Urolithiasis (urolithiasis) in dogs is a phenomenon of the formation and presence of uroliths in the urinary tract (kidneys, ureters, bladder and urethra). Uroliths ( uro– urine, lith– stone) - organized calculi consisting of minerals (primarily) and not a significant amount of organic matrix.
There are three main theories of the formation of urinary stones: 1. The theory of precipitation – crystallization; 2. Matrix-nucleation theory; 3. The theory of crystallization-inhibition. According to the first theory, oversaturation of urine with one or another type of crystals is put forward as the main reason for the formation of stones and, consequently, urolithiasis. In the theory of matrix nucleation, the presence of various substances in the urine that initiate the onset of urolith growth is considered as the reason for the formation of uroliths. With the theory of crystallization-inhibition, it has been suggested that the presence or absence of factors in the urine inhibiting or provoking the formation of stones. Urine oversaturation in dogs is considered to be the main cause of urolithiasis, other factors are less significant but may also contribute to the pathogenesis of stone formation.
Most canine uroliths are identified in the bladder or urethra. Struvite and oxalate are the predominant types of urinary stones, followed by urates, silicates, cystines and mixed types. Over the past twenty years, an increased percentage of oxalates has been noted, presumably this phenomenon has developed due to the beginning of the widespread use of industrial feed. An important cause of struvite formation in dogs is urinary tract infection. Below are the main factors that can increase the risk of morbidity in dogs with one or another type of urolithiasis.
Risk factors for canine oxalate-associated urolithiasis
Oxalate urinary stones are the most common type of urolith in dogs, and the incidence of urolithiasis with this type of stone has increased significantly over the last twenty years, along with a decrease in the prevalence of struvite. Oxalate urinary stones include calcium oxalate monohydrate or dihydrate, and the outer surface usually has sharp, jagged edges. One to many uroliths can form, and oxalate formation is characteristic of acidic dog urine.
Possible reasons for the increased incidence of oxalate uroliths in dogs include demographic and dietary changes in dog management during this period. These factors may include feeding with an acidifying diet (widespread use of industrial feed), an increase in the incidence of obesity and an increase in the percentage of representatives of breeds prone to the formation of a certain type of stones.
Breed predisposition to urolithiasis with the formation of oxalates was noted in representatives of such breeds as the Yorkshire Terrier, Shih Tzu, Miniature Poodle, Bichon Frize, Miniature Schnauzer, Pomeranian, Cairn Terrier, Maltese and Kesshund. Sexual predisposition has also been noted in small breed castrated males. Urolithiasis against the background of the formation of oxalate stones is more often observed in middle-aged and elderly animals (average age 8-9 years).
In general, the formation of uroliths is more associated with the acid-base balance of the animal body than with the specific pH and composition of urine. Dogs with oxalate urolithiasis often have transient hypercalcemia and hypercalciuria after feeding. So, uroliths can form against the background of hypercalcemia and the use of calciuretics (eg furosemide, prednisolone). Unlike struvites, urinary tract infection with oxalate uroliths develops as a complication of urolithiasis, and not as an underlying cause. Also, with the oxalate form of urolithiasis in dogs, there is a high relapse rate after stone extraction (about 25% -48%).
Risk Factors for Canine Urolithiasis with Struvite Formation
According to some reports, the percentage of struvite urinary stones in the total number is 40% -50%, but in recent years there has been a significant decrease in the incidence of struvite urolithiasis in favor of oxalate urolithiasis (see above). Struvites consist of ammonium, magnesium and phosphate ions, the shape is rounded (spherical, ellipsoidal and tetrahedral), the surface is often smooth. With struvite urolithiasis, both single and multiple uroliths with different diameters can form. Struvites in the urinary tract of dogs are more often localized in the bladder, but can also be noted in the kidneys and ureter.
The vast majority of canine struvite urinary stones are induced by a urinary tract infection (more commonly Staphylococcus intermedius but can also play a role Proteus mirabilis.). Bacteria have the ability to hydrolyze urea to ammonia and carbon dioxide, this is accompanied by an increase in urine pH and contributes to the formation of struvite urinary stones. In rare cases, the urine of dogs may become oversaturated with the minerals that make up struvite, and then, urolithiasis develops without the involvement of infection. Based on the possible causes of canine struvite urolithiasis, even if a negative urine culture is obtained, the search for infection continues and it is preferable to culture the bladder wall and / or calculus.
In case of urolithiasis of dogs with the formation of struvite uroliths, a breed predisposition was noted in such representatives as the Miniature Schnauzer, Bichon Frize, Cocker Spaniel, Shitzu, Miniature Poodle and Lhasa Apso. Age-related predisposition was noted in middle-aged animals, sexual predisposition in females (presumably due to an increased incidence of urinary tract infections). The American Cocker Spaniel may have a predisposition to form sterile struvites.
Risk Factors for Canine Urolithiasis with Urate Formation
Uric urinary stones account for about a quarter (25%) of all stones delivered to specialized veterinary laboratories. Urate stones consist of a monobasic ammonium salt of uric acid, are small in size, their shape is spherical, the surface is smooth, multiplicity of urolithiasis is characteristic, the color is from light yellow to brown (maybe green). Urate stones are usually easily crumbled; concentric bedding is determined at the fault. With urate urolithiasis, there is a certain predisposition to urolithiasis in males, presumably due to the smaller lumen of the urethra. Also, in case of urolithiasis in dogs with the formation of urates, a high percentage of relapses after extraction of stones is characteristic, it can be 30% -50%.
Unlike representatives of other breeds, the Dalmatian has a violation of purine metabolism, which leads to the release of an increased amount of uric acid and a predisposition to the formation of urates. It should be remembered that not all Dalmatians show the formation of urates, despite the congenital elevated level of uric acid in the urine of the animal, a clinically significant disease is determined in animals in 26% -34% of cases. In some other breeds (English Bulldog and Black Russian Terrier), a hereditary predisposition to impaired purine metabolism (similar to Dalmatians) and a tendency to urate form of urolithiasis may also be noted.
Another reason for the formation of urates is microvascular dysplasia of the liver, while there is a violation of the conversion of ammonia into urea and uric acid into allantoin. With the above violations of the liver, a mixed form of urolithiasis is more often noted, in addition to urates, struvites are also formed. A breed predisposition to the formation of this type of urolithiasis was noted in breeds predisposed to formation (eg Yorkshire Terrier, Miniature Schnauzer, Pekingese).
