Symptoms and treatment of urolithiasis in dogs. General urine analysis in dogs and cats

Urinalysis includes assessment physicochemical characteristics of urine and microscopy of sediment. This study allows you to evaluate renal function and other internal organs, as well as identify the inflammatory process in the urinary tract. Together with the general clinical analysis blood, the results of this study can tell quite a lot about the processes occurring in the body and, most importantly, indicate the direction of further diagnostic search.

Indications for the purpose of analysis:

Secondary ketonuria:
- thyrotoxicosis;
- Itsenko-Cushing's disease; overproduction of corticosteroids (tumor of the anterior pituitary gland or adrenal gland);

Hemoglobin.

Norm: dogs, cats - absent.

Hemoglobinuria is characterized by red or dark brown (black) urine and dysuria. Hemoglobinuria must be distinguished from hematuria, alkaptonuria, melaninuria, and porphyria. With hemoglobinuria, there are no red blood cells in the urine sediment, anemia with reticulocytosis and an increase in the level of indirect bilirubin in the blood serum are detected.

When does hemoglobin or myoglobin appear in the urine (hemoglobinuria)?

Hemolytic anemia.
- Severe poisoning (sulfonamides, phenol, aniline dyes,
- After an epileptic seizure.
- Transfusion of incompatible blood group.
-
- Sepsis.
- Severe injuries.

Microscopy of urinary sediment.

In urinary sediment, organized sediment is distinguished (cellular elements, cylinders, mucus, bacteria, yeast fungi) and unorganized (crystalline elements).
Red blood cells.

Norm: dogs, cats - 1 – 3 red blood cells in the field of view.
Everything above is hematuria.

Highlight:
- gross hematuria (when the color of urine is changed);
- microhematuria (when the color of urine is not changed, and red blood cells are detected only under a microscope).

In urinary sediment, red blood cells can be unchanged or changed. The appearance of altered red blood cells in the urine is significant diagnostic value, because they are most often of renal origin. Unchanged red blood cells are more likely to cause damage to the urinary tract (urolithiasis, cystitis, urethritis).

When does the red blood cell count increase (hematuria)?

Urolithiasis disease.
- Tumors of the genitourinary system.
- Glomerulonephritis.
- Pyelonephritis.
- Infectious diseases urinary tract (cystitis, tuberculosis).
- Kidney injury.
- Poisoning with benzene derivatives, aniline, snake venom, anticoagulants, poisonous mushrooms.

Leukocytes.

Norm: dogs, cats - 0–6 leukocytes in the field of view.

When does the white blood cell count increase (leukocyturia)?

Acute and chronic glomerulonephritis, pyelonephritis.
- Cystitis, urethritis, prostatitis.
- Stones in the ureter.
- Tubulointerstitial nephritis.

Epithelial cells.

Norm: dogs and cats – single or absent.

Epithelial cells have different origins:
- squamous epithelial cells (washed off with night urine from the external genitalia);
- transitional epithelial cells (lining the mucous membrane Bladder, ureters, pelvis, large ducts of the prostate gland);
- cells of the renal (tubular) epithelium (lining the renal tubules).

When does the number of epithelial cells increase?

Cell enhancement squamous epithelium has no significant diagnostic value. One can assume about improper preparation patient for analysis.

Cell enhancement transitional epithelium:
- intoxication;
- intolerance to anesthesia, medications, after operations;
- jaundice of various etiologies;
- urolithiasis (at the moment of stone passage);
- chronic cystitis;

Appearance of cells renal epithelium:
- pyelonephritis;
- intoxication (taking salicylates, cortisone, phenacetin, bismuth preparations, poisoning with heavy metal salts, ethylene glycol);
- tubular necrosis;

Cylinders.

Norm: dogs and cats are absent.

The appearance of casts (cylindruria) is a symptom of kidney damage.

When and what casts appear in a general urinalysis (cylindruria)?

Hyaline casts are found in all organic kidney diseases, their number depends on the severity of the condition and the level of proteinuria.

Grain cylinders:
- glomerulonephritis;
- pyelonephritis;
- kidney cancer;
- diabetic nephropathy;
- infectious hepatitis;
- osteomyelitis.

Waxy cylinders indicate severe kidney damage.

Leukocyte casts:
- acute pyelonephritis;
- exacerbation of chronic pyelonephritis;
- kidney abscess.

Red blood cell casts:
- kidney infarction;
- embolism;
- acute diffuse glomerulonephritis.

Pigment cylinders:
- prerenal hematuria;
- hemoglobinuria;
- myoglobinuria.

Epithelial casts:
- acute renal failure;
- tubular necrosis;
- acute and chronic glomerulonephritis.

Fat cylinders:
- chronic glomerulonephritis and pyelonephritis complicated by nephrotic syndrome;
- lipoid and lipoid-amyloid nephrosis;
- diabetic nephropathy.

Bacteria.

Fine urine in the bladder is sterile. Detection of bacteria in a urine test of more than 50,000 in 1 ml indicates infectious lesion organs of the urinary system (pyelonephritis, urethritis, cystitis, etc.). The type of bacteria can only be determined through bacteriological testing.

Yeast fungi.

The detection of yeast of the genus Candida indicates candidiasis, which most often occurs as a result of irrational antibiotic therapy, the use of immunosuppressants, and cytostatics.

Determining the type of fungus is only possible through bacteriological examination.

Slime.

Mucus is secreted by the epithelium of the mucous membranes. Normally absent or present in urine in small quantities. During inflammatory processes in lower sections urinary tract, the mucus content in the urine increases.

Crystals (disorganized sediment).

Urine is a solution of various salts, which can precipitate (form crystals) when the urine stands. The presence of certain salt crystals in the urinary sediment indicates a change in the reaction towards the acidic or alkaline side. Excessive salt content in urine contributes to the formation of stones and the development of urolithiasis.

When and what kind of crystals appear in a general urine test?
- Uric acid and its salts (urates): can normally be found in Dalmatians and English bulldogs; in dogs of other breeds and cats they are associated with liver failure and porosystemic anastomoses.
- Tripelphosphates, amorphous phosphates: often found in slightly acidic or alkaline urine in healthy dogs and cats; may be associated with cystitis.

Calcium oxalate:

Severe infectious diseases;
- pyelonephritis;
- diabetes;
- ethylene glycol poisoning;

Cystine:

Cirrhosis of the liver;
- viral hepatitis;
- state of hepatic coma
- Bilirubin: may occur in healthy dogs with concentrated urine or due to bilirubinuria.

Definitions of the concept " urolithiasis disease“You can give a lot. To put it simply, its essence is this: due to metabolic disorders in the body of dogs and cats, stones called uroliths or calculi form in the urine and urinary tract.

