate nephritis develops against the background of metabolic disorders uric acid. The pathology is characterized by bilateral kidney damage and the formation of urinary tract stones.

Interstitial nephritis - two groups

When the stone is localized in the pelvis, renal colic occurs. A feature of urate nephritis is the rapid formation of kidney failure. The pathology is often accompanied by a bacterial infection (glomerulonephritis, pyelonephritis, pyonephrosis).

Chronic tubulointerstitial nephropathy is manifested by severe urinary damage, combined with arterial hypertension. Against the background of the pathology, proteinuria appears, in which the level of urine protein does not exceed 2 grams per liter.

Half of the patients develop microhematuria. No stones are detected, but episodes of sand, azotemia, oliguria, and dehydration occur. A third of patients develop bilateral medullary cysts that do not exceed 3 cm in diameter.

Early onset of night urination, sclerotic kidney damage, high blood pressure indicates the presence of stenosis renal arteries, atherosclerosis with inflammatory process of interstitial tissue.

Acute uric acid nephropathy is characterized not only by nephritis. An increase in blood uric acid levels is accompanied by attacks renal colic, decrease in the total amount of urine, hypertensive crisis, urate crystalluria.

Infectious nephritis is formed due to chronic bacterial, viral or fungal lesions of the interstitium of the kidneys.

The drug type occurs while taking non-steroidal anti-inflammatory drugs (diclofenac) or hormonal drugs.

Did you know that blood cleansing of toxins is prescribed not only for the diagnosis of kidney failure? , contraindications. The essence of the procedure, preparation, and possible complications.

Read about the symptoms of acute and chronic forms of renal failure in adults and children.

Many people do not notice the signs of kidney disease, which leads to late diagnosis. Here you will learn about the symptoms that may indicate the presence of kidney disease in adults and children.

Symptoms of inflammation of the renal interstitium

The symptoms of acute and chronic interstitial nephritis differ. Expressed clinical form characterized by the following clinical signs:

1. Polyuria - discharge large quantity urine;
2. Hematuria – blood in urine;
3. Fever - alternating periods of increasing and decreasing temperature curve;
4. Lumbar pain.

Causative agents of infectious interstitial nephritis

Medicines that provoke inflammation of the interstitium of the kidneys:

• Methicillin;
• Cephalosporins;
• Tetracyclines;
• Penicillins;
• Antituberculosis drugs (ethambutol, rifampicin);
• Nonsteroidal drugs;
• Sulfonamides;
• Thiazide diuretics.

In literary sources there are facts of inflammation of the interstitium of the kidneys when taking allopurinol, cimetidine, phenylin, acyclovir, and some Chinese medicinal herbs.

The effect of taking certain drugs on kidney damage

Morphologically at this type Nosology can be traced to mononuclear infiltrates, around which non-caseating granulomas are located. Delayed hypersensitivity reactions are provoked by the T-cell component of immunity. They are accompanied by the synthesis of immunoglobulins, which affect the interstitial tissue of the kidneys.

Diagnosis is difficult due to non-specificity clinical picture diseases. Often the only sign of pathology is repeat wave fever, in which attacks of temperature up to 39 degrees are observed.

Delayed treatment leads to rapid development of renal failure.

The presence of the following changes in tests helps to identify kidney pathology:

1. Hematuria;
2. Proteinuria more than 2 grams per day;
3. Decline glomerular filtration;
4. Increased creatinine concentration;
5. Oliguria and polyuria;
6. Urinary syndrome.

Interstitial nephritis in children

A feature of the pathology in children is the rapid development of the clinical picture, the gradual formation of chronic changes. A child is rarely prone to developing kidney failure, since children are not prescribed medications.

IN childhood Analgesic nephropathy, which is characterized by necrosis of the renal papillae due to lack of painkillers, never appears.

Diagnostics

Principles for diagnosing interstitial nephritis:

1. Urinalysis to detect pyuria, microhematuria, proteinuria, eosinophiluria;
2. Biopsy of interstitial tissue for lympho- and monocytosis;
3. Signs of detection have diagnostic significance allergic reaction: skin rashes, drug-induced hepatitis, arthralgia.