Risk factors for canine urolithiasis with silicate stones
Silicate uroliths are also rare and cause urolithiasis in dogs (about 6.6% of the total number of urinary stones), they consist mostly of silicon dioxide (quartz), may contain small amounts of other minerals. The color of silicate urinary stones in dogs is gray-white or brownish, more often multiple uroliths are formed. A predisposition to the formation of silicate stones has been noted in dogs when fed a diet high in gluten grains (gluten) or soy peels. The relapse rate after stone removal is quite low. As with oxalate urolithiasis, urinary tract infection is seen as a complicating factor rather than a causative factor in the disease.
Risk factors for cystine-forming urolithiasis in dogs
Cystine uroliths are rarely found in dogs (about 1.3% of the total number of urinary stones), they are completely composed of cystine, they are small in size, spherical in shape. The color of cystine stones is light yellow, brown or green. The presence of cystine in the urine (cystinuria) is considered a hereditary pathology with impaired transport of cystine in the kidneys (± amino acids), the presence of cystine crystals in the urine is regarded as a pathology, but not all dogs with cystinuria form corresponding urinary stones.
A number of dog breeds have a breed predisposition to the disease, such as the English Mastiff, Newfoundland, English Bulldog, Dachshund, Tibetan Spaniel and Basset Hound. With cystine urolithiasis in dogs, an exceptional sexual predisposition was noted in males, with the exception of Newfoundland. The average age at development of the disease is 4-6 years. When removing stones, a very high percentage of recurrences of their formation was noted, it is about 47% –75%. As with oxalate urolithiasis, urinary tract infection is seen as a complicating factor rather than a causative factor in the disease.
Risk Factors for Canine Urolithiasis with Hydroxyapatite (Calcium Phosphate) Formation
This type of urolith is extremely rare in dogs, and appatites (calcium phosphate or calcium hydroxyl phosphate) often appear as a component of other urinary stones (more often struvite). Alkaline urine and hyperparathyroidism predispose to precipitation of hypoxiapatitis in urine. The following breeds have a predisposition to the formation of this type of urinary stones - Miniature Schnauzer, Bichon Frize, Shih Tzu and Yorkshire Terrier.
Clinical signs
Struvite urinary stones are more often found in females due to their increased susceptibility to urinary tract infections, however; clinically significant urethral obstruction is more common in males due to the narrower and longer urethra. Canine urolithiasis can occur at any age, but is more common in middle-aged and older animals. Urinary stones in dogs under 1 year of age are most often struvites and develop from a urinary tract infection. With the development of the oxalate form of urolithiasis in dogs, the development of stones is more often observed in males, especially in breeds such as the Miniature Schnauzer, Shitzu, Pomeranian, Yorkshire Terrier and Maltese. Also, canine oxalate urolithiasis occurs at an older age than struvite type of urolithiasis. Urates are more often formed in Dalmatians and English Bulldogs, as well as in dogs predisposed to development. Cystine uroliths also have a certain breed predisposition, the table below contains general information on the incidence of urolithiasis in dogs.
Table. Pedigree, gender and age predisposition for the formation of urinary stones in dogs.
|
Type of stones |
Morbidity |
|
Struvite |
Breed predisposition - Miniature Schnatzer, Bichon Frize, Cocker Spaniel, Shitsu, Miniature Poodle, Lhasa Apso. Sexual predisposition in females Age predisposition - middle age The main predisposing factor to the development of struvites is an infection of the urinary tract with urease-producing bacteria (ex. Proteus, Staphylococcus). |
|
Oxalates |
Breed predisposition - Miniature Schnauzer, Shitzu, Pomeranian, Yorkshire Terrier, Maltese, Lhasa Apso, Bichon Frize, Cairn Terrier, Miniature Poodle Sexual predisposition - in neutered males more often than in non-neutered males. Age-related predisposition - middle and old age. One of the predisposing factors is obesity |
|
Breed predisposition - Dalmatians and English Bulldogs The main factor predisposing to the development of urates is a portosystemic shunt, and, accordingly, is more often observed in predisposed breeds (eg Yorkshire Terrier, Miniature Schnauzer, Pekingese) |
|
|
Silicates |
Breed predisposition - German Shepherd, Old English Shepherd Sexual and age-related predisposition - middle-aged males |
|
Breed predisposition - Dachshund, Basset Hound, English Bulldog, Newfoundland, Chihuahua, Miniature Pinscher, Welsh Corgi, Mastiffs, Australian cow dog Sexual and age-related predisposition - middle-aged males |
|
|
Calcium phosphate |
Breed predisposition - Yorkshire Terrier |
The history of urolithiasis in dogs depends on the specific localization of the stone, the duration of its finding, various complications and diseases predisposing to the development of the stone (etc.).
When a urinary stone is found in the kidneys, animals are characterized by a prolonged asymptomatic course of urolithiasis, blood in the urine (hematuria) and signs of pain in the kidney area may be noted. When pyelonephritis develops, the animal may have fever, polydipsia / polyuria, and general depression. Ureteral stones in dogs are rarely diagnosed, dogs may show various signs of pain in the lumbar region, most animals often develop unilateral lesions without systemic involvement, and a stone can be found as an accidental finding against the background of renal hydronephrosis.
Bladder stones in dogs represent the overwhelming majority of cases of urolithiasis in dogs, complaints of the owner during treatment may be signs of difficult and frequent urination, sometimes hematuria occurs. Displacement of stones into the urethra of males can lead to partial or complete obstruction of the outflow of urine, in which case the primary complaints may be signs of stranguria, abdominal pain and signs of postrenal renal failure (eg, anorexia, vomiting, depression). In rare cases of complete obstruction of the outflow of urine, a complete rupture of the bladder with signs of a uroabdomen may develop. It should be remembered that canine urinary tract stones can be asymptomatic and are found as an incidental finding on plain radiographic examination.
Physical examination data for urolithiasis sin with weak specificity of signs. With unilateral hydronephrosis in dogs, an enlarged kidney (renomegaly) may be found during palpation. With obstruction of the ureters or urethra, soreness of the abdominal cavity can be determined, with a rupture of the urinary tract, signs of a uroabdomen and general depression develop. During physical examination, bladder stones can be detected only with a significant number or volume; on palpation, sounds of crepitus can be detected or an urolith of a significant size can be felt. With obstruction of the urethra, palpation of the abdomen can reveal an enlarged bladder, rectal palpation can reveal a stone with localization in the pelvic urethra, with localization of a stone in the urethra of the penis - in some cases it can be palpated. When trying to catheterize the bladder of an animal with urethral obstruction, a veterinarian doctor may detect mechanical resistance to the catheter.