Urine is a complex solution, which is a necessary medium for removing metabolic products from the body. Metabolic products (urea and creatinine) are excreted in the urine. minerals(calcium, magnesium, phosphate), electrolytes (sodium and potassium), water, urine pH varies depending on homeostatic maintenance acid-base balance. Any deviations from the norm can lead to the development of urolithiasis in animals. Mechanical blockage of the urinary tract by stones is the cause of urolithiasis. Stones can form both in the kidneys and in the urinary tract, but the clinical symptoms of urolithiasis are associated specifically with urinary tract disease.

Diagnosis. Urolithiasis is diagnosed when stones are detected in fresh urine, in the bladder by ultrasound or x-ray examination and detection of stones during surgery to remove them. The presence of stones in urine that has stood for more than an hour does not give grounds to draw a conclusion about urolithiasis, since uroliths can precipitate as a result of natural chemical reactions.

Uroliths vary greatly in composition - from homogeneous (cystines) to a complex mixture of minerals and even minerals and proteins. They also differ in appearance- from soft deposits of sandy material (mucoid plugs), which are mainly seen in cats and consist of a protein-like shell filled with mineral content, to hard smooth or uneven stones, consisting mainly of minerals and small matrices. We will not describe in detail the properties of each of the stones; this is not the purpose of this article. Fellow veterinarians engaged in in-depth study of this problem can refer to the relevant manuals.

The formation of stones occurs for the following reasons:

1. If the concentration of urolith components in the urine is higher than the possibility of their dissolution and excretion without the formation of a crystal.
2. Some types of crystals are sensitive to urine pH. Thus, struvite is formed only in alkaline urine (PH> 7.0). Calcium oxalates are generally not sensitive to urine pH.
3. The formation of large crystals that can cause obstruction (blockage) of the urinary tract should occur very quickly, because When crystals form slowly, they are washed out of the bladder before they can cause harm.
4. The presence of a nucleus (base) to begin the formation of a large urolith. These may be remnants of cells, suture material, bacteria and, according to some sources, viruses.
5. Some bacterial infections can contribute to the development of urolithiasis. Thus, some bladder infections contribute to the development of struvite-type urolithiasis in dogs (especially in bitches and puppies in the first year of life).

Clinical symptoms of urolithiasis

The presence of uroliths in the urinary tract can cause clinical symptoms that may or may not be noticed by the pet owner. This is especially true for cats, since they hide from their owners and their owners do not always see their act of urination. The main clinical symptom is the inability to urinate naturally or urination is difficult.

In this case, the animal often sits down (male cats, females) or raises its paw (males), tries to urinate, whines, cries, urine is released in drops, often with blood.

Palpation of the abdomen establishes the presence of a full bladder. This procedure in cats it can always be done, in dogs it can sometimes be palpated abdominal wall extremely difficult due to the tense powerful muscles of the abdominal wall.

There are several degrees of urolithiasis:

1. Subclinical urolithiasis. There may be no symptoms associated with the presence of uroliths in the urinary tract. Struvite, calcium oxalate and other calcium-containing uroliths are radioopaque and are found on x-rays. A urine test may show elevated crystals and an abnormal urine pH. These uroliths are usually struvite and sometimes calcium oxalate. Calcium oxalate stones often have a very uneven surface and can cause mild to severe symptoms of urinary tract inflammation, while smooth struvite or cystine stones often do not cause any clinical symptoms. Nephroliths rarely cause clinical symptoms other than hematuria until they move into the ureter, causing obstruction (blockage) and hydronephrosis.

2. Mild symptoms of urolithiasis:

• Slight increase in urinary frequency
• Mild hematuria - blood staining
• Slight increase in urination time
• Slight discomfort during urination
• Increased licking of the genitals

3. Severe symptoms:

• Pollakiuria - cats almost never leave their toilet, dogs constantly leak drops of urine
• Urinary tenesmus (to be distinguished from constipation)
• Severe hematuria - obvious blood in the urine
• Severe discomfort when urinating - vocalization and obvious pain
• On palpation, the bladder is greatly distended
• Polydipsia/polyuria in case of secondary renal failure
• General depression and anorexia

4. Symptoms that threaten the animal's life:

• Anuria (lack of urination)
• Weakness/collapse
• Dehydration
• On palpation, the bladder may not be found if it has burst or is anuric (otherwise it feels like a dense mass)
• Uremic halitosis may be detected
• Vomit
• Convulsions

For appointment adequate treatment The veterinarian must be able to assess the degree of development of urolithiasis.

Diagnosis of urolithiasis

Urolithiasis is confirmed:

• Clinical symptoms
• Palpation of uroliths in the bladder in dogs (in cats they are difficult to palpate)
• Plain x-rays show radioopaque uroliths
• Contrast radiographs for radiolucent and small (less than 2 mm in diameter) uroliths
• Discharge of uroliths during urination (they can be collected in a net)

Radiography is necessary to determine radioopacity, location of deposition, number and size of uroliths. Usually stones are present in several places at once, so examination of all urinary tracts is necessary.

Rice. 1. Calcium oxalate crystals in urine

In cats, urolithiasis usually resolves with the formation of struvite (tripelphosphate), but recently there have been increasing cases of detection of calcium oxalates in the urine of cats and, even worse, urolithiasis mixed type, when at a neutral urine pH level both struvite and oxalates are present in the urine. Many veterinarians neglect laboratory diagnosis, relying on the prevalence of struvite in cats. I think this approach is wrong.

In dogs, KSD can occur with the formation of all known uroliths, therefore, laboratory visual determination of the type of stones for dogs is very important for prescribing treatment. A 10-mL sample of fresh urine sediment should be microscopically examined immediately after collection at body temperature because time, cooling, or evaporation of the urine may accelerate crystal precipitation and produce false positive or paradoxical results. Most common crystals have a typical appearance in urine, and if their number is large, one can judge the composition of the urolith, or at least its outer layer.

Rice. 2. Struvite

Rice. 3. Struvite and red blood cells in urine

Treatment of urolithiasis

Choice proper treatment depends on the location(s) of uroliths:

Kidneys- nephroliths are very difficult to remove surgically, unless they are concentrated in one kidney. Then nephrectomy (kidney removal) is possible. With nephrolitas, the development of postrenal renal failure is possible. Dissolution of struvite uroliths is possible by prescribing a special diet.

Ureters- uroliths located in the ureters can be successfully removed surgically, but one should remember the possibility of developing postrenal renal failure.

Bladder- treatment depends on the type of uroliths. Struvite, urate, and sometimes cystine can be dissolved, and calcium oxalate and other calcium- and silica-containing uroliths can be removed surgically by conventional cystotomy (opening the bladder and removing stones).

