An increase in uric acid in a dog up to 1200. Urolithiasis (urolithiasis) in dogs
Urea is one of the products formed in the body during the breakdown of proteins. The normal blood urea concentration in dogs is 3.5–9.2 mmol/L (data may vary slightly between laboratories). It is formed in the liver and excreted through the kidneys in the urine. An increase or decrease in urea levels, therefore, indicates a dysfunction of these organs and a violation of metabolic processes.
Increased urea levels
Most often, an increase in urea levels is associated with difficulty removing it from the body, this is associated with a deterioration in kidney function. Along with urea, the level of serum creatinine also increases. An increase in the level of urea and other products of nitrogen metabolism in the blood is called azotemia. When the body begins to suffer from the accumulation of these products in the body, it is called uremia.
Urea can also increase with protein overfeeding of an animal (a lot of meat), with acute hemolytic anemia, stress, shock, vomiting, diarrhea, and acute myocardial infarction.
Reduced urea levels
A decrease in urea may be associated with a low intake of protein from food, severe liver diseases, for example, with portosystemic shunts. Increased urine output that occurs with hyperadrenocorticism, diabetes mellitus, and other metabolic disorders also leads to a decrease in its level.
As can be seen from the above, urea is not a specific indicator of any disease and is always assessed in conjunction with other tests carried out by a veterinarian.
The article was prepared by doctors of the therapeutic department "MEDVET"
© 2016 SEC "MEDVET"
A urine test is important for a person who can tell the doctor where and how it hurts, and even more so for a dog, which, unfortunately, cannot tell us about its pain.
However, if taking a urine test to a medical laboratory is normal, going to a veterinary laboratory with dog excrement is still quite rare.
Factors influencing the composition of urine in dogs
Urine that is excreted (diuresis) is a waste product of the body. Its composition is influenced by:
- pathological factors (infection, invasion,);
- physiological (pregnancy, estrus, weight, type of feeding);
- climatic (temperature, humidity).
Stress can affect the composition of your urine.
Conducting experiments and studies with clinically healthy animals, biologists calculated the parameters that are present in urine and characterize the physiological balance of the functioning of systems and organs.
Composition and parameters of the norm
The basis of urine is water, its normal content is 97–98%. The following components are included in its composition:
- organic;
- inorganic.
According to physical parameters, a dog’s urine should be yellow or light yellow (depending on the food consumed), transparent, and without a strong odor.
Normally, the color of urine should be yellow.
Table of organic components (norm for dogs)
Density
The specific gravity of urine is an indicator that characterizes how much the kidneys can concentrate urine by reabsorbing water.
The density of urine allows you to assess kidney activity.
pH Indicator of acid balance
Urine, normally, can be either acidic or alkaline. By this indicator we can judge the dog’s feeding diet. The more protein food is contained in the four-legged bowl, the more acidic the urine.
Protein feeds increase the acidity of urine.
The indicator will be acidified during fasting or prolonged physical activity, but this will not indicate pathology.
Protein
A substance consisting of amino acids should not normally leave the body.
The appearance of protein in the urine may sometimes not be associated with pathology. This phenomenon occurs with excessive physical exertion, as well as overfeeding the dog with food of animal origin, or when the diet is not balanced in protein.
The appearance of protein occurs during heavy physical exertion.
Glucose
An indicator that makes it possible to understand whether carbohydrate metabolism is occurring correctly in a dog.
Normally, all carbohydrates should be absorbed, but if there is an excess of them in the diet, then some of them will be excreted in the urine.
Excess glucose will be excreted in the urine.
Often this message is deceptive. Since diagnostic strips react to the level of ascorbic acid, and a dog can synthesize it in fairly high concentrations.
Bilirubin
A component of bile. The appearance of traces of bilirubin may indicate.
Detected bilirubin indicates liver pathologies.
Ketone bodies
If ketone bodies are found along with increased sugar content, this indicates.
Ketone bodies alone can be normal during prolonged fasting, or when there is an excess of fat in the dog’s diet.
Ketone bodies are released during fasting.
Microscopic studies
After settling, the urine releases sediment. Having examined it under a microscope, its components are divided into organic and mineral origin.
Under a microscope, the urine sediment is divided into parts.
Organic sediments
- Red blood cells can be found as organic. Such a “find” may indicate a pathology of the urinary tract.
- Leukocytes can be found normally, but not more than 1–2. If the quantity is higher, this indicates kidney pathology.
- Epithelial cells are always present in urine sediment, since the epithelial cover is constantly changing, but this indicator is more pronounced in females.
- If found increased number of cylinders , then this may indicate pathology of the kidneys and urinary system.
The presence of red blood cells indicates urinary tract disease.
Inorganic sediments
If the urine pH is acidic, then uric acid, calcium phosphate, and calcium sulfate may predominate. If the reaction is closer to alkaline, then amorphous phosphates, magnesium phosphate, calcium carbonate, tripel phosphate may be present.
When uric acid appears (normally it should not be present), we can talk about strong physical exertion on the dog, or overfeeding with meat food. In pathological processes such as uric acid diathesis, feverish conditions, tumor processes, uric acid will be present in significant quantities.
When you overfeed meat, uric acid appears.
If the dog's urine is closer to brick in color, then amorphous urates will precipitate. Under physiological conditions, such processes are impossible. The presence may indicate fever.
Oxalates
Oxalates (producers of oxalic acid) can be in units. If there are many of them in the field of view, then diabetes mellitus, pyelonephritis, and calcium pathology are possible.
The detection of calcium carbonate will not be a pathology if the dog is fed exclusively with food of plant origin, otherwise it will indicate.
If your dog is a Dalmatian Great Dane or a puppy, ammonium urate will be present in the urine normally. In other cases, it may indicate inflammation of the bladder.
In Dalmatian Great Danes, the presence of ammonium urate is normal.
Crystals and neoplasms
- If found tyrosine or leucine crystals , then the pathology can be caused by leukemia or phosphorus poisoning.
- On kidney tumors , or degenerative processes in them will be indicated by the presence of cholesterol crystals in the sediment.
Tyrosine crystals can be caused by leukemia.
Fatty acids
Sometimes fatty acids can be detected in the urine. Their presence indicates dystrophic changes in the renal tissue, namely the disintegration of the epithelium of the renal tubules.
The presence of fatty acids indicates changes in the kidney tissue.
Bacteriological urine analysis
The detection of bacteria in the field of view of a microscope cannot indicate pathology or normality, but the fact itself is a prerequisite for conducting bacterial analysis.
When inoculating urine on nutrient media and identifying the level ranging from 1000 to 10000 microbial bodies in one milliliter of urine, for females this will be the norm, but for males, it may indicate the onset of inflammatory processes in the genitourinary organs.
Such a urine test is carried out, as a rule, not so much to identify microflora, but to isolate a pure culture and subtitrate the sensitivity of antibiotics, which are then used to treat the animal.
Bacteriological analysis of urine is carried out to determine sensitivity to antibiotics.
Urine analysis for fungi
When sown on nutrient media, microscopic fungi germinate at certain temperatures. Normally, they are absent, but long-term treatment with antibiotics, as well as diabetes mellitus, can activate the growth of pathogenic microflora.
Urinalysis can be carried out qualitatively, using test systems (strips that are not always adapted for veterinary diagnostics) and quantitatively, in the laboratory.
If the initial analysis of the test system showed deviations in one direction or another, this is not yet a reason to panic. Quantitative measurements of urine parameters are necessary. Research should be carried out in a veterinary laboratory, and only one that has the right to conduct certain research.