The most radiopaque urinary stones are uroliths with a calcium content (calcium oxalates and phosphates), struvite is also well defined in a general radiographic study. The size and number of radiopaque stones is best determined by x-ray. Double contrast cystography and / or retrograde urethrography can be used to identify retntgenotranslucent stones. Ultrasound diagnostic methods are able to detect radiolucent stones of the ureter of the bladder and urethra, in addition, ultrasound can help in assessing the kidneys and ureter of the animal. When examining a dog with urolithiasis, radiographic and ultrasound research methods are usually used together, but, according to many authors, double contrast cystography is the most sensitive method for determining bladder stones.
Laboratory tests for a dog with urolithiasis include CBC, animal biochemical profile, CBC, and urine culture. With urolithiasis in dogs, even in the absence of obvious pyuia, hematuria and proteinuria, there is still a high probability of urinary tract infection, and it is preferable to use additional research methods (e.g. urine cytological examination, urine culture). A biochemical blood test can detect signs of liver failure (eg high blood urea nitrogen levels, hypoalbuminemia) in dogs with.
Diagnosis and differential diagnosis
Urinary stones should be suspected in all dogs with signs of urinary tract infection (eg, hematuria, stranguria, pollakiuria, urinary outflow obstruction). The list of differential diagnoses includes any form of bladder inflammation, neoplasms of the urinary tract, and granulomatous inflammation. The detection of uroliths as such is carried out by means of visual examination methods (radiogarfia, ultrasound), in rare cases - identification of uroliths is possible only intraoperatively. Determination of a specific type of urolith requires its examination in a specialized veterinary laboratory.
It should be remembered that the identification of most crystals in urine does not always indicate pathology (with the exception of cystine crystals), in many dogs with urolithiasis, the type of crystals found in urine may differ in composition from urinary stones, crystals may not be detected at all, or multiple crystals may be detected without the risk of urinary calculi formation.
Treatment
The finding of urinary stones in the urinary tract of dogs is not always associated with the development of clinical signs; in many cases, the presence of uroliths is not accompanied by any symptoms on the part of the animal. In the presence of uroliths, several options for the development of events can be noted: their asymptomatic presence; evacuation of small uroliths into the spring environment through the urethra; spontaneous dissolution of urinary stones; stopping growth or its continuation; accession of a secondary urinary tract infection (); partial or complete obstruction of the ureter or urethra (with blockage of the ureter, unilateral hydronephrosis may develop); the formation of polypoid inflammation of the bladder. The approach to a dog with urolithiasis largely depends on the manifestation of certain clinical signs.
Urethral obstruction is a medical emergency, and when it develops, a number of conservative measures can be taken to displace the stone either outward or back into the bladder. In females, rectal palpation with massage of the urethra and urolith towards the vagina may facilitate its exit from the urinary tract. In both females and males, the urethrohydropulsation technique can return the bladder back to the bladder and restore normal urine flow. In some cases, when the diameter of the urolith is less than the diameter of the urethra, a lowering urohydropopulsion can be used, when a sterile saline solution is injected into the bladder in an animal under anesthesia, followed by manual emptying in an attempt to lower the stones (the procedure can be performed several times).
After the stone has been displaced into the bladder, it can be removed by cytostomy, endoscopic laser lithotripsy, endoscopic basket extraction, laparoscopic cystotomy, dissolved by drug therapy, or destroyed by extracorporeal shock wave lithotripsy. The choice of method depends on the size of the animal, the equipment and the qualifications of the veterinarian. If it is impossible to move the stone out of the urethra, urethrotomy with subsequent stone extraction can be used in males.
Indications for surgical treatment of urolithiasis in dogs are such indicators as obstruction of the urethra and ureter; multiple recurrent episodes of urolithiasis; the lack of effect from attempts at conservative dissolution of stones for 4-6 weeks, as well as the personal preferences of the doctor. When localizing uroliths in the kidneys of dogs, pyelotomy or nephrotomy can be used, it should be remembered that in dogs, uroliths of the kidneys and bladder can also be crushed by means of extracorporeal shock wave lithotripsy. When urinary stones are found in the ureters and localized in the proximal areas, ureterectomy can be used; when localized in the distal regions, resection of the ureter can be used with the subsequent creation of a new connection with the bladder (ureteroneocystostomy).
Indications for conservative treatment of canine urolithiasis are the presence of soluble uroliths (struvites, urates, cystines, and possibly xanthines) as well as animals with concomitant diseases that increase the operational risk. Regardless of the composition of the urolith, general measures are taken in the form of increased water consumption (hence increased urine output), treatment of any underlying diseases (eg Cushing's disease), as well as bacterial therapy (primary or secondary). It should be remembered that bacterial infection (cystitis or pyelonephritis) makes a significant contribution to the development of urolithiasis in dogs, either as a trigger or as a supportive mechanism. The effectiveness of conservative dissolution of canine urinary stones is usually monitored by visual imaging (usually x-ray).
In struvite urolithiasis, the main reason for their formation in dogs is urinary tract infection, and they dissolve against the background of adequate antibiotic therapy, possibly with the combined use of dietary feeding. At the same time, the average period of dissolution of infected uroliths in dogs during treatment is about 12 weeks. With a sterile form of struvite urolithiasis in dogs, the time for the dissolution of urinary stones is much shorter and takes about 4-6 weeks. In dogs with struvite urolithiasis, a change in diet to dissolve stones may not be necessary, and stones will reverse development only with appropriate antibiotic therapy and increased water intake.
In dogs with urate form of urolithiasis, in an attempt to conservatively dissolve stones, allopurinol at a dose of 10-15 mg / kg PO x 2 times a day can be used, as well as alkalinization of urine by changing the diet. The efficiency of conservative dissolution of urates is less than 50% and takes 4 weeks on average. It should be remembered that a significant cause of urate formation in dogs is, and dissolution of stones can be noted only after surgical resolution of this problem.
In cystine uroliths in dogs, in an attempt to conservatively treat urolithiasis, 2-mercatopropionol glysine (2-MPG) 15-20 mg / kg PO x 2 times a day can be used, as well as feeding an alkalizing diet with a low protein content. Dissolution of cystine stones in dogs takes about 4-12 weeks.
Xanthine uroliths are treated with reduced allopurinol intake and a low purine diet and are likely to reverse. With oxalate uroliths, there are no proven methods for their dissolution and it is generally accepted that they are not subject to reverse development, despite all the measures taken.