Urethra- depending on how the uroliths lie, several types of treatment are used:

1) Manipulation - manual massage(often used for cats with sand plugs) or catheterization small polyurethane catheter (eg special catheter Jackson for cats or a medical subclavian catheter with a diameter of 0.6 - 0.8 mm).

Despite the fact that catheterization is often used to displace or break up uroliths in cats and some breeds of dogs, this method of treatment is the most dangerous for the following reasons:

• it injures the tissue, which leads to fibrosis and scarring with subsequent narrowing of the urethra;
• causes infection in the urinary tract.

2) Retrograde urethral lavage followed by dissolution (struvite, urate and cystine) or cystotomy (calcium oxalates, other uroliths containing calcium and silicon dioxide) is the only method of treating urethral urolithiasis.

Method of retrograde washing out of urethral stones

The animal is given general anesthesia or strong sedatives. Then the following steps are performed:

• Empty the bladder by cystocentesis (puncture of the bladder through the abdominal wall)
• Through the rectum, fingers compress the urethra opposite the pubis, below the urolith (an assistant is needed for this)
• A sterile catheter is inserted into the distal urethra
• Secure the penile part of the urethra around the catheter
• A sterile saline solution is injected into the catheter through a syringe.
• When the intraluminal pressure reaches the desired point, the assistant removes his fingers and releases the urethra
• Under the pressure of the saline solution, the urolith returns back to the bladder
• You can repeat the procedure several times

After retrograde lavage, recurrence of obstruction is very rare. This method, as a rule, is not used in cats; in males, this low-traumatic method is often recommended for use.

3) Urethrostomy used for males when manipulation or retrograde lavage has not been successful. A urethrostomy creates a permanent opening in the urethra. This method is used for recurrent obstructions of the penile urethra in cats and sometimes in males. Although this is the only method of treating animals with permanent urethral obstruction, it must be used with caution, because according to some data, in 17% of cases, urethrostomy in cats leads to postoperative urinary tract infection. In 10% of cats, urethrostomy and dietary changes also result in postoperative infection, while none of the cats treated with diet develop a urinary tract infection.

Dissolution

Struvite, urate and cystine stones can be dissolved. This is the only method for removing stones in animals with non-life-threatening urolithiasis. Dissolution is used for kidney or bladder stones. If a urinary tract infection is present, antibiotics are prescribed as part of treatment based on the results of urine culture and sensitivity testing. Treatment details are discussed below.

Struvites (magnesium ammonium phosphate, tripel phosphates). To dissolve struvite stones, it is enough to strictly adhere to special veterinary diets. They are represented quite widely on the Russian market; any veterinary clinic in Moscow and large Russian cities can offer a veterinary diet for your pet. We successfully use food from Purina (UR) and Hills (s/d, c/d).

These foods contribute to the acidification of urine, causing the dissolution of struvite. In addition, the high sodium content in these diets stimulates diuresis (urination), which helps flush the bladder and speed up the elimination of accumulated salts. For urolithiasis not complicated by bacterial infections, treatment with special diets brings positive results already 4-5 days after the start of treatment. It should be noted that contacting a veterinarian as early as possible and early diagnosis of urolithiasis contributes to speedy recovery animal and minimizes possible relapses of the disease. The owner's compliance with the animal's feeding regime is of great importance. THE ANIMAL CANNOT BE GIVEN ANYTHING ELSE EXCEPT A SPECIAL DIET!!!

Quality control of treatment is carried out laboratory research urine and x-ray diagnosis of the presence of stones in the bladder. If there are no stones in the urine and in the photographs, the treatment is considered effective and the owner’s task in the future is MANDATORY research urine at least once every six months. In our opinion, the optimal period for control testing is 3 months.

Laboratory assessment of urine pH, as well as the presence and analysis of urine sediment, determination of the type and quantity of urinary crystals.

Treatment of insoluble uroliths

-Calcium oxalates
Calcium oxalate uroliths are more common in certain breeds of dogs (Yorkshire terriers and miniature schnauzers), and in last years they began to occur noticeably more often, especially in cats.
Unfortunately, this type of crystal is completely insoluble, and treatment of this type Urolithiasis is performed exclusively surgically, by removing stones from the bladder. Sometimes 3-4 operations per year are required if the intensity of oxalate formation is very high.
To prevent relapses, it is necessary to reduce the concentration of calcium and oxalates in the urine. Prevention is possible with special diets (Hills x/d, Eucanuba Oxalat Urinary Formula, etc.). I repeat. PREVENTION. But not the dissolution of oxalate stones!

-Calcium phosphates
Calcium phosphate crystalluria manifests itself in various forms: both amorphous (calcium phosphates) and calcium hydrogen phosphates (brushite). These minerals are often present in mixed uroliths along with struvite, urate, or calcium oxalate. Most calcium phosphate crystals (with the exception of brushite) are sensitive to urine pH and form in alkaline urine.
A medical protocol for dissolving these uroliths has not yet been developed, so surgical removal and prevention of hypercalciuria (as in the case of calcium oxalate urolithiasis), but not urine alkalinization, are recommended.

-Silicon dioxide (silicates)
Silicate uroliths are rare in dogs. They are called "Jack stones." The etiopathogenesis of these uroliths is not completely clear, however, it is believed that the risk of the formation of these stones increases if the dog eats soil or types of vegetables contaminated with soil (rutabaga, beets). Personally, I have never encountered this type of urolithiasis.
For clinical symptoms, the only treatment is surgical removal of stones, and as a preventive measure, it is recommended to ensure that the dog does not eat soil or vegetation contaminated with it.

The most common uroliths that form in dogs are:

Tripelphosphates (magnesium ammonium phosphate)

Calcium oxalate

Salt uric acid

Less common uroliths include cystine, silica, calcium phosphate and xanthine.

Most often found in dogs are Struvite or tripelphosphates. In most cases, these stones are formed due to an infection in the urinary system. Microflora is often represented by Escherichia coli, Proteus, staphylococcus, Pseudomonas aeruginosa, etc. When urine is contaminated with bacteria, their accumulations adhere to the epithelium of the bladder and form microcolonies. During their life, microbes secrete the enzyme urease into the urine. Under the influence of the enzyme urease, the acidity of urine increases, which creates favorable conditions for struvite crystallization. Sterile struvite uroliths are very rare to form in dogs, but they have been found in the breed English cocker spaniels, which may indicate a genetic predisposition.

Treatment of urolithiasis in dogs

Therapeutic measures depend on the location of the urinary calculus, its chemical composition, as well as from individual characteristics body. Most often it involves dissolving crystals or stones, and if there is no reaction to conservative treatment surgical removal of large stones is used.