Urinalysis must be performed in a laboratory setting.
Conclusions
It is necessary to clearly understand that not having research results is better than having incorrect ones. Urine examination is intended not only to identify pathology, but also to differentiate the disease. Any inaccuracy can lead to the prescription of incorrect treatment, which in turn can lead to irreversible consequences.
Urine examination will help to identify pathologies in time.
Video about dog urine analysis
In dogs, urea is 4 - 6 mmol/liter (24 - 36 mg/dl).
In cats, urea is 6 - 12 mmol/liter (36 - 72 mg/dl).
Standards vary slightly from laboratory to laboratory.
For recalculation:
mmol/liter divided by 0.166 gives mg/dl. Mg/dl multiplied by 0.166 gives mmol/liter.
Increased in renal failure
In renal failure, urea increases.
Typically, an increase of up to 20 mmol/liter may not be externally noticeable.
If urea is more than 30 mmol/liter, then appetite worsens or disappears.
When urea is above 60 mmol/liter there is usually frequent vomiting, followed by vomiting blood.
Rare cases
Some animals with chronic renal failure can feel quite well and retain their appetite even with urea of 90 mmol/liter.
In our practice, there was a live animal with urea 160 mmol/liter.
Origin of urea
Approximately half of the urea is formed in the liver during biochemical protein reactions. The second half is also formed in the liver, but during the neutralization of ammonia coming from the intestines.
During fasting, a state of hypercatabolism develops and the formation of urea as a result of metabolic processes increases.
When defecation is delayed, especially with micro or macro bleeding in the intestines, the formation of ammonia sharply increases as a result of putrefactive processes, and as a result, urea in the blood increases.
Other cases of increased urea in the blood
High protein diet.
Putrefactive processes in the intestines as a result of dysbacteriosis, lack of bile, and eating not fresh foods.
Bleeding in the stomach or intestines.
With normally functioning kidneys, in all of the above cases, urea rarely exceeds 30 mmol/liter, at the same time creatinine remains within normal limits, and in case of renal failure, creatinine is also increased.
Cases of decreased blood urea
Prolonged protein fasting.
Cirrhotic changes in the liver. In this case, ammonia from the intestines is not completely converted into urea.
Polyuria, polydipsia. Along with more fluid, more urea is removed from the body. With PN, even with polyuria, urea in the blood remains elevated.
Toxicity of urea to the body
Urea is neutralized ammonia, so urea itself is not toxic.
But very high urea increases the osmolarity of the blood plasma, and this can have harmful effects on the body.
When a lot of urea is released from the blood into the stomach, the urea turns into ammonia, which irritates the walls of the stomach and intestines and increases ulcerative damage to the mucous membrane.
Urea is a marker of toxicosis
In general, urea is used in analyzes as a marker of the amount of toxic metabolic products of approximately the same molecular weight.
The formation and release of urea are not constant values, depending on many factors, therefore, even with the same numbers in the analyses, the general condition of the animals may be different.
How to correctly take blood tests for urea during PN
Urea tests can be done in whole blood, plasma or serum, depending on the capabilities of the instruments.
You can take blood at any time, in any condition, because with renal failure, fluctuations in indicators decrease.
Treatment of kidney failure in animals
Biochemical blood test.
A biochemical blood test is a laboratory diagnostic method that allows you to evaluate the functioning of many internal organs. A standard biochemical blood test includes the determination of a number of indicators that reflect the state of protein, carbohydrate, lipid and mineral metabolism, as well as the activity of some key enzymes in the blood serum.
For research, blood is taken strictly on an empty stomach into a test tube with a coagulation activator, and the blood serum is examined.
- General biochemical parameters.
Total protein.
Total protein is the total concentration of all blood proteins. There are different classifications of plasma proteins. They are most often divided into albumin, globulins (all other plasma proteins) and fibrinogen. The concentration of total protein and albumin is determined by biochemical analysis, and the concentration of globulins by subtracting the concentration of albumin from the total protein.
Promotion:
- dehydration,
- inflammatory processes,
- tissue damage,
- diseases accompanied by activation of the immune system (autoimmune and allergic diseases, chronic infections, etc.),
- pregnancy.
False overestimation of protein can occur with lipemia (chylosis), hyperbilirubinemia, significant hemoglobinemia (hemolysis).
Demotion:
- overhydration,
- bleeding,
- nephropathy
- enteropathy,
- strong exudation,
- ascites, pleurisy,
- lack of protein in food,
- long-term chronic diseases characterized by depletion of the immune system (infections, neoplasms),
- treatment with cytostatics, immunosuppressants, glucocorticosteroids, etc.
During bleeding, the concentration of albumin and globulins decreases in parallel, however, in some disorders accompanied by protein loss, the albumin content decreases primarily, since the size of its molecules is smaller compared to other plasma proteins.
Normal value
Dog 55-75 g/l
Cat 54-79 g/l
Albumen
A homogeneous plasma protein containing a small amount of carbohydrates. An important biological function of albumin in plasma is to maintain intravascular colloid osmotic pressure, thereby preventing plasma from leaving the capillaries. Therefore, a significant decrease in albumin levels leads to the appearance of edema and effusions in the pleural or abdominal cavity. Albumin serves as a carrier molecule, transporting bilirubin, fatty acids, drugs, free cations (calcium, copper, zinc), some hormones, and various toxic agents. It also collects free radicals and binds mediators of inflammatory processes that pose a danger to tissues.
Promotion:
- dehydration
Disorders that would be accompanied by increased albumin synthesis are not known.
Demotion:
- overhydration;
- bleeding,
- nephropathy and enteropathy,
- severe exudation (for example, burns);
- chronic liver failure,
- lack of protein in food,
- malabsorption syndrome,
- insufficiency of exocrine pancreatic function
Normal value
Dog 25-39 g/l
Cat 24-38 g/l
Bilirubin.
Bilirubin is produced in macrophages by enzymatic catabolism of the heme fraction from various hemeproteins. Most of the circulating bilirubin (about 80%) is formed from “old” red blood cells. Dead “old” red blood cells are destroyed by reticuloendothelial cells. The oxidation of heme produces biliverdin, which is metabolized to bilirubin. The remaining portion of circulating bilirubin (about 20%) is formed from other sources (destruction of mature red blood cells in the bone marrow containing heme, muscle myoglobin, enzymes). The bilirubin thus formed circulates in the bloodstream, being transported to the liver in the form of a soluble bilirubin-albumin complex. Bilirubin bound to albumin can be easily removed from the blood by the liver. In the liver, bilirubin binds to glucuronic acid under the influence of glucuronyltransferases. Bound bilirubin includes bilirubin monoglucuronide, which predominates in the liver, and bilirubin diglucuronide, which predominates in bile. Bound bilirubin is transported into the bile capillaries, from where it enters the bile ducts and then into the intestines. In the intestine, bound bilirubin undergoes a series of transformations to form urobilinogen and stercobilinogen. Stercobilinogen and small amounts of urobilinogen are excreted in feces. The main amount of urobilinogen is reabsorbed in the intestine, reaching the liver through the portal circulation and being re-excreted by the gallbladder.
Serum bilirubin levels rise when bilirubin production exceeds its metabolism and excretion from the body. Clinically, hyperbilirubinemia is expressed by jaundice (yellow pigmentation of the skin and sclera).