Pathogenesis of acute interstitial nephritis

When collecting anamnesis, clinical examination, palpation, you should pay attention to some features:

• Taking medications;
• Urinary syndrome with the release of no more than 2 grams of protein per day;
• Renal failure with hypertension;
• Tubular disorders with concentration defect;
• Hyperproteinemia, increase in ESR;
• Extrarenal fever.

Confirm morphological changes kidneys are possible using clinical and instrumental diagnostic methods (ultrasound, urography, tomography).

Treatment

Treatment involves eliminating the etiological factor, eliminating symptoms, and preventing complications. In case of kidney failure, hemodialysis is required to cleanse the blood of toxins.

The principle of hemodialysis by diffusion

Diet for inflammation of the interstitial tissue of the kidneys

Diet for inflammatory changes interstitial tissue of the kidneys:

1. Eating low-calorie foods;
2. Limiting purine diet;
3. Drink plenty of alkaline drinks;
4. The daily amount of protein is no more than one gram per kilogram;
5. The fat concentration is equal to the protein content;
6. Use fish oil provides nephroprotective effect.

Inflammation of the renal glomeruli disrupts the main function of the kidneys - cleaning the blood from metabolic products. Find out why it is a common diagnosis. How to resist this and what is the treatment of glomerular inflammation based on?

Read about the symptoms of female pyelonephritis. The course of the disease in the chronic and acute stages.

Prevention of tubulointerstitial nephritis

Preventive measures include limiting the intake of purine compounds, timely treatment of high blood pressure, prevention negative influence blood toxins on the kidneys.

Should not be taken unnecessarily medicines, which can provoke inflammation of the interstitial tissue of the kidneys.

Video on the topic

I didn’t know that diet and antibiotics could complicate nephritis. I suffer from this disease, periodically there are exacerbations. but I never thought that many foods need to be limited during this period. Now I will know!

Description:

Interstitial (IN) is inflammatory disease kidneys of a non-infectious (abacterial) nature with localization of the pathological process in the interstitial (interstitial) tissue and damage to the tubular apparatus of the nephrons. This is an independent nosological form of the disease. Unlike, in which the interstitial tissue and renal tubules are also affected, interstitial nephritis is not accompanied destructive changes renal tissue, and the inflammatory process does not extend to the cups and pelvis. The disease is still little known to practical doctors.

Clinical diagnosis of interstitial nephritis, even in specialized nephrological institutions, presents great difficulties due to the lack of characteristic clinical and laboratory criteria that are pathognomonic only for it, as well as due to its similarity with other forms of nephropathy. Therefore, the most reliable and convincing method for diagnosing ID so far is needle biopsy kidneys

Because in conditions clinical practice IN is still diagnosed relatively rarely, and there is still no accurate data on the frequency of its distribution. However, according to the information available in the literature, last decades There is a clear trend towards an increase in the frequency of this disease among the adult population. This is due not only to the improvement of methods for diagnosing IN, but also to the broader impact on the kidneys of those factors that cause its occurrence (especially drugs) (B. I. Shulutko, 1983; J. P. Zalkalns, 1990, etc. ).

There are acute interstitial nephritis (AIN) and chronic interstitial nephritis (CIN), as well as primary and secondary. Since in this disease not only interstitial tissue, but also tubules are always involved in the pathological process, along with the term “interstitial nephritis” it is considered legitimate to use the term “tubulointerstitial nephritis”. Primary IN develops without any previous kidney damage (disease). Secondary IN usually complicates the course of pre-existing kidney disease or diseases such as multiple myeloma, leukemia, vascular lesions kidney, oxalate, etc. (S. O. Androsova, 1983).

Acute interstitial nephritis (AIN) can occur at any age, including newborns and the elderly, but the vast majority of patients are registered at the age of 20-50 years.