Before starting treatment comprehensive examination patient. It includes a clinical examination, clinical and biochemical tests blood, urine analysis, urine culture to determine the sensitivity of microflora to antibiotics, ultrasonography, X-ray to determine the size of large stones.

Dissolution of struvite stones

Drugs are used to reduce the urine acidity level to less than 6.0, but more often individually selected dietary diets are used that promote the dissolution of struvite. In dogs consuming these diets, the amount of protein entering the body, phosphate and magnesium is reduced and the amount of sodium increases. As a result of consumption of this diet, the volume of urine excreted increases, the urine becomes unsaturated, and this is an unfavorable environment for crystallization. When taking specialized diets, it is not recommended to eat other foods or treats, but access to drinking water must be open 24/7.

Antibacterial therapy

For selection antibacterial therapy It is necessary to carry out laboratory culture of urine to determine sensitivity to antibiotics. Most staphylococci and Proteus are sensitive to amoxicillin. A urease inhibitor (acetohydroxamic acid) is used when resistance to antibiotics develops; it blocks the urease enzyme, resulting in acidification of the urine and subsequent dissolution of struvite.

After four weeks of treatment, a repeated comprehensive examination is carried out, which includes blood biochemistry, urine analysis, ultrasound and x-rays. After treatment, urine acidity should normalize: 6.0-6.5, specific gravity should be no more than 1.025. The radiograph shows a decrease in size of the stones. With positive dynamics, treatment can last up to 20 weeks, but a follow-up examination is required every 4 weeks. Stones that do not decrease in size after 8 weeks may not be struvite or the feeding regimen is not being followed. Such stones must be surgically removed.

Prevention

The main method of preventing the formation of struvite stones is to maintain sterile urine, so it is important to have your pet's urine tested periodically. If fresh urine has alkaline reaction, urine culture must be done and the animal must be treated based on the results of the analysis.

It is also important to carry out periodic preventive examinations after the stones have dissolved. the main objective is to prevent the development of urinary tract infections by urease-producing microbes. A diet is also used to maintain normal urine acidity and urine acidity must be monitored weekly in the morning after an overnight fast; owners conduct this study on their own.

General clinical urine examination includes the determination of physical properties, chemical composition and microscopic examination of sediment.

Physical properties.

QUANTITY.

Fine The daily amount of urine averages 20-50 ml per kg body weight for dogs and 20-30 mg per kg body weight for cats.

Increased daily diuresis - polyuria.
Causes:
1. Convergence of edema;
2. Diabetes mellitus (Diabetes maleus) (together with a positive level of glucose in the urine and high specific gravity of urine);
3. Glomerulonephritis, amyloidosis, pyelonephritis (together with negative glucose levels, high specific gravity of urine and severe proteinuria);
4. Cushing's syndrome, hypercalcemia, hypokalemia, tumors, uterine diseases (pyometra), hyperthyroidism, liver disease (together with negative glucose levels, high specific gravity of urine and negative or mild proteinuria)
5. Chronic renal failure or diuresis after acute renal failure (together with low specific gravity of urine and increased levels of urea in the blood);
6. Diabetes insipidus (Diabetes insipidus) (together with low specific gravity of urine, which does not change when testing with fluid deprivation and a normal level of urea in the blood);
7. Psychogenic craving for drinking (together with low specific gravity of urine, which increases when testing with fluid deprivation and a normal level of urea in the blood)
Often causes polydipsia.

Decreased daily diuresis - oliguria.
Causes:
1. Profuse diarrhea;
2. Vomiting;
3. Increase in edema (regardless of its origin);
4. Too little fluid intake;

Lack of urine or too little urine (lack of urination or urine formation) - anuria.
Causes:
a) Prerenal anuria (arising due to extrarenal causes):
1. Severe blood loss (hypovolemia - hypovolemic shock);
2. Acute heart failure (cardiogenic shock);
3. Spicy vascular insufficiency(vascular shock);
4. Uncontrollable vomiting;
5. Severe diarrhea.
b) Renal (secretory) anuria (associated with pathological processes in the kidneys):
1. Acute jades;
2. Necronephrosis;
3. Transfusion of incompatible blood;
4. Severe chronic kidney disease.
c) Obstructive (excretory) anuria (impossibility of urination):
1. Blockage of the ureters with stones;
2. Compression of the ureters by tumors developing near the ureters (neoplastic tumors of the uterus, ovaries, bladder, metastases from other organs.

COLOR

Normal urine color is straw yellow.
Color change may be due to the release of coloring compounds formed during organic changes or under the influence of food, drugs or contrast agents.

Red or red-brown (meat slop color)
Causes:
1. Macrohematuria;
2. Hemoglobinuria;
3. The presence of myoglobin in the urine;
4. The presence of porphyrin in the urine;
5. The presence of certain medications or their metabolites in the urine.

Dark yellow color (may have a greenish or greenish-brown tint, the color of dark beer)
Causes:
1. Excretion of bilirubin in the urine (with parenchymal or obstructive jaundice).

Greenish yellow color
Causes:
1. High content of pus in the urine.

Dirty brown or gray color
Causes:
1. Pyuria with alkaline urine reaction.

Very dark, almost black color
Causes:
1. Hemoglobinuria in acute hemolytic anemia.

Whitish color
Causes:
1. Phosphaturia (presence in urine large quantity phosphates).
It should be taken into account that if urine sits for a long time, its color may change. As a rule, it becomes more saturated. When urobilin is formed from colorless urobilinogen under the influence of light, urine becomes dark yellow (to orange). If methemoglobin is formed, the urine becomes dark brown color. In addition, changes in odor may be associated with the use of certain medications, feed or feed additives.

TRANSPARENCY

Normal urine is clear.

Cloudy urine can be caused by:
1. The presence of red blood cells in the urine;
2. The presence of leukocytes in the urine;
3. The presence of epithelial cells in the urine;
4. The presence of bacteria in the urine (bacteruria);
5. The presence of fatty droplets in the urine;
6. The presence of mucus in the urine;
7. Precipitation of salts.

In addition, the clarity of urine depends on:
1. Salt concentrations;
2. pH;
3. Storage temperatures ( low temperature promotes the precipitation of salts);
4. Duration of storage (during long-term storage, salts precipitate).

SMELL

Normally, the urine of dogs and cats has a mild, specific odor.

A change in odor may be caused by:
1. Acetonuria (the appearance of the smell of acetone in diabetes mellitus);
2. Bacterial infections (ammonia, unpleasant odor);
3. Taking antibiotics or food additives (special specific smell).

DENSITY

Normal density of urine in dogs 1.015-1.034 (minimum - 1.001, maximum 1.065), in cats - 1.020-1.040.
Density is a measure of the kidneys' ability to concentrate urine.