Valery Shubin, veterinarian, Balakovo
Urea is one of the products formed in the body during the breakdown of proteins. Normal blood urea concentration in dogs is 3.5-9.2 mmol / L (data may vary slightly from laboratory to laboratory). It is formed in the liver and excreted through the kidneys in the urine. An increase or decrease in the level of urea, therefore, indicates a violation of the function of these organs, a violation of metabolic processes.
Increased urea levels
Most often, an increase in the level of urea is associated with a difficulty in excreting it from the body, this is due to a deterioration in kidney function. Together with urea, the serum creatinine level also rises. An increase in blood levels of urea and other products of nitrogen metabolism is called azotemia. When the body begins to suffer from the accumulation of these products in the body, then they talk about uremia.
Urea can also increase with protein overfeeding of the animal (a lot of meat), with acute hemolytic anemia, stress, shock, vomiting, diarrhea, acute myocardial infarction.
Decreased urea levels
A decrease in urea may be associated with a low intake of proteins from food, severe liver diseases, for example, with portosystemic shunts. The increased excretion of urine 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 evaluated in conjunction with other studies conducted by a veterinarian.
The article was prepared by doctors of the therapeutic department "MEDVET"
© 2016 Specialized Exhibition Center "MEDVET"
Portosystemic shunts (PSS) represent a direct vascular connection of the portal vein with systemic circulation, so that substances with portal blood are sent from the intestinal tract bypassing the liver without hepatic metabolism. Dogs with PSS are very likely to develop ammonium urate uroliths. These uroliths are found in both males and bitches 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 degradation products of purine. In most dogs, it is converted by hepatic urease to allantoin. (Bartgesetal., 1992). However, in PSS, the uric acid formed as a result of purine metabolism practically does not pass through the liver. Consequently, it is not fully converted to allantoin, which leads to a pathological increase in serum uric acid concentration. When examining 15 dogs with PSS in a teaching hospital at the University of Minnesota, a serum uric acid concentration of 1.2-4 mg / dl was determined, in healthy dogs this concentration is 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 partly determined by its concentration in serum. Due to the nortosystem shunting of blood, the concentration of uric acid in the serum increases, and, accordingly. in the urine. The uroliths that form during PSS are usually composed of ammonium urates. Ammonium urates are formed because 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 into urea, therefore, its concentration in the systemic circulation increases. An increased concentration of circulating ammonia leads to an increased excretion of ammonia in the urine. The result of bypassing the portal blood of hepatic metabolism is an increase in the systemic concentration 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 in oversaturated urine leads to the formation of ammonium urate uroliths.
Clinical symptoms
Urate uroliths in PSS are usually formed in the bladder, therefore, sick animals will develop symptoms of urinary tract disease - hematuria, dysuria, pollakiuria and urinary disorders. When the urethra is obstructed, symptoms of anuria and post-azotemia are observed. Some dogs with bladder stones have no symptoms of urinary tract disease. Despite the fact that uroliths of ammonium urate can form in the renal pelvis, they are very rarely found there. A PSS dog may have symptoms of hepatoencephalopathy - tremors, drooling, seizures, bleeding, and stunted growth
Diagnostics
Rice. 1. Micrograph of urea sediment in a 6-year-old male Miniature Schnauzer. Urinary sediment contains crystals of ammonium urate (unstained, magnification 100)
Rice. 2. Double contrast cystogram -
ma 2-year-old male Lhasa Apso with PSSh.
Three radiolucent nodules are shown.
ment and a decrease in the size of the liver. At
analysis of nodules, remote surgeons
in a physical way, it was revealed that they were
100% composed of ammonium urate
Lab tests
In dogs with PSS, crystalluria with ammonium urate is often found (Fig. 1), which is an indicator of possible calculus formation. The specific gravity of urine may be low due to the decreased concentration of urine in the medulla of the nights. Another common disorder in dogs with PSS is microcytic anemia. Serum biochemical tests in dogs with PSS are generally normal, with the exception of low blood urea nitrogen levels caused by insufficient conversion of ammonia to urea.
Sometimes there is an increase in the activity of alkaline phosphatase and alanine aminotransfrase, and the concentration of albumin and glucose may be low. Serum uric acid concentration will increase, but these values should be interpreted with caution due to the unreliability of spectrophotometric methods for the analysis of uric acid (Felice et al., 1990). In dogs with PSS, liver function test results will include an increase in serum bile acid concentration before and after feeding, an increase in blood and plasma ammonia concentrations before and after administration of ammonium chloride, and an increase in bromsulfalein retention.
X-ray examinations
Ammonium urate uroliths can be radiolucent. therefore, it is sometimes impossible to identify them on conventional x-rays. However, abdominal x-rays show a decrease in liver size due to liver atrophy resulting from portosystemic shunting of the blood. Psnomegaly is sometimes observed with PSS, its meaning is unclear. Uroliths of ammonium urate in the bladder can be seen on double contrast cystography (Fig. 2) or on 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 the urethra, and with ultrasound scanning, 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 study requires sedation or general anesthesia. The condition of the kidneys can be assessed in terms of the presence of calculi in the renal pelvis, however, excretory urography is a more reliable way of examining the nocturnal and ureters.
Treatment
Although it is possible for dogs without PSS to dissolve ammonium urate uroliths medically using a low-purine alkaline diet in combination with allonurinol, drug therapy will not be effective in dissolving calculi in dogs with PSS. The efficacy of allopurinol may be altered in these animals due to biotransformation of the short half-life drug to the long half-life oxypurinol (Bartgesetal., 1997). Also, drug dissolution may be ineffective if the uroliths contain other minerals in addition to ammonium urates.In addition, when allopurinol is prescribed, xanthine may form, which will interfere with dissolution
Urate urocystoliths, which are usually small, round, and smooth, can be removed from the bladder with urohydropulsion during urination. However, the success of this procedure depends on the size of the uroliths, the diameter of which must be smaller than the narrowest part of the urethra. Therefore, such calculus removal should not be performed in dogs with PSS.
Since drug dissolution is ineffective, clinically active calculi must be surgically removed. If possible, calculi should be removed during surgical correction of PSS. If the calculi are not removed at this moment, 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 PSSH, the calculi may dissolve on their own, since they consist of ammonium urates. New research is needed to confirm or refute this hypothesis. Also, using an alkaline, low-purine diet may prevent the growth of existing calculi or facilitate their dissolution after ligation with PSS.