Direct bilirubin
It is conjugated bilirubin, soluble and highly reactive. An increase in the level of direct bilirubin in the blood serum is associated with reduced excretion of the conjugated pigment from the liver and biliary tract and manifests itself in the form of cholestatic or hepatocellular jaundice. A pathological increase in the level of direct bilirubin leads to the appearance of this pigment in the urine. Since indirect bilirubin is not excreted in the urine, the presence of bilirubin in the urine highlights the increase in serum levels of conjugated bilirubin.
Indirect bilirubin
The serum concentration of unconjugated bilirubin is determined by the rate at which newly synthesized bilirubin enters the blood plasma and the rate of elimination of bilirubin by the liver (hepatic bilirubin clearance).
Indirect bilirubin is calculated by calculation:
indirect bilirubin = total bilirubin - direct bilirubin.
Promotion
- accelerated destruction of red blood cells (hemolytic jaundice),
- hepatocellular disease (hepatic and extrahepatic origin).
Chylosis can cause a falsely elevated bilirubin level, which should be taken into account if a high bilirubin level is determined in a patient in the absence of jaundice. “Chylous” blood serum becomes white, which is associated with an increased concentration of chylomicrons and/or very low-density lipoproteins. Most often, chyle is the result of a recent meal, but in dogs it can be caused by diseases such as diabetes, pancreatitis, and hypothyroidism.
Demotion
No clinical significance.
Normal value:
Total bilirubin
Dog – 2.0-13.5 µmol/l
Cat – 2.0-10.0 µmol/l
Direct bilirubin
Dog – 0-5.5 µmol/l
Cat – 0-5.5 µmol/l
Alanine aminotransferase (ALT)
ALT is an endogenous enzyme from the group of transferases, widely used in medical and veterinary practice for laboratory diagnosis of liver damage. It is synthesized intracellularly, and normally only a small part of this enzyme enters the blood. If the energy metabolism of liver cells is disrupted by infectious factors (for example, viral hepatitis) or toxic, this leads to an increase in the permeability of cell membranes with the passage of cytoplasmic components into the serum (cytolysis). ALT is an indicator of cytolysis, the most studied and most indicative of even minimal liver damage. ALT is more specific for liver disorders than AST. Absolute ALT values still do not directly correlate with the severity of liver damage and with predicting the development of the pathological process, and therefore serial determinations of ALT over time are the most appropriate.
Increased:
- liver damage
- use of hepatotoxic drugs
Downgraded:
- pyridoxine deficiency
- repeated hemodialysis
- sometimes during pregnancy
Normal value:
Dog 10-58 units/l
Cat 18-79 units/l
Aspartate aminotransferase (AST)
Aspartate aminotransferase (AST) is an endogenous enzyme from the group of transferases. Unlike ALT, which is found mainly in the liver, AST is present in many tissues: myocardium, liver, skeletal muscle, kidney, pancreas, brain tissue, spleen, being a less characteristic indicator of liver function. At the level of liver cells, AST isoenzymes are found both in the cytosol and in the mitochondria.
Increased:
— Toxic and viral hepatitis
— Necrosis of liver tissue
— Acute myocardial infarction
— Administration of opioids to patients with biliary tract diseases
An increase and rapid decrease suggests extrahepatic biliary obstruction.
Downgraded:
— Azotemia
Normal value:
Dog – 8-42 units/l
Cat – 9-45 units/l
An increase in ALT that exceeds an increase in AST is characteristic of liver damage; if the AST indicator increases more than the ALT increases, then this, as a rule, indicates problems with the myocardial cells (heart muscle).
γ - glutamyltransferase (GGT)
GGT is an enzyme localized on the membrane of cells of various tissues, catalyzing the reaction of transamination or transamination of amino acids in the process of their catabolism and biosynthesis. The enzyme transfers γ-glutamyl from amino acids, peptides and other substances to acceptor molecules. This reaction is reversible. Thus, GGT is involved in the transport of amino acids across the cell membrane. Therefore, the highest enzyme content is observed in the membrane of cells with high secretory and absorption capacity: liver tubules, bile duct epithelium, nephron tubules, small intestinal villi epithelium, pancreatic exocrine cells.
Since GGT is associated with epithelial cells of the bile duct system, it has diagnostic value in cases of liver dysfunction.
Increased:
- cholelithiasis
- in dogs with increasing concentrations of glucorticosteroids
- hyperthyroidism
- hepatitis of extra- or intrahepatic origin, liver neoplasia,
- acute pancreatitis, pancreatic cancer
- exacerbation of chronic glomerulonephritis and pyelonephritis,
Downgraded:
Normal value
Dog 0-8 units/l
Cat 0-8 units/l
Unlike ALT, which is found in the cytosol of hepatocytes and is therefore a sensitive marker of damage to cell integrity, GGT is found exclusively in mitochondria and is released only when there is significant tissue damage. Unlike in humans, anticonvulsants used in dogs do not cause an increase in GGT activity or it is minimal. In cats with liver lipidosis, ALP activity increases to a greater extent than GGT. Colostrum and breast milk contain high GGT activity in the early stages of feeding, so GGT levels are elevated in newborns.
Alkaline phosphatase.
This enzyme is found mainly in the liver (bile tubules and bile duct epithelium), kidney tubules, small intestine, bones and placenta. This is an enzyme associated with the cell membrane that catalyzes the alkaline hydrolysis of a wide variety of substances, during which the phosphoric acid residue is separated from its organic compounds.
The total activity of alkaline phosphatase in the circulating blood of healthy animals consists of the activity of liver and bone isoenzymes. The proportion of activity of bone isoenzymes is greatest in growing animals, while in adults their activity may increase with bone tumors.
Promotion:
- impaired bile flow (cholestatic hepatobiliary disease),
- nodular liver hyperplasia (develops with aging),
- cholestasis,
- increased osteoblast activity (at a young age),
— diseases of the skeletal system (bone tumors, osteomalacia, etc.)
— pregnancy (an increase in alkaline phosphatase during pregnancy occurs due to the placental isoenzyme).
- May be associated with hepatic lipidosis in cats.
Demotion:
- hypothyroidism,
— hypovitaminosis C.
Normal value
Dog 10-70 units/l
Cat 0-55 units/l
Alpha amylase
Amylase is a hydrolytic enzyme involved in the breakdown of carbohydrates. Amylase is produced in the salivary glands and pancreas, then enters the oral cavity or the lumen of the duodenum, respectively. Such organs as the ovaries, fallopian tubes, small and large intestines, and liver also have significantly lower amylase activity. In blood serum, pancreatic and salivary amylase isoenzymes are isolated. The enzyme is excreted by the kidneys. Therefore, an increase in serum amylase activity leads to an increase in urinary amylase activity. Amylase can form large complexes with immunoglobulins and other plasma proteins, which does not allow it to pass through the glomeruli, as a result of which its content in the serum increases, and amylase activity in the urine is normal.
Increased:
— Pancreatitis (acute, chronic, reactive).
- Neoplasms of the pancreas.
— Blockage of the pancreatic duct (tumor, stone, adhesions).
- Acute peritonitis.
— Diabetes mellitus (ketoacidosis).
— Diseases of the biliary tract (cholelithiasis, cholecystitis).
- Kidney failure.
— Traumatic lesions of the abdominal cavity.
Downgraded:
— Acute and chronic hepatitis.
- Pancreatic necrosis.
- Thyrotoxicosis.
- Myocardial infarction.
Normal values:
Dog – 300-1500 units/l
Cat – 500-1200 units/l
Pancreatic amylase.