They matter
1. The state of hydration of the animal;
2. Drinking and eating habits;
3. Ambient temperature;
4. Injected drugs;
5. Functional status or quantity renal tubules.

Reasons for increased urine density:
1. Glucose in the urine;
2. Protein in urine (in large quantities);
3. Medicines (or their metabolites) in the urine;
4. Mannitol or dextran in urine (as a result of intravenous infusion).

Reasons for decreased urine density:
1. Diabetes mellitus;
3. Acute kidney damage.

We can talk about adequate kidney response, when, after a short abstinence from drinking water, the specific gravity of urine rises to the average norm. The kidney reaction is considered inadequate if the specific gravity does not rise above the minimum values ​​when abstaining from water intake - isosthenuria (severely reduced ability to adapt).
Causes:
1. Chronic renal failure.

Chemical research.

pH

Normal urine pH Dogs and cats can be either slightly acidic or slightly alkaline, depending on the protein content of the diet. On average, urine pH ranges from 5-7.5 and is more often slightly acidic.

Increasing urine pH (pH>7.5) - alkalization of urine.
Causes:
1. Eating plant foods;
2. Profuse sour vomiting;
3. Hyperkalemia;
4. Resorption of edema;
5. Primary and secondary hyperparathyroidism (accompanied by hypercalcemia);
6. Metabolic or respiratory alkalosis;
7. Bacterial cystitis;
8. Introduction of sodium bicarbonate.

A decrease in urine pH (pH about 5 and below) - acidification of urine.
Causes:
1. Metabolic or respiratory acidosis;
2. Hypokalemia;
3. Dehydration;
4. Fever;
5. Fasting;
6. Long-term muscle load;
7. Diabetes mellitus;
8. Chronic renal failure;
9. Introduction of acid salts (for example, ammonium chloride).

PROTEIN

Normally there is protein in urine absent or its concentration is less than 100 mg/l.
Proteinuria- the appearance of protein in the urine.

Physiological proteinuria- cases of temporary appearance of protein in the urine, not associated with diseases.
Causes:
1. Taking a large amount of feed from increased content squirrel;
2. Strong physical exercise;
3. Epileptic seizures.

Pathological proteinuria There are renal and extrarenal.

Extrarenal proteinuria can be extrarenal and postrenal.

Extrarenal extrarenal protenuria is more often temporary mild degree(300 mg\l).
Causes:
1. Heart failure;
2. Diabetes mellitus;
3. Fever;
4. Anemia;
5. Hypothermia;
6. Allergy;
7. Use of penicillin, sulfonamides, aminoglycosides;
8. Burns;
9. Dehydration;
10. Hemoglobinuria;
11. Myoglobinuria.
Severity of proteinuria is not a reliable indicator of the severity of the underlying disease and its prognosis.

Extrarenal postrenal proteinuria(false proteinuria, accidental proteinuria) rarely exceeds 1 g/l (except in cases severe pyuria) and is accompanied by the formation of a large sediment.
Causes:
1. Cystitis;
2. Pyelitis;
3. Prostatitis;
4. Urethritis;
5. Vulvovaginitis.
6. Bleeding in the urinary tract.

Renal proteinuria occurs when protein enters the urine in the kidney parenchyma. In most cases, it is associated with increased permeability of the renal filter. In this case, a high protein content in the urine is detected (more than 1 g/l). At microscopic examination Urine sediment reveals cylinders.
Causes:
1. Acute and chronic glomerulonephritis;
2. Acute and chronic pyelonephritis;
3. Severe chronic heart failure;
4. Kidney amyloidosis;
5. Kidney neoplasms;
6. Kidney hydronephrosis;
7. Lipoid nephrosis;
8. Nephrotic syndrome;
9. Immune diseases with damage to the renal glomeruli by immune complexes;
10. Severe anemia.

Renal microalbuminuria- the presence of protein in the urine in concentrations below the sensitivity of reagent strips (from 1 to 30 mg\100 ml). Is an early sensitive indicator of various chronic diseases kidney

Paraproteinuria- the appearance in the urine of a globulin protein that does not have the properties of antibodies (Bence Jones protein), consisting of light chains of immunoglobulins that easily pass through glomerular filters. This protein is secreted in plasmacytoma. Paraproteinuria develops without primary damage to the kidney glomeruli.

Tubular proteinuria- the appearance of small proteins in the urine (α1-microglobulin, β2-microglobulin, lysozyme, retinol-binding protein). They are normally present in the glomerular filtrate, but are reabsorbed into renal tubules. When the epithelium of the renal tubules is damaged, these proteins appear in the urine (determined only by electrophoresis). Tubular proteinuria is an early indicator of renal tubular damage in the absence of concomitant changes in circulating urea and creatinine levels.
Causes:
1. Medicines(aminoglycosides, cyclosporine);
2. Heavy metals(lead);
3. Analgesics (non-steroidal anti-inflammatory substances);
4. Ischemia;
5. Metabolic diseases (Fanconi-like syndrome).

False positive protein counts, obtained using a test strip, are characteristic of alkaline urine (pH 8).

False negative protein counts, obtained using a test strip are due to the fact that test strips show, first of all, the level of albumin (paraproteinuria and tubular proteinuria are not detected) and their content in urine is above 30 mg\100 ml (microalbuminuria is not detected).
Proteinuria assessment should be carried out taking into account clinical symptoms (fluid accumulation, edema) and other laboratory parameters (blood protein level, albumin-to-globulin ratio, urea, creatinine, serum lipids, cholesterol levels).

GLUCOSE

Normally, there is no glucose in the urine.

Glucosuria- presence of glucose in urine.

1. Glucosuria with high urine specific gravity(1.030) and elevated level blood glucose (3.3 - 5 mmol/l) is a criterion for diabetes mellitus (Diadetes mellitus).
It must be taken into account that in animals with diabetes mellitus Type 1 (insulin-dependent) can significantly change the renal glucose threshold (the concentration of glucose in the blood, above which glucose begins to enter the urine). Sometimes, with persistent normoglycemia, glucosuria persists (the renal glucose threshold is reduced). And with the development of glomerulosclerosis, the renal glucose threshold increases, and glucosuria may not occur even with severe hyperglycemia.

2.Renal glycosuria- is registered at the average specific gravity of urine and normal level blood glucose. A marker of tubular dysfunction is deterioration of reabsorption.
Causes:
1. Primary renal glycosuria in some dog breeds (Scottish terriers, Norwegian Elkhounds, mixed breed dogs);
2. A component of general dysfunction of the renal tubules - Fanconi-like syndrome (may be hereditary or acquired; glucose, amino acids, small globulins, phosphate and bicarbonate are excreted in the urine; described in Besenges, Norwegian Elkhounds, Shetland Sheepdogs, Miniature Schnauzers);
3. Use of certain nephrotoxic drugs.
4. Acute renal failure or aminoglycoside toxicity - if the level of urea in the blood is elevated.