Prophylaxis
After ligation with PSSH, ammonium urates stop precipitating if normal blood flow goes through the liver. However, for animals that cannot be ligated with PSS, or with partial ligation of PSS, there is a risk of formation of ammonium urate uroliths. For these animals, constant monitoring of the composition of urine is needed to prevent the precipitation of ammonium urate crystals. With crystalluria, additional preventive measures must be taken. Monitoring the concentration of ammonia in the blood plasma after feeding allows you to detect its increase, despite the absence of clinical symptoms. Measurement of serum uric acid concentration also detects an increase. Consequently, the concentration of ammonia and uric acid in the urine of these animals will also be increased, which increases the risk of the formation of ammonium urate uroliths. In a study at the University of Minnesota, 4 dogs with inoperable PSS were fed a low purine alkalizing 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, during which there was no recurrence of the formation of uroliths of ammonium urate.
If preventive measures are needed, a low-protein, alkalizing diet should be followed. Allopurinol is not recommended for dogs with PSS.
Blood chemistry.
A biochemical blood test is a laboratory diagnostic method that allows you to evaluate the work of many internal organs. A standard biochemical blood test includes the determination of a number of indicators reflecting the state of protein, carbohydrate, lipid and mineral metabolism, as well as the activity of some key serum enzymes.
For the study, blood is taken strictly on an empty stomach in a test tube with a coagulation activator, and blood serum is examined.
- General biochemical parameters.
Total protein.
Total protein is the total concentration of all blood proteins. There are various classifications of plasma proteins. Most often they are divided into albumin, globulins (all other plasma proteins) and fibrinogen. The concentration of total protein and albumin is determined using biochemical analysis, and the concentration of globulins is determined by subtracting the concentration of albumin from the total protein.
Increase:
- 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 (chylemia), hyperbilirubinemia, significant hemoglobinemia (hemolysis).
Decrease:
- 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.
With bleeding, the concentration of albumin and globulins decreases in parallel, however, in some disorders accompanied by loss of protein, the content of albumin mainly decreases, since the size of its molecules is smaller in comparison with other plasma proteins.
Normal value
Dog 55-75 g / l
Cat 54-79 g / l
Albumen
Homogeneous plasma protein containing small amounts of carbohydrates. An important biological function of albumin in plasma is to maintain intravascular colloidal osmotic pressure, thereby preventing the release of plasma from 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, binds mediators of inflammatory processes that are dangerous to tissues.
Increase:
- dehydration
Disorders that would be accompanied by increased albumin synthesis are not known.
Decrease:
- overhydration;
- bleeding,
- nephropathy and enteropathy,
- severe exudation (eg 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 hemproteins. Most of the circulating bilirubin (about 80%) is formed from "old" erythrocytes. Dead "old" erythrocytes are destroyed by reticuloendothelial cells. When heme is oxidized, biliverdin is formed, which is metabolized to bilirubin. The rest of the circulating bilirubin (about 20%) is formed from other sources (destruction of mature erythrocytes 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. Albumin-bound bilirubin can be easily removed from the blood by the liver. In the liver, bilirubin binds to glucuronic acid under the influence of glucuronyl transferases. Bound bilirubin includes bilirubin monoglucuronide, which predominates in the liver, and bilirubin diglucuronide, which predominates in bile. The bound bilirubin is transported to the bile capillaries, from where it enters the biliary tract and then to the intestines. In the intestine, bound bilirubin undergoes a series of transformations with the formation of urobilinogen and stercobilinogen. Stercobilinogen and a small amount of urobilinogen are excreted in the faeces. The main amount of urobilinogen is reabsorbed in the intestine, reaching the liver through the portal circulation and re-excreted by the gallbladder.
Serum bilirubin levels rise when its 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 bound bilirubin, soluble and highly reactive. An increase in the level of direct bilirubin in the blood serum is associated with a decreased excretion of conjugated pigment from the liver and biliary tract and manifests itself in the form of cholestatic or hepatocellular jaundice. An abnormal increase in the level of direct bilirubin leads to the appearance of this pigment in the urine. Since indirect bilirubin is not excreted in urine, the presence of bilirubin in urine emphasizes an increase in serum bound bilirubin levels.
Indirect bilirubin
The serum concentration of unconjugated bilirubin is determined by the rate at which the newly synthesized bilirubin enters the blood plasma and the rate of elimination of bilirubin by the liver (hepatic clearance of bilirubin).
Indirect bilirubin is calculated by calculation:
indirect bilirubin = total bilirubin - direct bilirubin.
Enhancement
- accelerated destruction of red blood cells (hemolytic jaundice),
- hepatocellular disease (hepatic and extrahepatic origin).
Chilesis can cause a falsely overestimated value of the bilirubin content, which should be taken into account if a high bilirubin level is determined in a patient in the absence of jaundice. "Chyle" 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 mellitus, pancreatitis, hypothyroidism.
Downgrade
It has no clinical significance.
Normal value:
Total bilirubin
Dog - 2.0-13.5 μmol / L
Cat - 2.0-10.0 μmol / l
Bilirubin direct
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 bloodstream. If the energy metabolism of liver cells is disturbed by infectious factors (for example, viral hepatitis) or toxic, then 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 even for the detection of minimal liver damage. ALT is more specific for liver disorders than AST. The absolute ALT values still do not directly correlate with the severity of liver damage and with the prediction of the development of the pathological process, and therefore, serial ALT determinations over time are most appropriate.
Increased:
- liver damage
- the use of hepatotoxic drugs
Decreased:
- 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 occurs 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 isozymes are found both in the cytosol and in the mitochondria.
Increased:
- Toxic and viral hepatitis
- Liver tissue necrosis
- Acute myocardial infarction
- Administration of opioids to patients with biliary tract diseases
Increase and rapid decline suggests obstruction of the biliary extrahepatic tract.
Decreased:
- Azotemia
Normal value:
Dog - 8-42 units / l
Cat - 9-45 units / l
An increase in ALT exceeding an increase in AST is characteristic of liver damage; if the AST index rises more than the ALT rises, then this, as a rule, indicates the problems of myocardial cells (heart muscle).
γ - glutamyl transferase (GGT)
GGT is an enzyme localized on the cell membrane of various tissues, catalyzing the reaction of transamination or transamination of amino acids during 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 content of the enzyme is noted in the membrane of cells with a high secretory and absorption capacity: hepatic tubules, biliary epithelium, nephron tubules, epithelium of the villi of the small intestine, pancreatic exocrine cells.
Since GGT is associated with epithelial cells of the bile duct system, it has diagnostic value in liver dysfunction.