Amylase is an enzyme that catalyzes the breakdown (hydrolysis) of complex carbohydrates (starch, glycogen and some others) into disaccharides and oligosaccharides (maltose, glucose). In animals, much of the amylase activity is due to the small intestinal mucosa and other extrapancreatic sources. With the participation of amylase in the small intestine, the process of digesting carbohydrates is completed. Various disruptions of processes in the acinar cells of the exocrine part of the pancreas, increased permeability of the pancreatic duct and premature activation of enzymes lead to “leakage” of enzymes inside the organ.
Promotion:
- kidney failure
- severe inflammatory bowel diseases (perforation of the small intestine, volvulus),
- long-term treatment with glucocorticosteroids.
Demotion :
- inflammation,
- necrosis or tumor of the pancreas.
Normal value
Dog 243.6-866.2 units/l
Cat 150.0-503.5 units/l
Glucose.
Glucose is the main source of energy in the body. As part of carbohydrates, glucose enters the body with food and is absorbed into the blood from the jejunum. It can also be synthesized by the body mainly in the liver and kidneys from non-carbohydrate components. All organs have a need for glucose, but especially a lot of glucose is used by brain tissue and red blood cells. The liver regulates blood glucose levels through glycogenesis, glycolysis, and gluconeogenesis. In the liver and muscles, glucose is stored in the form of glycogen, which is used to maintain the physiological concentration of glucose in the blood, primarily in the intervals between meals. Glucose is the only source of energy for the work of skeletal muscle under anaerobic conditions. The main hormones influencing glucose homeostasis are insulin and deregulating hormones - glucagon, catecholamines and cortisol.
Promotion:
- insulin deficiency or tissue resistance to insulin,
– pituitary tumors (common in cats),
- acute pancreatitis,
- renal failure,
- taking certain medications (glucocorticosteroids, thiazide diuretics, intravenous administration of fluids containing glucose, progestins, etc.),
- severe hypothermia.
Short-term hyperglycemia is possible with head injuries and central nervous system lesions.
Demotion:
- pancreatic tumor (insulinoma),
— hypofunction of endocrine organs (hypocortisolism);
- liver failure,
- cirrhosis of the liver;
- prolonged fasting and anorexia;
— congenital portosystemic shunts;
- idiopathic juvenile hypoglycemia in dogs of small and hunting breeds,
- insulin overdose,
- heatstroke
With prolonged contact of blood serum with red blood cells, a drop in glucose is possible, since red blood cells actively consume it, so it is advisable to centrifuge the blood as quickly as possible. The glucose level in uncentrifuged blood decreases by approximately 10% per hour.
Normal value
Dog 4.3-7.3 mmol/l
Cat 3.3-6.3 mmol/l
Creatinine
Creatine is synthesized in the liver, and after release, 98% of it enters muscle tissue, where it is phosphorylated. The resulting phosphocreatine plays an important role in storing muscle energy. When this muscle energy is needed to carry out metabolic processes, phosphocreatine is broken down into creatinine. Creatinine is a stable nitrogenous constituent of the blood, unaffected by most foods, exercise, or other biological constants, and is associated with muscle metabolism.
Impaired renal function reduces creatinine excretion, causing an increase in serum creatinine levels. Thus, creatinine concentrations approximately characterize the level of glomerular filtration. The main value of determining serum creatinine is the diagnosis of renal failure.
Serum creatinine is a more specific and sensitive indicator of renal function than urea.
Promotion:
- acute or chronic renal failure.
Caused by prerenal causes causing a decrease in glomerular filtration rate (dehydration, cardiovascular diseases, septic and traumatic shock, hypovolemia, etc.), renal associated with severe diseases of the kidney parenchyma (pyelonephritis, leptospirosis, poisoning, neoplasia, congenital disorders, trauma, ischemia) and postrenal - obstructive disorders that prevent the excretion of creatinine in the urine (obstruction of the urethra, ureter or rupture of the urinary tract).
Demotion :
- age-related decrease in muscle mass.
Normal value
Dog 26-130 µmol/l
Cat 70-165 µmol/l
Urea
Urea is formed as a result of the catabolism of amino acids from ammonia. Ammonia formed from amino acids is toxic and is converted by liver enzymes into non-toxic urea. The main part of the urea that then enters the circulatory system is easily filtered and excreted by the kidneys. Urea can also passively diffuse into the interstitial tissue of the kidneys and return to the bloodstream. Passive diffusion of urea depends on the rate of urine filtration - the higher it is (for example, after intravenous administration of diuretics), the lower the level of urea in the blood.
Promotion:
- renal failure (may be caused by prerenal, renal and postrenal disorders).
Demotion
- low intake of protein into the body,
- liver diseases.
Normal value
Dog 3.5-9.2 mmol/l
Cat 5.4-12.1 mmol/l
Uric acid
Uric acid is the end product of purine catabolism.
Uric acid is absorbed in the intestine, circulates in the blood as ionized urate, and is excreted in the urine. In most mammals, elimination is carried out by the liver. Hepatocytes, using urease, oxidize uric acid to form water-soluble allantoin, which is excreted by the kidneys. Decreased uric acid metabolism combined with decreased ammonia metabolism during portosystemic shunting leads to the formation of urate crystals with the formation of urate stones (urolithiasis).
In portosystemic shunting (PSS), uric acid formed as a result of purine metabolism practically does not pass through the liver, since PSSs represent a direct vascular connection from the portal vein to the systemic circulation, bypassing the liver.
The predisposition of dogs with pSS to urate urolithiasis is associated with concomitant hyperuricemia, hyperammonemia, hyperuricuria and hyperammoniuria. Since uric acid does not reach the liver in pSS, it is not completely converted to allantoin, which leads to a pathological increase in serum uric acid concentration. In this case, uric acid is freely filtered by the glomeruli, reabsorbed in the proximal tubules and secreted into the tubular lumen of the proximal nephrons. Thus, the concentration of uric acid in urine is determined in part by its concentration in serum.
Dalmatian Dogs are predisposed to the formation of urate crystals due to a particular metabolic disorder of the liver, leading to incomplete oxidation of uric acid.
Promotion
- uric acid diathesis
- leukemia, lymphoma
- anemia caused by vitamin B12 deficiency
- some acute infections (pneumonia, tuberculosis)
- diseases of the liver and biliary tract
- diabetes mellitus
- dermatological diseases
- kidney diseases
- acidosis
Demotion:
- diet poor in nucleic acids
- use of diuretics
Normal value
Dog<60 мкмоль/л
Cat<60 мкмоль/л
Lipase
Pancreatic lipase is an enzyme secreted in large quantities into the duodenum with pancreatic juice and catalyzing the hydrolysis of triglycerides to fatty acids and monoglycerides. Lipase activity is also observed in the stomach, liver, adipose and other tissues. Pancreatic lipase acts on the surface of lipid droplets formed in the intestine.
Promotion :
- perforation of the small intestine,
- chronic renal failure,
- use of corticosteroids,
- postoperative period
Demotion
- hemolysis.
Normal value
Dog<500 ед/л
Cat<200 ед/л
Cholesterol
Determination of cholesterol levels characterizes lipid status and metabolic disorders.
Cholesterol (cholesterol) is a secondary monohydric alcohol. Free cholesterol is a component of cell plasma membranes. Its esters predominate in blood serum. Cholesterol is a precursor to sex hormones, corticosteroids, bile acids and vitamin D. Most of the cholesterol (up to 80%) is synthesized in the liver, and the rest enters the body with products of animal origin (fatty meat, butter, eggs). Cholesterol is insoluble in water; its transport between tissues and organs occurs due to the formation of lipoprotein complexes.