3. Glucosuria with reduced specific gravity of urine(1.015 - 1.018) may be with the introduction of glucose.
4. Moderate glycosuria occurs in healthy animals with a significant nutritional load with high carbohydrate content feeds.

False positive result when determining glucose in urine with test strips, it is possible in cats with cystitis.

False negative result when determining glucose in urine with test strips, it is possible in dogs in the presence of ascorbic acid(it is synthesized in dogs in varying quantities).

BILIRUBIN

Normally, there is no bilirubin in cat urine., concentrated dog urine may contain trace amounts of bilirubin.

Bilirubinuria- the appearance of bilirubin (direct) in the urine.
Causes:
1. Parenchymal jaundice (damage to the liver parenchyma);
2. Obstructive jaundice (impaired bile outflow).

Used as an express method for differential diagnosis hemolytic jaundice - bilirubinuria is not typical for them, since indirect bilirubin does not pass through the kidney filter.

UROBILINOGEN

The upper limit of normal for urobilinogen in urine about 10 mg/l.

Urobilinogenuria- increased levels of urobilinogen in urine.
Causes:
1. Increased hemoglobin catabolism: hemolytic anemia, intravascular hemolysis (transfusion of incompatible blood, infections, sepsis), pernicious anemia, polycythemia, resorption of massive hematomas;
2. Increased formation of urobilinogen in gastrointestinal tract: enterocolitis, ileitis;
3. Increased formation and reabsorption of urobilinogen during inflammation of the biliary system - cholangitis;
4. Liver dysfunction: chronic hepatitis and cirrhosis of the liver, toxic liver damage (poisoning with organic compounds, toxins in infectious diseases and sepsis); secondary liver failure(heart and circulatory failure, liver tumors);
5. Liver bypass surgery: liver cirrhosis with portal hypertension, thrombosis, renal vein obstruction.

Of particular diagnostic importance is:
1. For lesions of the liver parenchyma in cases without jaundice;
2. For differential diagnosis parenchymal jaundice from obstructive jaundice, in which there is no urobilinogenuria.

KETONE BODIES

Normally, there are no ketone bodies in urine.

Ketonuria- the appearance of ketone bodies in the urine (as a result of accelerated incomplete oxidation of fatty acids as an energy source).
Causes:
1. Severe decompensation of type 1 diabetes mellitus (insulin-dependent) and long-term type II diabetes (non-insulin-dependent) with depletion of pancreatic beta cells and the development of absolute insulin deficiency.
2. Severe - hyperketonemic diabetic coma;
3. Precomatose states;
4. Cerebral coma;
5. Long fasting;
6. Severe fever;
7. Hyperinsulinism;
8. Hypercatecholemia;
9. Postoperative period.

NITRITES

Normally, there are no nitrites in the urine.

The appearance of nitrites in the urine indicates infection of the urinary tract, since many pathogenic bacteria reduce nitrates present in the urine into nitrites.
Of particular diagnostic importance when determining asymptomatic urinary tract infections (at risk are animals with prostate tumors, patients with diabetes mellitus, after urological operations or instrumental procedures on the urinary tract).

erythrocytes

Normally, there are no red blood cells in the urine or physiological microhematuria is allowed when examined with test strips of up to 3 red blood cells/μl of urine.

Hematuria- the content of red blood cells in the urine is more than 5 in 1 μl of urine.

Gross hematuria- can be installed with the naked eye.

Microhematuria- can only be detected using test strips or microscopy. Often caused by cystocentesis or catheterization.

Hematuria, originating from the bladder and urethra.
In approximately 75% of cases, gross hematuria is often combined with dysuria and pain on palpation.
Causes:
1. Stones in the bladder and urethra;
2. Infectious or drug-induced (cyclophosphamide) cystitis;
3. Urethritis;
4. Tumors of the bladder;
5. Injuries to the bladder and urethra (crushing, ruptures).
The admixture of blood only at the beginning of urination indicates bleeding between the neck of the bladder and the opening of the urethra.
An admixture of blood predominantly at the end of urination indicates bleeding in the bladder.

Hematuria originating from the kidneys (approximately 25% of cases of hematuria).
Uniform hematuria from the beginning to the end of urination. In this case, microscopy of the sediment reveals erythrocyte casts. Such bleeding is relatively rare, is combined with proteinuria and is less intense compared to bleeding in the urinary tract.
Causes:
1. Physical overload;
2. Infectious diseases(leptospirosis, septicemia);
3. Hemorrhagic diathesis of various etiologies;
4. Coagulopathies (dicoumarol poisoning);
5. Consumption coagulopathy (DIC syndrome);
6. Kidney injuries;
7. Thrombosis of renal vessels;
8. Kidney neoplasms;
9. Acute and chronic glomerulonephritis;
10. Pyelitis, pyelonephritis;
11. Glomerulo- and tubulonephrosis (poisoning, taking medications);
12. Strong venous stasis;
13. Displacement of the spleen;
14. Systemic lupus erythematosus;
15. Overdose of anticoagulants, sulfonamides, methenamine.
16. Idiopathic renal hematuria.
Bleeding, occurring independently of urination, are localized in the urethra, prepuce, vagina, uterus (estrus) or prostate gland.

HEMOGLOBIN, MYOGLOBIN

Normally absent when examined with test strips.

Causes of myoglobinuria:
1. Muscle damage (creatine kinase levels increase in the circulating blood).
Hemoglobinuria is always accompanied by hemoglobinemia. If hemolyzed red blood cells are found in the urinary sediment, the cause is hematuria.

Microscopic examination of sediment.

There are elements of organized and unorganized urine sediment. The main elements of organized sediment are erythrocytes, leukocytes, epithelium and casts; unorganized - crystalline and amorphous salts.

EPITHELIUM

Fine in the urine sediment, single cells of squamous (urethra) and transitional epithelium (pelvis, ureters, bladder) are found in the field of view. The renal epithelium (tubules) is normally absent.

Squamous epithelial cells. Normally, it occurs in larger quantities in females. Detection of layers of flat epithelium and horny scales in the sediment is a sign of squamous metaplasia of the mucous membrane of the urinary tract.

Transitional epithelial cells.
Reasons for the significant increase in their number:
1. Spicy inflammatory processes in the bladder and renal pelvis;
2. Intoxication;
3. Urolithiasis;
4. Neoplasms of the urinary tract.