Increased:
- cholelithiasis
- in dogs, with an increase in the concentration of glucorticosteroids
- hyperthyroidism
- hepatitis of extra- or intrahepatic origin, liver neoplasia,
- acute pancreatitis, pancreatic cancer
- exacerbation of chronic glomerulonephritis and pyelonephritis,
Decreased:
Normal value
Dog 0-8 units / l
Cat 0-8 units / l
In contrast to ALT, which is contained in the cytosol of hepatocytes and therefore is a sensitive marker of a violation of the integrity of cells, GGT is found exclusively in mitochondria and is released only with significant tissue damage. Unlike in humans, anticonvulsants used in dogs do not induce an increase in GGT activity or it is minimal. In cats with liver lipidosis, ALP activity is increased to a greater extent than GGT. Colostrum and breast milk in the early stages of feeding contain a high activity of GGT, therefore, the level of GGT in newborns is increased.
Alkaline phosphatase.
This enzyme is found primarily in the liver (bile duct and bile duct epithelium), kidney tubules, small intestine, bones, and placenta. It is an enzyme associated with the cell membrane that catalyzes the alkaline hydrolysis of a wide variety of substances, during which the remainder of phosphoric acid is cleaved from its organic compounds.
The total alkaline phosphatase activity in the circulating blood of healthy animals consists of the activity of hepatic and bone isoenzymes. The proportion of the activity of bone isoenzymes is greatest in growing animals, while in adults their activity can increase with bone tumors.
Increase:
- violation of the flow of bile (cholestatic hepatobiliary disease),
- nodular liver hyperplasia (develops with aging),
- cholestasis,
- increased activity of osteoblasts (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).
- In cats, it may be associated with hepatic lipidosis.
Decrease:
- 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 formed in the salivary glands and pancreas, then enters the oral cavity or duodenal lumen, respectively. Organs such as the ovaries, fallopian tubes, small and large intestines, and the liver also have significantly lower amylase activity. In the 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-sized complexes with immunoglobulins and other plasma proteins, which does not allow it to pass through the renal glomeruli, as a result of which its content in serum increases, and normal amylase activity is observed in urine.
Increased:
- Pancreatitis (acute, chronic, reactive).
- Neoplasms of the pancreas.
- Blockage of the pancreatic duct (tumor, calculus, adhesions).
- Acute peritonitis.
- Diabetes mellitus (ketoacidosis).
- Diseases of the biliary tract (cholelithiasis, cholecystitis).
- Renal failure.
- Traumatic lesions of the abdominal cavity.
Decreased:
- 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) to disaccharides and oligosaccharides (maltose, glucose). In animals, a significant part of the amylase activity is due to the mucous membrane of the small intestine and other extra-pancreatic sources. With the participation of amylase in the small intestine, the process of digestion of carbohydrates is completed. Various disturbances of processes in the acinous cells of the exocrine pancreas, increased permeability of the pancreatic duct and premature activation of enzymes lead to the "leakage" of enzymes inside the organ.
Increase:
- renal failure
- severe inflammatory bowel disease (perforation of the small intestine, volvulus),
- long-term treatment with glucocorticosteroids.
Downgrade :
- inflammation,
- necrosis or swelling of the pancreas.
Normal value
Dog 243.6-866.2 units / l
Cat 150.0-503.5 units / l
Glucose.
Glucose is the body's main source of energy. As part of carbohydrates, glucose enters the body with food and is absorbed into the bloodstream 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 tissues and erythrocytes. 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 between meals. Glucose is the only source of energy for skeletal muscle to function under anaerobic conditions. The main hormones affecting glucose homeostasis are insulin and the deregulating hormones glucagon, catecholamines, and cortisol.
Increase:
- insulin deficiency or tissue resistance to insulin,
- pituitary tumors (found in cats),
- acute pancreatitis,
- renal failure,
- taking certain medications (glucocorticosteroids, thiazide diuretics, intravenous fluids containing glucose, progestins, etc.),
- severe hypothermia.
Short-term hyperglycemia is possible with head trauma and CNS lesions.
Decrease:
- a tumor of the pancreas (insulinoma),
- hypofunction of endocrine organs (hypocorticism);
- 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 erythrocytes, a drop in glucose is possible, since erythrocytes actively consume it, so it is advisable to centrifuge the blood as soon as possible. Non-centrifuged blood glucose is reduced by about 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 it enters muscle tissue by 98%, where it is phosphorylated. The formed phosphocreatine plays an important role in the storage of muscle energy. When this muscle energy is required for metabolic processes, phosphocreatine is broken down to creatinine. Creatinine is a persistent nitrogenous constituent of the blood, independent of most foods, exercise or other biological constants, and is associated with muscle metabolism.
Renal dysfunction reduces the excretion of creatinine, causing an increase in serum creatinine levels. Thus, creatinine concentrations roughly characterize the level of glomerular filtration. The main value of serum creatinine determination is the diagnosis of renal failure.
Serum creatinine is a more specific and more sensitive indicator of renal function than urea.
Increase:
- acute or chronic renal failure.
It is caused by prerenal reasons causing a decrease in the glomerular filtration rate (dehydration, cardiovascular diseases, septic and traumatic shock, hypovolemia, etc.), renal associated with severe diseases of the renal 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 urinary tract rupture).
Downgrade :
- age-related decrease in muscle mass.
Normal value
Dog 26-130 μmol / l
Cat 70-165 μmol / l
Urea
Urea is formed by 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 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.
Increase:
- renal failure (may be due to prerenal, renal and postrenal disorders).
Downgrade
- low intake of protein in the body,
- liver disease.
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 intestines, 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. A decrease in uric acid metabolism, combined with a weakening of 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 PSS is a direct vascular connection of the portal vein with 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 enter the liver during 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 partly determined by its concentration in serum.
Dalmatian mastiffs are prone to the formation of urate crystals due to a particular metabolic disorder of the liver, leading to incomplete oxidation of uric acid.
Enhancement
- uric acid diathesis
- leukemia, lymphoma
- anemia caused by vitamin B12 deficiency
- some acute infections (pneumonia, tuberculosis)
- diseases of the liver and biliary tract
- diabetes
- dermatological diseases
- kidney disease
- acidosis
Decrease:
- a 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 noted in the stomach, liver, adipose and other tissues. Pancreatic lipase acts on the surface of lipid droplets formed in the intestine.
Enhancement :
- perforation of the small intestine,
- chronic renal failure,
- the use of corticosteroids,
- postoperative period
Downgrade
- hemolysis.
Normal value
Dog<500 ед/л
Cat<200 ед/л
Cholesterol
Determination of cholesterol level 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 of 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 animal products (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, sex differences in concentration appear, which is associated with the action of sex hormones. Estrogens lower and androgens raise total cholesterol levels.