Symptoms:

Character and severity clinical manifestations OIN depends on severity general body and on the degree of activity of the pathological process in the kidneys. The first subjective symptoms of the disease usually appear 2-3 days after the start of treatment with antibiotics (most often penicillin or its semi-synthetic analogs) due to exacerbation of chronic and other diseases that precede the development of AIN. In other cases, they occur several days after the administration of nonsteroidal anti-inflammatory drugs, diuretics, cytostatics, administration of radiocontrast agents, serums, and vaccines. Most patients complain of general weakness, sweating, headache, aching pain in the lumbar region, drowsiness, decreased or loss of appetite, nausea. Often the mentioned symptoms are accompanied by chills with fever, muscle aches, sometimes polyarthralgia, skin allergic rashes. IN in some cases the development of moderate and short-term symptoms is possible. are not typical for IINs and, as a rule, are absent. Dysuric phenomena are not usually observed. In the vast majority of cases, from the first days it is noted with low relative density of urine (hyposthenuria). Only in very severe cases of AIN at the onset of the disease is there a significant decrease (oliguria) in urine until the development (combined, however, with hyposthenuria) and other signs of ARF. At the same time, the following is detected: slight (0.033-0.33 g/l) or (less often) moderately pronounced (from 1.0 to 3.0 g/l), microhematuria, small or moderate, with a predominance of hyaline, and in severe cases - and the appearance of granular and waxy casts. Oxalaturia and calciuria are often detected.

The origin of proteinuria is primarily associated with a decrease in protein reabsorption by the epithelium proximal sections tubules, however, the possibility of secretion of a special (specific) tissue protein Tamm-Horsfall into the lumen of the tubules is not excluded (B. I. Shulutko, 1983).

The mechanism of microhematuria is not entirely clear.

Pathological changes in urine persist throughout the disease (for 2-4-8 weeks). Polyuria and hyposthenuria last especially long (up to 2-3 months or more). Oliguria, which is sometimes observed in the first days of the disease, is associated with an increase in intratubular and intracapsular pressure, which leads to a drop in effective filtration pressure and a transient decrease in glomerular filtration rate. Along with a decrease in concentration ability, a violation of the nitrogen excretory function of the kidneys develops early (also in the first days) (especially in severe cases), which is manifested by hyperazotemia, i.e., an increase in the level of urea and creatinine in the blood. It is typical that hyperazotemia develops against the background of polyuria and hyposthenuria. It is also possible to have a disorder of electrolyte balance (hypokalemia, hypochloremia) and acid-base balance with symptoms of acidosis. The severity of the mentioned kidney disorders in the regulation of nitrogen balance, acid-base balance and water-electrolyte homeostasis depends on the severity of the pathological process in the kidneys and reaches its greatest extent in the case of acute renal failure.

As a consequence of the inflammatory process in the kidneys and general intoxication, characteristic changes in the peripheral blood: small or moderately expressed with a slight shift to the left, often - increase in ESR. In severe cases, development is possible. At biochemical research blood, C-reactive protein, elevated levels of DPA test, sialic acids, fibrinogen (or fibrin), dysproteinemia with hyper-a1- and a2-globulinemia are detected.

When assessing the clinical picture of AIN and its diagnosis, it is important to keep in mind that in almost all cases, and already in the first days from the onset of the disease, signs of renal failure develop varying degrees severity: from slight increase in the blood the level of urea and creatinine (in mild cases) to the typical picture of acute renal failure (in severe cases). It is characteristic that the development of anuria (severe oliguria) is possible, but not at all necessary. More often develops against the background of polyuria and hyposthenuria.

In the vast majority of cases, the symptoms of renal failure are reversible and disappear after 2-3 weeks, but the impairment of the concentration function of the kidneys persists, as already noted, for 2-3 months or more (sometimes up to a year).

Taking into account the characteristics of the clinical picture of the disease and its course, the following variants (forms) of IIN are distinguished (B.I. Shulutko, 1981).

1. Expanded form, which is characterized by all of the above clinical symptoms And laboratory signs of this disease.

2. A variant of AIN, which proceeds according to the type of “banal” (ordinary) acute renal failure with prolonged anuria and increasing hyperazotemia, with the phasic development of the pathological process characteristic of acute renal failure and its very severe course, requiring the use of acute when helping the patient.

3. “Abortive” form with its characteristic absence of the anuria phase, early development polyuria, slight and short-term hyperazotemia, favorable course and fast recovery nitrogen excretion and concentration (within 1-1.5 months) kidney functions.