Epithelial cells of the urinary tubules (renal epithelium).
Reasons for their appearance:
1. Jades;
2. Intoxication;
3. Circulatory failure;
4. Necrotic nephrosis (in case of poisoning with sublimate, antifreeze, dichloroethane) - epithelium in very large quantities;
5. Kidney amyloidosis (rarely in the albuminemic stage, often in the edematous-hypertensive and azotemic stage);
6. Lipoid nephrosis (desquamated renal epithelium is often found fat-degenerated).
If conglomerates of epithelial cells are detected, especially those varying moderately or significantly in shape and/or size, further cytological examination to determine the possible malignancy of these cells.

LEUKOCYTES

Normally there are no leukocytes or single leukocytes per field of view may be observed (0-3 leukocytes per field of view at a magnification of 400).

Leukocyturia- more than 3 leukocytes in the field of view of the microscope at a magnification of 400.
Piuria- over 60 leukocytes in the field of view of the microscope at a magnification of 400.

Infectious leukocyturia, often pyuria.
Causes:
1. Inflammatory processes in the bladder, urethra, renal pelvis.
2. Infected discharge from the prostate, vagina, uterus.

Aseptic leukocyturia.
Causes:
1. Glomerulonephritis;
2. Amyloidosis;
3. Chronic interstitial nephritis.

erythrocytes

Normally, urine sediment contains no or single in the preparation (0-3 in the field of view at a magnification of 400).
The appearance or increase in the number of red blood cells in urine sediment is called hematuria.
For reasons, see above in the section “ Chemical research urine."

CYLINDERS

Fine In the urine sediment, hyaline and granular casts can be detected - single in the preparation - with unchanged urine.
Urinary cylinders not contained in alkaline urine. Neither the number nor the type of urinary casts indicates the severity of the disease and is not specific for any kidney damage. The absence of casts in urine sediment does not indicate the absence of kidney disease.

Cylindruria- presence in urine increased number cylinders of any type.

Hyaline casts consist of protein that gets into the urine due to stagnation or an inflammatory process.
Reasons for appearance:
1. Proteinuria not associated with kidney damage (albuminemia, venous congestion in the kidneys, heavy physical activity, cooling);
2. Feverish conditions;
3. Various organic lesions kidneys, both acute and chronic;
4. Dehydration.
There is no correlation between the severity of proteinuria and the number of hyaline casts, since the formation of casts depends on the pH of the urine.

Grainy cylinders- consist of tubular epithelial cells.
Reasons for education:
1. The presence of severe degeneration in the tubular epithelium (necrosis of the tubular epithelium, kidney inflammation).
Waxy cylinders.
Reasons for appearance:
1. Severe defeats renal parenchyma (both acute and chronic).

Red blood cell casts are formed from accumulations of red blood cells. Their presence in urine sediment indicates the renal origin of hematuria.
Causes:
1. Inflammatory diseases kidney;
2. Bleeding into the kidney parenchyma;
3. Kidney infarctions.

Leukocyte casts- are quite rare.
Reasons for appearance:
1. Pyelonephritis.

SALT AND OTHER ELEMENTS


The precipitation of salts depends on the properties of urine, in particular on its pH.

In acidic urine, the following precipitates:
1. Uric acid
2. Uric acid salts;
3. Calcium phosphate;
4. Calcium sulfate.

In urine that gives a basic (alkaline) reaction, the following precipitate:
1. Amorphous phosphates;
2. Tripelphosphates;
3. Neutral magnesium phosphate;
4. Calcium carbonate;
5. Crystals of sulfonamides.

Crystalluria- the appearance of crystals in the urinary sediment.

Uric acid.
Fine There are no uric acid crystals.
Reasons for appearance:
1. Pathologically acidic urine pH in renal failure ( early loss in sediment - within an hour after urination);
2. Fever;
3. Conditions accompanied by increased tissue breakdown (leukemia, massive decaying tumors, pneumonia in the resolution stage);
4. Heavy physical activity;
5. Uric acid diathesis;
6. Feeding exclusively meat feed.

Amorphous urates- Urate salts give urine sediment a brick-pink color.
Fine- single in the field of view.
Reasons for appearance:
1. Acute and chronic glomerulonephritis;
2. Chronic renal failure;
3. “Congestive kidney”;
4. Fever.

Oxalates- salts of oxalic acid, mainly calcium oxalate.
Fine oxalates are rare in the field of view.
Reasons for appearance:
1. Pyelonephritis;
2. Diabetes mellitus;
3. Disorders of calcium metabolism;
4. After epileptic attacks;
5. Ethylene glycol (antifreeze) poisoning.

Triple phosphates, neutral phosphates, calcium carbonate.
Fine none.
Reasons for appearance:
1. Cystitis;
2. Abundant reception plant feed;
3. Vomiting.
May cause the development of stones.

Acid ammonium urate.
Fine absent.
Reasons for appearance:
1. Cystitis with ammonia fermentation in the bladder;
2. Uric acid renal infarction in newborns.
3. Insufficiency of the liver, especially with congenital portosystemic shunts;
4. In Dalmatian dogs in the absence of pathology.

Cystine crystals.
Fine absent.
Reasons for appearance: cytinosis (congenital disorder of amino acid metabolism).

Crystals of leucine, tyrosine.
Fine none.
Reasons for appearance:
1. Acute yellow atrophy of the liver;
2. Leukemia;
3. Phosphorus poisoning.

Cholesterol crystals.
Fine none.


Reasons for appearance:
1. Amyloid and lipoid dystrophy of the kidneys;
2. Kidney neoplasms;
3. Kidney abscess.

Fatty acid.
Fine none.
Causes of appearance (very rare):
1. Fatty degeneration kidney;
2. Disintegration of the epithelium of the renal tubules.

Hemosiderin- a breakdown product of hemoglobin.
Fine absent.
Reasons for appearance - hemolytic anemia with intravascular hemolysis of red blood cells.

Hematoidin- a breakdown product of hemoglobin that does not contain iron.
Fine absent.
Reasons for appearance:
1. Calculous (associated with the formation of stones) pyelitis;
2. Kidney abscess;
3. New growths of the bladder and kidneys.

BACTERIA

Normally there are no bacteria or determined in urine obtained during spontaneous urination or using a catheter, in an amount of no more than 2x103 bact.\ml of urine.

The quantitative content of bacteria in the urine is of decisive importance.
- 100,000 (1x105) or more microbial bodies per ml of urine - indirect sign inflammation in the urinary organs.
- 1000 - 10000 (1x103 - 1x104) microbial bodies per ml of urine - raises suspicion of inflammatory processes in the urinary tract. In females this amount may be normal.
- less than 1000 microbial bodies per ml of urine are regarded as the result of secondary pollution.