Increased:
- hyperlipoproteinemia
- obstruction of the biliary tract: cholestasis, biliary cirrhosis;
- nephrosis;
- diseases of the pancreas;
- hypothyroidism, diabetes mellitus;
- obesity.
Decreased:
- 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 conversion of creatine phosphate to creatinine in the presence of ADP, which is converted into ATP, which is a source of energy for muscle contraction.
The active form of CPK is a dimer consisting of subunits M and B, respectively, there are 3 CPK isoenzymes: BB (contained in the brain), MV (in the myocardium), and MM (in skeletal muscle 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 less than in animals of other species, therefore, in them, one should pay attention to even a slight excess of the upper limit of the standard interval.
Often in cats with anorexia, CPK levels can rise and fall several days after appropriate maintenance nutrition.
Enhancement
- damage to skeletal muscles (trauma, surgery, muscular dystrophies, polymyositis, etc.).
- after significant physical exertion,
- epileptic seizures
- myocardial infarction (2-3 hours after the lesion, and after 14-30 hours it reaches a maximum, a decrease in the level occurs 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 be increased.
Decrease:
- 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 during glycolysis. With adequate oxygen supply, lactate does not accumulate in the blood, but is neutralized and excreted. With oxygen deficiency, the enzyme tends to accumulate, causing muscle fatigue, disrupting tissue respiration. High LDH activity is inherent in many tissues. There are 5 LDH isoenzymes: 1 and 2 are presented mainly in the heart muscle, in 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 in a particular tissue, the method of glucose oxidation depends - aerobic (to CO2 and H2O) or anaerobic (to lactic acid).
Since the enzyme activity is high in tissues, even relatively small tissue damage or weak hemolysis leads to a significant increase in LDH activity in the circulating blood. From this it follows that any diseases accompanied by the destruction of cells that contain LDH isozymes are accompanied by an increase in its activity in the blood serum.
Enhancement
- myocardial infarction,
- damage and degeneration of skeletal muscles,
- necrotic lesion of the kidneys and liver,
- cholestatic liver diseases,
- pancreatitis,
- pneumonia,
- hemolytic anemias, etc.
Downgrade
It has no clinical significance.
Normal value
Dog 23-220 units / l
Cat 35-220 units / l
The degree of increase in LDH activity in myocardial infarction does not correlate with the size of the lesion of the heart muscle and can only serve as an indicative factor for the prognosis of the disease. In general, being not a specific laboratory marker, the change in the LDH level should be assessed only in combination with the values of other laboratory parameters (CPK, AST, etc.), as well as the data of instrumental diagnostic methods. It is also important not to forget that even a 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 cleavage of choline esters (acetylcholine, etc.) with the formation of choline and the corresponding acids. There are two types of enzyme: true (acetylcholinesterase) - which plays an important role in the transmission of nerve impulses (located in the nervous tissue and muscles, erythrocytes), and false (pseudocholinesterase) - serum, present in the liver and pancreas, muscles, heart, brain ... ChE performs a protective function in the body, in particular, prevents the inactivation of acetylcholinesterase, hydrolyzing the inhibitor of this enzyme, butyrylcholine.
Acetylcholineserase is a strictly specific enzyme that hydrolyzes acetylcholine, which is involved in signal transmission through the endings of nerve cells and is one of the most important neurotransmitters in the brain. With a decrease in the activity of ChE, acetylcholine accumulates, which first leads to an acceleration of the conduction of nerve impulses (excitation) and then to blocking the transmission of nerve impulses (paralysis). This causes disorganization of all body processes, and in case of severe poisoning, it can be fatal.
Measurement of the ChE level in blood serum can be useful in case of poisoning with insecticides or various toxic compounds inhibiting the enzyme (organophosphates, phenothiazines, fluorides, various alkaloids, etc.)
Enhancement
- diabetes;
- mammary cancer;
- nephrosis;
- hypertension;
- obesity;
Downgrade
- liver damage (cirrhosis, metastatic liver damage)
- muscular dystrophies, dermatomyositis
Normal value
Dog 2200-6500 E / l
Cat 2000-4000 E / l
Calcium. Ionized calcium.
In blood plasma, calcium is present in three forms:
1) in combination with organic and inorganic acids (a very small percentage),
2) in the form associated with proteins,
3) in ionized form Ca2 +.
Total calcium includes the total concentration of all three forms. Of the total calcium, 50% is ionized calcium and 50% is associated with albumin. Physiological shifts rapidly alter calcium binding. In a biochemical blood test, both the level of total calcium in the blood serum and the concentration of ionized calcium are measured separately. 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 a variety of metabolic processes. Calcium ions take part in the regulation of the most important physiological and biochemical processes: neuromuscular excitement, blood coagulation, secretion processes, maintenance of membrane integrity and transport across membranes, many enzymatic reactions, the release of hormones and neurotransmitters, the intracellular action of a number of hormones, is involved 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 the concentration of Ca2 + in the body can cause many pathologies. With a decrease in calcium, 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 shifts in the level of total calcium in the blood plasma. The binding of calcium to plasma proteins depends on pH: acidosis promotes the conversion of calcium into an ionized form, and alkalosis increases protein binding, 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 on a feedback mechanism. Calcium metabolism is influenced by estrogens, corticosteroids, growth hormone, glucagon and T4. PTH is the main physiological regulator of blood calcium concentration. The main signal affecting 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 depot in bones. When Ca2 + falls, the opposite process takes place. PTH is secreted by the cells of the parathyroid glands, and when the calcium concentration falls, the secretion of PTH increases. PTH stimulates the release of calcium from bones, reabsorption of Ca in the renal tubules.
Increase:
- hyperalbuminemia
- malignant tumors
- primary hyperparathyroidism;
- hypocorticism;
- osteolytic lesions of bones (osomyelitis, myeloma);
- idiopathic hypercalcemia (cats);
Decrease:
- hypoalbuminemia;
- alkalosis;
- primary hypoparathyroidism;
- chronic or acute renal failure;
- secondary renal hyperparathyroidism;
- pancreatitis;
- unbalanced diet, vitamin D deficiency;
- eclampsia or postpartum paresis;
- disorders of 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; it is part of hemoglobin, cytochromes and other biologically important compounds. Iron is an essential element for the formation of red blood cells, is involved in the transfer of oxygen and tissue respiration. It also participates in a number of redox reactions, the work of the immune system, and collagen synthesis. Developing erythroid cells take from 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 number of glands and its chemical form. Under the action of hydrochloric acid in the stomach, iron oxides ingested with food go into a soluble form and bind in the stomach with mucin and various small molecules that keep iron in a soluble state suitable for absorption in the alkaline medium of the small intestine. Under normal conditions, only a small percentage of dietary iron is absorbed into the bloodstream. Iron absorption increases with its lack 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 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 hyperchromic anemia,
- liver diseases,
- administration of corticosteroids
- lead intoxication
Decreased:
- vitamin deficiency B12;
- 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, it is present in gastric juice, secretions of the pancreas and intestines, sweat, 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 contributes to 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 introduction of chlorine, occurs with vomiting and the appointment of diuretics, as a result of the loss of H + and Cl- ions;
the chlorine-resistant type, uncorrected by the introduction 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.
