An increase in uric acid in a dog up to 1200. Urolithiasis (urolithiasis) in dogs
Portosystemic shunts (PSS) are a direct vascular connection of the portal vein with the systemic circulation, so that substances in the portal blood are directed from intestinal tract bypassing the liver without hepatic metabolism. Dogs with PSS are very likely to develop ammonium urate uroliths. These uroliths occur in both males and females and are usually, but not always, diagnosed in animals older than 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, uric acid, formed as a result of purine metabolism, practically does not pass through the liver. Consequently, it is not completely converted to allantoin, which leads to a pathological increase in the serum concentration of uric acid. In a study of 15 dogs with PSS at the University of Minnesota Teaching Hospital, 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 glomerulus, reabsorbed in the proximal tubules, and secreted into the tubular lumen of the distal proximal nephrons.
Thus, the concentration of uric acid in the urine is partly determined by its concentration in the serum. Due to the northosystemic shunting of the blood, the concentration of uric acid in the serum increases, and, accordingly. in urine. The uroliths that form in PSS are usually composed of ammonium urate. Ammonium urate is formed because the urine becomes supersaturated with ammonia and uric acid due to 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, where it is converted to urea. In dogs with PSS, a small amount of ammonia is converted to urea, so 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 the portal blood bypass of hepatic metabolism is an increase in systemic concentrations of uric acid and ammonia, which are excreted in the urine. If the saturation of urine with ammonia and uric acid exceeds the solubility of ammonium urates, they precipitate. Precipitation under conditions of supersaturated urine leads to the formation of ammonium urate uroliths.
Clinical symptoms
Urate uroliths in PSS usually form in the bladder, therefore, affected animals will develop symptoms of the disease. urinary tract- hematuria, dysuria, pollakiuria and impaired urination. With obstruction of the urethra, symptoms of anuria and post-spinal azotemia are observed. Some dogs with bladder stones do not have symptoms of urinary tract disease. Although ammonium urate uroliths can form in the renal pelvis, they are rarely found there. A dog with PSS may have symptoms of hepatoencephalopathy—tremors, drooling, seizures, bleeding, and stunted growth.
Diagnostics
Rice. 1. Micrograph of urine sediment from a 6-year-old miniature schnauzer male. Urinary sediment contains ammonium urate crystals (unstained, magnification x 100)
Rice. 2. Double contrast cystogram
mother of a 2-year-old male Lhasa Apso with PSSh.
Three radiolucent concretions are shown.
ment and a decrease in the size of the liver. At
analysis of stones, remote surgical
scientifically, it was found that they
100% consisted of ammonium urates
Laboratory tests
In dogs with PSS, crystalluria with ammonium urate is often found (Fig. 1), which is an indicator of possible stone formation. The specific gravity of the urine may be low due to the decreased concentration of urine in the nocturnal medulla. Another common disorder in dogs with PSS is microcytic anemia. Serum chemistry tests in dogs with PSS are usually normal, except for a low blood urea nitrogen concentration caused by inadequate conversion of ammonia to urea.
Sometimes there is an increase in the activity of alkaline phosphatase and alanine aminotransfsrazy, and the concentration of albumin and glucose may be low. Serum uric acid concentration will be elevated, however, 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, the results of liver function tests will be an increase in serum bile acid concentrations before and after feeding, an increase in blood and plasma ammonia concentrations before and after ammonium chloride administration, and an increase in bromsulfalein retention.
X-ray studies
Ammonium urate uroliths may be radiolucent. therefore, sometimes they cannot be identified on plain x-rays. However, an abdominal x-ray can show a decrease in the size of the liver due to its atrophy, which was the result of portosystemic shunting of the blood. Rsnomegaly is sometimes observed in PSS, its significance is unclear. Ammonium urate uroliths in the bladder can be seen on double contrast cystography (Figure 2) or on ultrasonography. If uroliths are present in the urethra, then contrast retrography is needed to determine their size, number, and location. In assessing the urinary tract, double contrast cystography and retrograde contrast urethrography have several advantages over abdominal ultrasound. On contrast images, both the bladder and urethra are visible, and with ultrasound scanning- just the bladder. The number and size of stones can also be determined by contrast cystography. The main disadvantage contrast radiography 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 stones in the renal pelvis, but excretory urography is a more reliable way to examine the kidneys and ureters.