Normally, urine obtained by cystocentesis should contain no bacteria at all.
When examining a general urine test, only the fact of bacteriuria is stated. In a native preparation, 1 bacterium in an oil immersion field of view corresponds to 10,000 (1x104) bact./ml, but bacteriological testing is necessary to accurately determine the quantitative characteristics.
The presence of a urinary tract infection can be signaled by simultaneously detected bacteriuria, hematuria and pyuria.

Yeast fungi

Normally none.
Reasons for appearance:
1. Glucosuria;
2. Antibiotic therapy;
3. Long-term storage of urine.

Urolithiasis (urolithiasis)– a disease associated with the formation of urinary stones in the kidneys (nephrolitas) or urinary tract (urolitis). Urine stones can form both in the upper urinary tract (kidneys and ureters) and in the lower (bladder, urethra). Bladder stones are the most common; kidney stones are quite rare, averaging 5-10%.

Urinary stones vary in their composition and frequency of occurrence. The most common stones are those consisting of ammonium magnesium phosphate (struvite) - up to 60-70% of all stones, the second most common are calcium oxalate stones (up to 10-20%), more rare are urate stones (consisting of uric acid, sodium urate or ammonium urate), cystine, xanthine and mixed stones. However, with cystine and urate stones, the prevalence is very breed dependent.

The factors that contribute to the crystallization and formation of urolith are diverse and can be divided into external (exogenous) and internal (endogenous). External factors include the feeding conditions of the animal, mineral composition water and its saturation with mineral salts. TO internal factors include the animal’s own diseases that contribute to the cause of urolithiasis. For example, hyperparathyroidism, porto-caval shunts, inflammatory processes in the genitourinary system, genetically determined metabolic abnormalities. Thus, reliable factors predisposing to the development of urolithiasis include the following reasons: oversaturation of urine with minerals at a certain urine pH; deficiency in the urine of certain factors that stabilize the composition of urine; stagnation of urine and long intervals between bladder emptyings; increased crystalloid loss caused by increased intestinal absorption; an increase in the formation of crystalloids due to the activity of bacteria capable of breaking down urea, which leads to alkalinization of urine.

Struvite urolithiasis- crystals of this composition can form in dogs at any age (usually the average age is 4-6 years). A breed predisposition has been identified in miniature schnauzers; this is believed to be due to a violation of local defense mechanisms in the urinary tract. The risk group also includes breeds such as,. Struvite is much more common in females than in males. These stones are often accompanied by a urinary tract infection and are radiopaque. Urine pH is usually alkaline.

Oxalate urolithiasis– the average age of dogs with this type of stone is 7-8 years, but can occur at any age. Mainly males are affected. A breed predisposition has been noted in miniature schnauzers. Oxalates form in acidic urine and are radiopaque. Promotes of calcium oxalate stone formation include hypercalciuria (eg, due to hyperparathyroidism), hyperoxaluria, hypocitraturia, and defects in crystal growth inhibitors (nephrocalcin). Role bacterial infection in the formation of this type of uroliths is not great.

Urate urolithiasis– crystals of this type are most often formed in Dalmatians, which is caused by a genetic disorder in the metabolism of purines in the body. The average age of the disease in this breed is 3.5 years, but it can appear much earlier. Also, breeds with impaired portal blood flow (congenital porto-systemic shunts) are susceptible to this type of urolithiasis. This is first and foremost Yorkshire Terrier, miniature schnauzer, Irish wolfhound, Australian Shepherd, Maltese, Cairn Terrier. With this pathology, urolithiasis manifests itself mainly before 1 year. It is more common in males with acidic and neutral urine. X-ray contrast is not stable.

Cystine urolithiasis– associated with cystinuria, caused by a genetically determined disorder in the reabsorption of cystine in the renal tubules. Not all dogs with cystinuria form stones. They mainly form in males at the age of 3-5 years (but the first episode can occur between 1, 5 and 3 years). They are practically never found in females. Breeds at risk are dachshund, English bulldog, Yorkshire terrier, Irish Terrier, Chihuahua. Uroliths usually form in acidic urine. These uroliths are radiopaque.

Clinical manifestations of urolithiasis in dogs depend on the location, size and number of stones. The main symptoms are pollakiuria (frequent urination), dysuria (painful, difficult and frequent urination), hematuria (blood in the urine). Stones displaced into the urethra can cause partial or complete obstruction with the development of postrenal renal failure. Animals with portocaval shunts may have symptoms of hepatic encephalopathy. Stones in the upper urinary tract may for a long time remain asymptomatic (if there is no ureteral obstruction) further leading to the development.

Diagnosis diagnosed using plain radiography (for radiopaque stones), . In unclear cases, double contrast cystography or excretory urography. General and biochemical blood tests, a general urinalysis and a blood test are also recommended. urine culture. Unfortunately, a urine test cannot accurately indicate a specific type of stone, since the crystals found in the urine may not correspond to the type of urolith in the bladder or kidneys. Also, in the presence of stones, crystalluria may be absent, and vice versa, crystalluria does not yet provide grounds for diagnosing urolithiasis and does not indicate the obligatory presence of stones in the urinary tract. After removing the stones, it is necessary to examine them to make a final diagnosis.

Treatment of urolithiasis in dogs depends on the presence or absence of urethral or ureteral obstruction, and general condition animal. Urethral obstruction is relieved using the following methods - retrograde urohydropropulsion (pushing stones from the urethra into the bladder), catheterization of the bladder with a thin catheter, urethrotomy or urethrostomy. Next, the stones are removed from the bladder using a cystotomy. In animals with struvite, urate, and cystine stones, conservative therapy aimed at dissolving the stones may be recommended. The main disadvantage is the duration of treatment (from several weeks to several months). To dissolve struvite, special diets are used that limit protein, calcium, phosphorus, magnesium, and maintain urine pH at a certain level, as well as antibiotic therapy (in the presence of a urinary tract infection). In the presence of urates, special diets are also used (with limited proteins and purines), which contribute to the alkalization of urine, xanthine oxidase inhibitors (allopurinol) are used, and in case of porto-caval shunts, their ligation is carried out. For cystine stones, therapeutic diets are also necessary, with protein restrictions affecting urine pH, penicillamine D or alpha-mercapto-propionyl-glycine are used. Oxalate stones are insoluble and must be surgically removed. With the aim of further prevention oxalate stones, it is also necessary to eliminate the cause of hypercalcemia (if hypercalcemia has been identified). To prevent recurrence of stone formation (as after surgical removal, and after conservative therapy), it is necessary to adhere to a therapeutic diet and conduct control examinations of the animal (X-rays, ultrasound, urine tests) at certain intervals.