4. “Focal” form, in which the clinical symptoms of AIN are weakly expressed, erased, changes in urine are minimal and inconsistent, hyperazotemia is either absent or insignificant and quickly transient. This form is more characterized by acutely occurring polyuria with hyposthenuria, rapid (within a month) restoration of renal concentration function and disappearance pathological changes in urine. This is the easiest option and the most favorable outcome for IUI. In outpatient settings, it usually passes as an “infectious-toxic kidney.”

With AIN, the prognosis is most often favorable. Typically, the disappearance of the main clinical and laboratory symptoms of the disease occurs in the first 2-4 weeks from its onset. During this period, urine and peripheral blood parameters normalize, and normal level urea and creatinine in the blood, polyuria with hyposthenuria persists much longer (sometimes up to 2-3 months or more). Only in rare cases, with a very severe course of AIN with pronounced symptoms of acute renal failure, an unfavorable outcome is possible. Sometimes AIN can become chronic, mainly when it is diagnosed late and improper treatment, non-compliance by patients with medical recommendations.

Causes:

The causes of AIN can be varied, but more often its occurrence is associated with taking medications, especially antibiotics (penicillin and its semisynthetic analogues, aminoglycosides, cephalosporins, rifampicin, etc.). Often etiological factors IUIs include sulfonamides, non-steroidal anti-inflammatory drugs (indomethacin, methindol, brufen, etc.), analgesics, immunosuppressants (azathioprine, imuran, cyclophosphamide), diuretics, barbiturates, captopril, allopurinol. Cases of the development of AIN as a result of taking cimetidine after the administration of radiocontrast agents have been described. It may be a consequence of increased individual sensitivity of the body to various chemicals, intoxication with ethylene glycol, ethanol (I. R. Lazovsky, 1974; B. I. Shulutko, T. G. Ivanova, 1978).

OIN, which occurs under the influence of the mentioned medicinal, chemical and toxic substances, as well as with the administration of serums, vaccines and other protein preparations, is designated as a toxicoallergic variant of this disease. Cases of AIN with severe acute renal failure, sometimes developing in patients after viral and bacterial infections, are designated as post-infectious IN, although the influence of antibiotics cannot always be excluded. In some cases, the cause of AIN cannot be determined, and then they speak of idiopathic AIN.

Treatment:

For treatment the following is prescribed:

Patients with AIN should be hospitalized in a hospital, if possible, with a nephrological profile. Since in most cases this disease proceeds favorably, without severe clinical manifestations, then special treatment not required. Crucial has the abolition of the drug that caused the development of AIN. The rest is carried out symptomatic therapy, a diet limiting foods rich in animal proteins, mainly meat. Moreover, the degree of such restriction depends on the severity of hyperazotemia: the higher it is, the less it should be daily consumption squirrel. At the same time, significant restriction of table salt and liquid is not required, since fluid retention in the body and edema are not observed with AIN. On the contrary, due to polyuria and intoxication of the body, additional fluid intake is recommended in the form of fortified drinks (fruit drinks, jelly, compotes, etc.), and often intravenous administration solutions of glucose, rheopolyglucin and other detoxification agents. If AIN is more severe and is accompanied by oliguria, diuretics (Lasix, furosemide, uregit, hypothiazide, etc.) are prescribed in individually selected doses (depending on the severity and duration of oliguria). Antihypertensive drugs rarely prescribed because arterial hypertension It is not always observed, and if it does happen, it is moderately expressed and is of a transient nature. With prolonged polyuria and possible violation electrolyte balance (hypokalemia, hypochloremia and hyponatremia) is corrected under the control of the content of these electrolytes in the blood and their daily excretion in the urine. If necessary, acidosis should be combated.

In general, it is advisable to avoid prescribing medications whenever possible, especially if the course of the disease is favorable and there is no need for this absolute readings. It is advisable to limit yourself to desensitizing agents in the form antihistamines(tavegil, diazolin, diphenhydramine, etc.), calcium supplements, ascorbic acid. In more severe cases, inclusion in the complex is indicated therapeutic measures glucocorticosteroids - prednisolone 30-60 mg per day (or metipred in appropriate doses) for 2-4 weeks, i.e. until the clinical and laboratory manifestations of AIN disappear or significantly decrease. In case of severe development, it becomes necessary to use acute hemodialysis.