With age, the level of cholesterol in the blood increases, and gender differences in concentration appear, which is associated with the action of sex hormones. Estrogens reduce, and androgens increase, total cholesterol levels.
Increased:
- hyperlipoproteinemia
— obstruction of the biliary tract: cholestasis, biliary cirrhosis;
- nephrosis;
- diseases of the pancreas;
- hypothyroidism, diabetes mellitus;
- obesity.
Downgraded:
- severe hepatocellular damage;
- hyperthyroidism;
- myeloproliferative diseases;
- steatorrhea with malabsorption;
- fasting;
- chronic anemia (megaloblastic / sideroblastic);
- inflammation, infection.
Normal value:
Dog – 3.8-7.0 mmol/l
Cat – 1.6-3.9 mmol/l
Creatine phosphokinase (CPK)
Creatine phosphokinase is an enzyme in the cytoplasm of skeletal muscle and myocardial cells that catalyzes the reversible reaction of converting creatine phosphate into creatinine in the presence of ADP, which is converted into ATP, which is the source of energy for muscle contraction.
The active form of CPK is a dimer consisting of subunits M and B, respectively, there are 3 isoenzymes of CPK: BB (found in the brain), MB (in the myocardium), and MM (in skeletal muscles and myocardium). The degree of increase depends on the nature of the damage and the initial level of the enzyme in the tissue. In cats, the content of CPK in tissues is relatively lower than in animals of other species, so in them one should pay attention to even a slight excess of the upper limit of the standard interval.
Often in cats suffering from anorexia, CPK levels may rise and fall several days after appropriate maintenance feeding.
Promotion
- damage to skeletal muscles (trauma, surgery, muscular dystrophy, polymyositis, etc.).
- after significant physical activity,
- epileptic seizures
- myocardial infarction (2-3 hours after the lesion, and after 14-30 hours it reaches a maximum, the level decreases on 2-3 days).
- metabolic disorders (phosphofructokinase deficiency in dogs, hypothyroidism, hypercortisolism, malignant hyperthermia).
When muscle tissue is damaged, along with CPK, enzymes such as LDH and AST will also increase.
Demotion:
- decrease in muscle mass
Normal value
Dog 32-220 units/l
Cat 150-350 units/l
Lactate dehydrogenase LDH
A cytosolic enzyme that catalyzes the reversible conversion of lactate to pyruvate with the participation of NADH in the process of glycolysis. With a full supply of oxygen, lactate in the blood does not accumulate, but is neutralized and eliminated. With oxygen deficiency, the enzyme tends to accumulate, causing muscle fatigue and disrupting tissue respiration. High LDH activity is inherent in many tissues. There are 5 LDH isoenzymes: 1 and 2 are present mainly in the heart muscle, erythrocytes and kidneys, 4 and 5 are localized in the liver and skeletal muscles. LDH 3 is characteristic of lung tissue. Depending on which of the five isoforms of the enzyme is found in a particular tissue, the method of glucose oxidation depends - aerobic (to CO2 and H2O) or anaerobic (to lactic acid).
Since enzyme activity is high in tissues, even relatively minor tissue damage or mild hemolysis leads to a significant increase in LDH activity in the circulating blood. It follows from this that any diseases accompanied by the destruction of cells that contain LDH isoenzymes are accompanied by an increase in its activity in the blood serum.
Promotion
- myocardial infarction,
- damage and dystrophy of skeletal muscles,
- necrotic damage to the kidneys and liver,
- cholestatic liver diseases,
- pancreatitis,
- pneumonia,
- hemolytic anemia, etc.
Demotion
Has no clinical significance.
Normal value
Dog 23-220 units/l
Cat 35-220 units/l
The degree of increase in LDH activity during myocardial infarction does not correlate with the size of the lesion in the heart muscle and can only serve as an indicative factor for prognosis of the disease. In general, being a non-specific laboratory marker, changes in LDH levels should be assessed only in combination with the values of other laboratory parameters (CPK, AST, etc.), as well as data from instrumental diagnostic methods. It is also important not to forget that even slight hemolysis of blood serum leads to a significant increase in LDH activity.
Cholinesterase ChE
Cholinesterase is an enzyme belonging to the class of hydrolases that catalyzes the breakdown of choline esters (acetylcholine, etc.) with the formation of choline and corresponding acids. There are two types of enzyme: true (acetylcholinesterase) - which plays an important role in the transmission of nerve impulses (located in nervous tissue and muscles, red blood cells), and false (pseudocholinesterase) - serum, present in the liver and pancreas, muscles, heart, brain . ChE performs a protective function in the body, in particular, it prevents the inactivation of acetylcholinesterase by hydrolyzing the inhibitor of this enzyme - butyrylcholine.
Acetylcholine serase is a strictly specific enzyme that hydrolyzes acetylcholine, which takes part in the transmission of signals through the endings of nerve cells and is one of the most important neurotransmitters in the brain. With a decrease in ChE activity, acetylcholine accumulates, which first leads to an acceleration of the conduction of nerve impulses (excitation) and then to a blocking of the transmission of nerve impulses (paralysis). This causes disorganization of all body processes, and in severe poisoning can lead to death.
Measuring the level of ChE in blood serum can be useful in case of poisoning with insecticides or various toxic compounds that inhibit the enzyme (organophosphorus, phenothiazines, fluorides, various alkaloids, etc.)
Promotion
- diabetes;
- breast cancer;
- nephrosis;
- hypertension;
- obesity;
Demotion
- liver damage (cirrhosis, metastatic liver disease)
- muscular dystrophy, dermatomyositis
Normal value
Dog 2200-6500 U/l
Cat 2000-4000 U/l
Calcium. Ionized calcium.
Calcium is present in blood plasma in three forms:
1) in combination with organic and inorganic acids (a very small percentage),
2) in protein-bound form,
3) in ionized form Ca2+.
Total calcium includes the total concentration of all three forms. Of total calcium, 50% is ionized calcium and 50% is bound to albumin. Physiological changes rapidly alter calcium binding. In a biochemical blood test, both the level of total calcium in the blood serum and separately the concentration of ionized calcium are measured. Ionized calcium is determined in cases where it is necessary to determine the calcium content, regardless of the albumin level.
Ionized calcium Ca2+ is a biologically active fraction. Even a slight increase in plasma Ca2+ can lead to death due to muscle paralysis and coma.
In cells, calcium serves as an intracellular mediator that affects various metabolic processes. Calcium ions take part in the regulation of the most important physiological and biochemical processes: neuromuscular excitation, blood coagulation, secretion processes, maintenance of membrane integrity and transport through membranes, many enzymatic reactions, release of hormones and neurotransmitters, intracellular action of a number of hormones, participates in the process of bone mineralization. Thus, they ensure the functioning of the cardiovascular and neuromuscular systems. The normal course of these processes is ensured by the fact that the concentration of Ca2+ in the blood plasma is maintained within very narrow limits. Therefore, a violation of Ca2+ concentration in the body can cause many pathologies. When calcium levels drop, the most dangerous consequences are ataxia and seizures.
Changes in the concentration of plasma proteins (primarily albumin, although globulins also bind calcium) are accompanied by corresponding changes in the level of total calcium in the blood plasma. The binding of calcium to plasma proteins depends on pH: acidosis promotes the transition of calcium into an ionized form, and alkalosis increases binding to proteins, i.e. reduces the concentration of Ca2+.