Decreased:
- general overhydration,
- indomitable 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, and only small amounts are present in bones and blood. Potassium is concentrated mainly in skeletal muscles, liver and myocardium. From damaged cells, potassium is released into the blood. All potassium entering 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 the feces. Regardless of the amount of potassium supplied from the outside, it is excreted daily by the kidneys, as a result of which severe hypokalemia quickly sets in.
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 cardiac contraction and cardiac output. Potassium and sodium ions are of great importance in the regulation of 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.
The increase and decrease in serum potassium levels are caused by disturbances in the internal and external balance of potassium. The external balance factor is: potassium intake with food, acid-base balance, mineralocorticoid function. Factors of internal balance include the function of adrenal hormones, which stimulate its excretion. Mineralocorticoids directly affect the secretion of potassium in the distal tubules, glucocorticosteroids act in an indirect way, increasing the 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,
- the appointment of anti-inflammatory nonsteroidal drugs,
- prescribing K-sparing diuretics,
Decreased:
- the appointment of non-potassium-sparing diuretics.
- diarrhea, vomiting,
- taking laxatives,
- profuse sweating,
- severe burns.
Hypokalemia associated with a decrease in urinary K + excretion, but without metabolic acidosis or alkalosis:
- parenteral therapy without additional potassium intake,
- fasting, anorexia, malabsorption,
- rapid growth of cell mass in the treatment of anemia with iron, vitamin B12 or folic acid preparations.
Hypokalemia associated with increased K + excretion and metabolic acidosis:
- renal tubular acidosis (RCA),
- diabetic ketoacidosis.
Hypokalemia associated with increased K + excretion and normal pH (usually renal origin):
- recovery from obstructive nephropathy,
- the appointment 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 body fluids, 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 is also retained in other body fluids, such as gastric juice, pancreatic juice, bile, intestinal juice, sweat, and CSF. A relatively large amount of sodium is found in cartilage and slightly less in bones. The total amount of sodium in bones increases with age, and the proportion of sodium reserves decreases. This proportion is clinically important as it represents a reservoir for sodium loss and acidosis.
Sodium is the main component of the osmotic pressure of a fluid. All movements of sodium cause movement of certain quantities of water. The volume of extracellular fluid directly depends on the total amount of sodium in the body. Plasma sodium concentration is identical to that in the extracellular fluid.
Increased:
- the use of diuretics,
- diarrhea (in young animals)
- Cushing's syndrome,
Decreased:
A decrease in the volume of extracellular fluid is observed when:
- jade with loss of salt,
- glucocorticoid deficiency,
- osmotic diuresis (diabetes with glucosuria, condition after violation of urinary tract obstruction),
- renal tubular acidosis, metabolic alkalosis,
- ketonuria.
A moderate increase in the volume of extracellular fluid 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 total sodium levels are observed when:
- congestive heart failure (serum sodium 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 in the body, present in any tissue.
In the cell, phosphorus is mainly involved in the metabolism of carbohydrates and fats or is associated with proteins, and only a small part is in the form of a phosphate ion. Phosphorus is a part of bones and teeth, is one of the constituents of nucleic acids, phospholipids of cell membranes, also participates in maintaining acid-base balance, in storing and transferring energy, in enzymatic processes, stimulates muscle contraction and is necessary to maintain the activity of neurons. The kidneys are the main regulators of phosphorus homeostasis.
Increased:
- Osteoporosis.
- The use of cytostatics (cell cytolysis and release of phosphates into the blood).
- Acute and chronic renal failure.
- Breakdown of bone tissue (with malignant tumors)
- Hypoparathyroidism,
- Acidosis
- Hypervitaminosis D.
- Portal cirrhosis.
- Healing of bone fractures (bone callus formation).
Decreased:
- Osteomalacia.
- Syndrome of malabsorption.
- 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 growth 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 amounts 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 in plasma, 25% is bound to proteins, and the rest 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 mechanism of blood coagulation. 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 the muscle cell, magnesium acts as a calcium antagonist.
Lack of magnesium leads to the mobilization of calcium from the bones, therefore it is recommended to take calcium levels into account when assessing magnesium levels. From a clinical point of view, magnesium deficiency causes neuromuscular diseases (muscle weakness, tremors, tetany and seizures) and can cause cardiac arrhythmias.
Increased:
- iatrogenic causes
- renal failure
- dehydration;
- diabetic coma
- hypothyroidism;
Decreased:
- 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,
- the 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, the last trimester of pregnancy, insulin treatment for diabetic coma;
- eclampsia,
- osteolytic bone tumors,
- progressive Paget bone disease,
- 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 the total content of bile acids (FA) in the circulating blood is a functional test of the liver due to a special process of FA recycling, called enterohepatic circulation. The main components involved in the recirculation of bile acids are the hepatobiliary system, the terminal ileum and the portal vein system.
Circulatory disorders in the portal vein system in most animals are associated with portosystemic shunting. Portsystemic shunt is an anastamosis between the veins of the gastrointestinal tract and the caudal vena cava, due to which the blood flowing from the intestine does not undergo cleansing 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 before meals is usually retained in the gallbladder. Food intake stimulates the release of cholecystokinin from the intestinal wall, which causes contraction of the gallbladder. There is individual physiological variability in the amount of stored bile and the degree of contraction of the gallbladder during stimulation with food, and the ratio between these values changes in some sick animals.
When the concentration of circulating bile acids is within or near the standard range, such physiological fluctuations can cause postprandial bile acid levels to be similar or less than fasting levels. In dogs, this can also occur when bacteria overgrow in the small intestine.
An increase in the content of bile acids in the blood, secondary to liver disease or portosystemic shunting, is accompanied by their increased excretion in the urine. In dogs and cats, the determination of the bile acid / creatinine ratio in urine is a fairly sensitive test for the diagnosis of liver disease.
It is important to study the level of bile acids on an empty stomach and 2 hours after eating.
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 intestine 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, which is characteristic of many liver diseases.
Normal value:
Dog 0-5 μmol / l
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