Three hormones are involved in calcium homeostasis: parathyroid hormone (PTH), calcitriol (vitamin D), and calcitonin, which act on three organs: bones, kidneys, and intestines. They all work using a feedback mechanism. Calcium metabolism is influenced by estrogens, corticosteroids, growth hormone, glucagon and T4. PTH is the main physiological regulator of calcium concentration in the blood. The main signal influencing the intensity of the secretion of these hormones is the change in ionized Ca in the blood. Calcitonin is secreted by parafollicular c-cells of the thyroid gland in response to an increase in Ca2+ concentration, while it disrupts the release of Ca2+ from the labile calcium store in the bones. When Ca2+ falls, the reverse process occurs. PTH is secreted by the cells of the parathyroid glands and as calcium concentrations fall, PTH secretion increases. PTH stimulates the release of calcium from the bones and the reabsorption of Ca in the renal tubules.
Promotion:
- hyperalbuminemia
- malignant tumors
- primary hyperparathyroidism;
- hypocortisolism;
— osteolytic bone lesions (ostomyelitis, myeloma);
— idiopathic hypercalcemia (cats);
Demotion:
- hypoalbuminemia;
- alkalosis;
- primary hypoparathyroidism;
- chronic or acute renal failure;
- secondary renal hyperparathyroidism;
- pancreatitis;
- unbalanced diet, vitamin D deficiency;
- eclampsia or postpartum paresis;
- impaired absorption from the intestine;
- hypercalcitonism;
- hyperphosphatemia;
- hypomagnesemia;
- enterocolitis;
- blood transfusion;
- idiopathic hypocalcemia;
- extensive soft tissue injury;
Iron
Iron is an important component of heme-containing enzymes and is part of hemoglobin, cytochromes and other biologically important compounds. Iron is a necessary element for the formation of red blood cells and is involved in oxygen transfer and tissue respiration. It also participates in a number of redox reactions, the functioning of the immune system, and collagen synthesis. Developing erythroid cells take up 70 to 95% of the iron circulating in the plasma, and hemoglobin accounts for 55 to 65% of the total iron content in erythrocytes. Iron absorption depends on the age and health of the animal, the state of iron metabolism in the body, as well as the amount of iron and its chemical form. Under the influence of gastric hydrochloric acid, iron oxides ingested in food become soluble and bind in the stomach with mucin and various small molecules that keep iron in a soluble state, suitable for absorption in the alkaline environment of the small intestine. Under normal conditions, only a small percentage of iron from food enters the bloodstream. Iron absorption increases with its deficiency in the body, increased erythropoiesis or hypoxia and decreases with its high total content in the body. More than half of all iron is part of hemoglobin.
It is advisable to test blood for iron on an empty stomach, since there are daily fluctuations in its level with maximum values in the morning. The level of iron in the serum depends on a number of factors: absorption in the intestine, accumulation in the liver, spleen, bone marrow, destruction and loss of hemoglobin, synthesis of new hemoglobin.
Increased:
- hemolytic anemia,
- folate deficiency hyperochromic anemia,
- liver diseases,
- administration of corticosteroids
- lead intoxication
Downgraded:
— vitamin B12 deficiency;
- iron deficiency anemia;
- hypothyroidism;
- tumors (leukemia, myeloma);
— infectious diseases;
- blood loss;
— chronic liver damage (cirrhosis, hepatitis);
- gastrointestinal diseases.
Chlorine
Chlorine is the main anion of extracellular fluids, present in gastric juice, pancreatic and intestinal secretions, sweat, and cerebrospinal fluid. Chlorine is an important regulator of extracellular fluid volume and plasma osmolarity. Chlorine maintains cell integrity through its effect on osmotic pressure and acid-base balance. In addition, chlorine promotes the retention of bicarbonate in the distal renal tubules.
There are two types of metabolic alkalosis with hyperchloremia:
the chlorine-sensitive type, which can be corrected by the administration of chlorine, occurs with vomiting and the administration of diuretics, as a result of the loss of H+ and Cl- ions;
the chlorine-resistant type, uncorrected by the administration of chlorine, is observed in patients with primary or secondary hyperaldosteronism.
Increased:
- dehydration,
- chronic hyperventilation with respiratory acidosis,
- metabolic acidosis with prolonged diarrhea,
- hyperparathyroidism,
- renal tubular acidosis,
- traumatic brain injury with damage to the hypothalamus,
- eclampsia.
Downgraded:
- general overhydration,
- uncontrollable vomiting or gastric aspiration with alkalosis with hypochloremia and hypokalemia,
- hyperaldosteronism,
- Cushing's syndrome,
— ACTH-producing tumors,
- burns of varying degrees,
- congestive heart failure,
- metabolic alkalosis,
- chronic hypercapnia with respiratory failure,
Normal value:
Dog – 96-122 mmol/l
Cat – 107-129 mmol/l
Potassium
Potassium is the main electrolyte (cation) and a component of the intracellular buffer system. Almost 90% of potassium is concentrated inside the cell, with only small amounts present in the bones and blood. Potassium is concentrated mainly in skeletal muscles, liver and myocardium. Potassium is released from damaged cells into the blood. All potassium that enters the body with food is absorbed in the small intestine. Normally, up to 80% of potassium is excreted in the urine, and the rest in feces. Regardless of the amount of potassium supplied from the outside, it is excreted daily by the kidneys, resulting in rapid hypokalemia.
Potassium is a vital component for the normal formation of membrane electrical phenomena, it plays an important role in the conduction of nerve impulses, muscle contractions, acid-base balance, osmotic pressure, protein anabolism and glycogen formation. Together with calcium and magnesium, K+ regulates heart contraction and cardiac output. Potassium and sodium ions are of great importance in regulating acid-base balance by the kidneys.
Potassium bicarbonate is the main intracellular inorganic buffer. With potassium deficiency, intracellular acidosis develops, in which the respiratory centers react with hyperventilation, which leads to a decrease in pCO2.
Increases and decreases in serum potassium levels are caused by disturbances in the internal and external potassium balance. The external balance factor is: dietary potassium intake, acid-base balance, mineralocorticoid function. Factors of internal balance include the function of adrenal hormones, which stimulate its excretion. Mineralocorticoids directly affect potassium secretion in the distal tubules; glucocorticosteroids act indirectly, increasing glomerular filtration rate and urinary excretion, as well as increasing sodium levels in the distal tubules.
Increased:
- massive muscle injuries
- destruction of the tumor,
- hemolysis, disseminated intravascular coagulation syndrome,
- metabolic acidosis,
- decompensated diabetes mellitus,
- renal failure,
- prescription of anti-inflammatory non-steroidal drugs,
- prescription of K-sparing diuretics,
Downgraded:
- prescription of non-potassium-sparing diuretics.
- diarrhea, vomiting,
- taking laxatives,
- profuse sweating,
- severe burns.
Hypokalemia associated with decreased urinary K+ excretion, but without metabolic acidosis or alkalosis:
- parenteral therapy without additional potassium supplementation,
- starvation, anorexia, malabsorption,
- rapid growth of cell mass when treating anemia with iron, vitamin B12 or folic acid.
Hypokalemia associated with increased K+ excretion and metabolic acidosis:
- renal tubular acidosis (RTA),
- diabetic ketoacidosis.
Hypokalemia associated with increased K+ excretion and normal pH (usually of renal origin):
- recovery after obstructive nephropathy,
- prescription of penicillins, aminoglycosides, cisplatin, mannitol,
- hypomagnesemia,
- monocytic leukemia
Normal values:
Dog – 3.8-5.6 mmol/l
Cat – 3.6-5.5 mmol/l
Sodium
In body fluids, sodium is in an ionized state (Na+). Sodium is present in all fluids of the body, mainly in the extracellular space, where it is the main cation, and potassium is the main cation in the intracellular space. The predominance of sodium over other cations persists in other body fluids, such as gastric juice, pancreatic juice, bile, intestinal juice, sweat, and CSF. Relatively large amounts of sodium are found in cartilage and slightly less in bones. The total amount of sodium in bones increases with age, and the proportion stored decreases. This lobe is clinically important because it represents a reservoir for sodium loss and acidosis.
Sodium is the main component of fluid osmotic pressure. All movements of sodium cause movement of certain amounts of water. The volume of extracellular fluid directly depends on the total amount of sodium in the body. The sodium concentration in plasma is identical to the concentration in the interstitial fluid.
Increased:
- use of diuretics,
- diarrhea (in young animals)
- Cushing's syndrome,
Downgraded:
A decrease in the volume of extracellular fluid is observed when:
- jade with salt loss,
- glucocorticoid deficiency,
- osmotic diuresis (diabetes with glucosuria, condition after obstruction of the urinary tract),
- renal tubular acidosis, metabolic alkalosis,
- ketonuria.
A moderate increase in extracellular fluid volume and a normal level of total sodium is observed with:
- hypothyroidism,
- pain, stress
- sometimes in the postoperative period
An increase in the volume of extracellular fluid and an increase in the level of total sodium is observed with:
- congestive heart failure (serum sodium level is a predictor of mortality),
- nephrotic syndrome, renal failure,
- cirrhosis of the liver,
- cachexia,
- hypoproteinemia.
Normal value:
Dog – 140-154 mmol/l
Cat – 144-158 mmol/l
Phosphorus
After calcium, phosphorus is the most abundant mineral element in the body, present in all tissues.
In the cell, phosphorus mainly takes part in the metabolism of carbohydrates and fats or is associated with proteins, and only a small part is in the form of phosphate ion. Phosphorus is part of bones and teeth, is one of the components of nucleic acids, phospholipids of cell membranes, is also involved in maintaining acid-base balance, storing and transferring energy, in enzymatic processes, stimulates muscle contraction and is necessary to maintain neuronal activity. The kidneys are the main regulators of phosphorus homeostasis.
Increased:
— Osteoporosis.
- Use of cytostatics (cytolysis of cells and release of phosphates into the blood).
— Acute and chronic renal failure.
— Bone tissue breakdown (for malignant tumors)
— Hypoparathyroidism,
— Acidosis
— Hypervitaminosis D.
- Portal cirrhosis.
— Healing of bone fractures (formation of bone “callus”).
Downgraded:
- Osteomalacia.
- Malabsorption syndrome.
- Severe diarrhea, vomiting.
— Hyperparathyroidism is the primary and ectopic synthesis of hormones by malignant tumors.
- Hyperinsulinemia (in the treatment of diabetes mellitus).
— Pregnancy (physiological phosphorus deficiency).
— Deficiency of somatotropic hormone (growth hormone).
Normal value:
Dog – 1.1-2.0 mmol/l
Cat – 1.1-2.3 mmol/l
Magnesium
Magnesium is an element that, although found in small quantities in the body, is of great importance. About 70% of the total amount of magnesium is found in bones, and the rest is distributed in soft tissues (especially skeletal muscles) and in various fluids. Approximately 1% is found in plasma, 25% is bound to proteins, and the remainder remains in ionized form. Most magnesium is found in the mitochondria and nucleus. In addition to its plastic role as a constituent of bones and soft tissues, Mg has many functions. Together with sodium, potassium and calcium ions, magnesium regulates neuromuscular excitability and the blood clotting mechanism. The actions of calcium and magnesium are closely related; a deficiency of one of the two elements significantly affects the metabolism of the other (magnesium is necessary for both intestinal absorption and calcium metabolism). In muscle cells, magnesium acts as a calcium antagonist.
Magnesium deficiency leads to calcium mobilization from bones, so it is recommended to consider calcium levels when assessing magnesium levels. From a clinical point of view, magnesium deficiency causes neuromuscular diseases (muscle weakness, tremors, tetany and convulsions), and can cause cardiac arrhythmias.
Increased:
- iatrogenic causes
- kidney failure
- dehydration;
- diabetic coma
- hypothyroidism;
Downgraded:
— diseases of the digestive system: malabsorption or excessive loss of fluids through the gastrointestinal tract;
- renal diseases: chronic glomerulonephritis, chronic pyelonephritis, renal tubular acidosis, diuretic phase of acute tubular necrosis,
- use of diuretics, antibiotics (aminoglycosides), cardiac glycosides, cisplatin, cyclosporine;
- endocrine disorders: hyperthyroidism, hyperparathyroidism and other causes of hypercalcemia, hyperparathyroidism, diabetes mellitus, hyperaldosteronism,
- metabolic disorders: excessive lactation, last trimester of pregnancy, insulin treatment of diabetic coma;
- eclampsia,
- osteolytic bone tumors,
- progressive Paget's disease of bones,
- acute and chronic pancreatitis,
- severe burns,
- septic conditions,
- hypothermia.
Normal value:
Dog – 0.8-1.4 mmol/l
Cat – 0.9-1.6 mmol/l
Bile acids
Determination of total bile acids (BA) in the circulating blood is a liver function test due to a special process of bile acid recycling called enterohepatic circulation. The main components involved in the recycling of bile acids are the hepatobiliary system, the terminal ileum and the portal vein system.
Circulation disorders in the portal vein system in most animals are associated with portosystemic shunting. Portsystemic shunt is an anastomosis between the veins of the gastrointestinal tract and the caudal vena cava, due to which the blood flowing from the intestines does not undergo purification in the liver, but immediately enters the body. As a result, compounds that are toxic to the body, primarily ammonia, enter the bloodstream, causing severe disorders of the nervous system.
In dogs and cats, most of the bile produced is usually stored in the gallbladder before meals. Eating stimulates the release of cholecystokinin from the intestinal wall, which causes contraction of the gallbladder. There is individual physiological variability in the amount of bile stored and the degree of gallbladder contraction during food stimulation, and the relationship between these values changes in some sick animals.
When circulating bile acid concentrations are within or close to the standard range, such physiological fluctuations can cause postprandial bile acid levels to be similar to or even lower than fasting levels. In dogs, this can also occur when there is an overgrowth of bacteria in the small intestine.
Increased levels of bile acids in the blood, secondary to liver disease or portosystemic shunting, are accompanied by increased excretion in the urine. In dogs and cats, determination of the bile acids/creatinine ratio in urine is a fairly sensitive test for diagnosing liver diseases.
It is important to study the level of bile acids on an empty stomach and 2 hours after meals.
Rarely, there may be false negative results resulting from severe intestinal malabsorption.
Increased:
— hepatobiliary diseases, in which there is a violation of the secretion of fatty acids through the biliary tract (obstruction of the intestines and bile ducts, cholestasis, neoplasia, etc.);
- circulatory disorders in the portal vein system,
— portsystemic shunt (congenital or acquired);
— terminal stage of liver cirrhosis;
- microvascular dysplasia of the liver;
- impairment of the ability of hepatocytes to absorb fatty acids, characteristic of many liver diseases.
Normal value:
Dog 0-5 µmol/l
Portosystemic shunts (PSS) provide a direct vascular connection from the portal vein to the systemic circulation, so that substances in the portal blood are diverted from the intestinal tract to bypass the liver without hepatic metabolism. Dogs with pSS are very likely to develop ammonium urate uroliths. These uroliths occur in both males and females and are usually, but not always, diagnosed in animals over 3 years of age. The predisposition of dogs with pSS to urate urolithiasis is associated with concomitant hyperuricemia, hyperammonemia, hyperuricuria and hyperammoniuria.
However, not all dogs with pSS have ammonium urate uroliths.
Etiology and pathogenesis
Uric acid is one of several breakdown products of purine. In most dogs it is converted by hepatic urease to allantoin. (Bartgesetal., 1992). However, in pSS, little or no uric acid produced from purine metabolism passes through the liver. Consequently, it is not completely converted to allantoin, resulting in an abnormal increase in serum uric acid concentration. When examining 15 dogs with pSS at the University of Minnesota teaching hospital, the serum uric acid concentration was determined to be 1.2-4 mg/dL; in healthy dogs, this concentration was 0.2-0.4 mg/dL (Lulichetal., 1995). Uric acid is freely filtered by the glomeruli, reabsorbed in the proximal tubules and secreted into the tubular lumen of the distal proximal nephrons.
Thus, the concentration of uric acid in urine is determined in part by its concentration in serum. Due to northosystemic blood shunting, the concentration of uric acid in the serum increases, and, accordingly. in urine. Uroliths that form in pSS usually consist of ammonium urate. Ammonium urate is formed because the urine becomes supersaturated with ammonia and uric acid due to the diversion of blood from the portal system directly into the systemic circulation.
Ammonia is produced mainly by bacterial colonies and is absorbed into the portal circulation. In healthy animals, ammonia enters the liver, and there it is converted into urea. In dogs with pSS, a small amount of ammonia is converted to urea, so its concentration in the systemic circulation increases. Increased concentrations of circulating ammonia result in increased urinary ammonia excretion. The result of portal blood bypass of hepatic metabolism is an increase in systemic concentrations of uric acid and ammonia, which are excreted in the urine. If the saturation of urine with ammonia and uric acid exceeds the solubility of ammonium urates, they precipitate. Precipitation under conditions of supersaturated urine leads to the formation of ammonium urate uroliths.
Clinical symptoms
Urate uroliths in pSS usually form in the bladder, therefore, affected animals will develop symptoms of urinary tract disease - hematuria, dysuria, pollakiuria and urinary dysfunction. With urethral obstruction, symptoms of anuria and post-nasal azotemia are observed. Some dogs with bladder stones do not have symptoms of urinary tract disease. Despite the fact that ammonium urate uroliths can also form in the renal pelvis, they are found there very rarely. The PSS dog may have symptoms of hepatoencephalopathy - tremors, drooling, seizures, bleeding and slow growth
Diagnostics
Rice. 1. Microphotograph of urine sediment from a 6-year-old male miniature schnauzer. Urine sediment contains crystals of ammonium urate (unstained, magnification x 100)
Rice. 2. Double contrast cystogram
ma of a 2-year-old male Lhasa Apso with PSS.
Three radiolucent concretions are shown.
ment and a decrease in liver size. At
analysis of stones removed by surgery
chemically, it was revealed that they are
100% consisted of ammonium urate
Laboratory tests
Ammonium urate crystalluria is often found in dogs with pSS (Figure 1), which is an indicator of possible stone formation. Urine specific gravity may be low due to decreased concentration of urine in the nocturnal medulla. Another common disorder in dogs with pSS is microcytic anemia. Serum chemistry tests in dogs with pSS are generally normal, except for low blood urea nitrogen concentrations caused by insufficient conversion of ammonia to urea.
Sometimes there is an increase in the activity of alkaline phosphatase and alanine aminotransferase, and the concentration of albumin and glucose may be low. Serum uric acid concentrations will be elevated, but these values should be interpreted with caution due to the unreliability of spectrophotometric methods for uric acid analysis. (Felicee et al., 1990). In dogs with pSS, liver function test results will include increased serum bile acid concentrations before and after feeding, increased blood and plasma ammonia concentrations before and after ammonium chloride administration, and increased bromsulfalein retention.
X-ray studies
Ammonium urate uroliths may be radiolucent. therefore, sometimes they cannot be identified on regular x-rays. However, an X-ray of the abdominal cavity can show a decrease in the size of the liver due to its atrophy, which was the result of portosystemic shunting of the blood. Rsnomegaly is sometimes observed in pSS; its significance is unclear. Ammonium urate uroliths in the bladder can be seen with double-contrast cystography (Figure 2) or ultrasound. If uroliths are present in the urethra, then contrast retrography is necessary to determine their size, number and location. When assessing the urinary tract, double contrast cystography and retrograde contrast urethrography have several advantages over abdominal ultrasound. Contrast images show both the bladder and urethra, but ultrasound scans show only the bladder. The number and size of stones can also be determined by contrast cystography. The main disadvantage of contrast radiography of the urinary tract is its invasiveness, since this examination requires sedation or general anesthesia. The condition of the kidneys can be assessed in terms of the presence of stones in the renal pelvis, but excretory urography is a more reliable way to examine the kidneys and ureters.
Treatment
Although it is possible to medically dissolve ammonium urate uroliths in dogs without pSS using an alkaline low-purine diet in combination with allonurinol, drug therapy will not be effective in dissolving stones in dogs with pSS. The effectiveness of allopurinol may be altered in these animals due to the biotransformation of the short half-life drug to the long half-life oxypurinol (Bartgesetal.,1997). Also, drug dissolution may be ineffective if uroliths contain other minerals in addition to ammonium urates. In addition, when allopurinol is prescribed, xanthine may be formed, which will interfere with dissolution
Urate urocystoliths, which are usually small, round and smooth, can be removed from the bladder using urohydropulsion during urination. However, the success of this procedure depends on the size of the uroliths, the diameter of which should be smaller than the narrowest part of the urethra. Therefore, dogs with pSS should not undergo this type of stone removal.
Because drug dissolution is ineffective, clinically active stones must be removed surgically. Whenever possible, stones should be removed during surgical correction of pSS. If the stones are not removed at this point, then hypothetically it can be assumed that in the absence of hyperuricuria and a decrease in the concentration of ammonia in the urine after surgical correction of pSS, the stones can dissolve on their own, since they consist of ammonium urates. New research is needed to confirm or refute this hypothesis. Also, the use of an alkaline diet with low purine content can prevent the growth of existing stones or promote their dissolution after ligation of psci.
Prevention
After ligation of the PSS, ammonium urate ceases to precipitate if normal blood flow passes through the liver. However, for animals in which PSS ligation cannot be performed, or where PSS is partially ligated, there is a risk of the formation of ammonium urate uroliths. These animals require constant monitoring of urine composition to prevent the precipitation of ammonium urate crystals. In case of crystalluria, additional preventive measures must be taken. Monitoring the concentration of ammonia in the blood plasma after feeding can detect its increase, despite the absence of clinical symptoms. Measurement of serum uric acid concentration also reveals its increase. Consequently, the concentrations of ammonia and uric acid in the urine of these animals will also be increased, increasing the risk of ammonium urate uroliths. In a study at the University of Minnesota, 4 dogs with inoperable pSS were treated with an alkalinizing, low-purine diet. (PrescriptionDietCanineu/d, Hill'sPetProduct, TopekaKS), which led to a decrease in the saturation of urine with ammonium urates to a level below their precipitation. In addition, the symptoms of genatoencephalopathy disappeared. These dogs lived for 3 years without recurrence of ammonium urate uroliths.
If preventive measures are necessary, a low-protein, alkalinizing diet should be used. The use of allopurinol is not recommended for dogs with pSS.