Treatment
Although it is possible for dogs without PSS to dissolve ammonium urate uroliths medically with an alkaline diet with low content purine in combination with allonurinol, drug therapy will not be effective in dissolving stones in dogs with PSS. The efficacy of allopurinol may vary in these animals due to biotransformation of the drug with short period half-life to oxypurinol with a long half-life (Bartgesetal., 1997). Also, drug dissolution may be ineffective if uroliths contain other minerals besides ammonium urate. In addition, when allopurinol is administered, xanthine may be formed, which will interfere with dissolution
Urate urocystoliths, which are usually small, round, and smooth, can be removed from the bladder by urohydropulsion during urination. However, the success of this procedure depends on the size of the uroliths, which should be smaller than the narrowest part of the urethra. Therefore, dogs with PSS should not have similar stone removal.
Since drug dissolution is ineffective, clinically active stones must be removed. surgically. If possible, stones should be removed during surgical correction PSSH. If the calculi are not removed at this point, then hypothetically it can be assumed that in the absence of hyperuricuria and a decrease in the concentration of ammonia in the urine after surgical correction of PSSh, the calculi can dissolve themselves, since they are composed of ammonium urates. More research is needed to confirm or refute this hypothesis. Also, the use of an alkaline diet low in purine may prevent the growth of existing stones or promote their dissolution after PSSh ligation.
Prevention
After PSSh ligation, ammonium urate stops precipitating if normal blood flow through the liver. However, there is a risk of ammonium urate urolith formation in animals that cannot be PSSh ligated, or where PSSh is partially ligated. For these animals, constant monitoring of the composition of the urine is needed to prevent the precipitation of ammonium urate crystals. With crystalluria, additional preventive measures must be taken. Post-feeding monitoring of plasma ammonia concentration can detect an increase despite the absence of clinical symptoms. Measurement of serum uric acid concentration also reveals its increase. Consequently, the concentration of ammonia and uric acid in the urine of these animals will also be elevated, which increases the risk of ammonium urate uroliths. In a study at the University of Minnesota, 4 dogs with inoperable PSS were treated with an alkalizing, low purine diet. (PrescriptionDietCanineu/d, Hill'sPetProduct, TopekaKS), which led to a decrease in the saturation of urine with ammonium urates to a level below their precipitation. In addition, the symptoms of genatoencephalopathy disappeared. These dogs lived for 3 years without recurrence of ammonium urate uroliths.
If preventive measures are needed, a low-protein alkalinizing diet should be used. The use of allopurinol is not recommended for dogs with PSS.
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 stones consisting of minerals (primarily) and a small amount of organic matrix.
There are three main theories of the formation of urinary stones: 1. Theory of precipitation-crystallization; 2. Theory of matrix nucleation; 3. Theory of crystallization-inhibition. According to the first theory, the 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 in the urine of various substances that initiate the onset of urolith growth is considered as the cause of the formation of uroliths. Under the theory of crystallization-inhibition, an assumption was made about the presence or absence in the urine of factors that inhibit or provoke the formation of stones. Oversaturation of urine with salts in dogs is considered as the main cause of urolithiasis, other factors play a less significant role, but may also contribute to the pathogenesis of stone formation.
Most canine uroliths are identified in the bladder or urethra. The predominant type of urinary stones are struvite and oxalate, followed by urate, silicate, cystine 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 feeds. An important reason struvite formation in dogs is a 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 oxalate-forming urolithiasis in dogs
Oxalate urinary stones are the most common type of canine uroliths, and the incidence of urolithiasis with this type of stone has increased significantly over the past twenty years, along with a decrease in incidence with a predominance of struvites. Oxalate urinary stones are composed of calcium oxalate monohydrate or dihydrate and usually have sharp, jagged edges on the outer surface. From one to many uroliths can form, the formation of oxalates is characteristic of acidic dog urine.
Possible reasons for the increased incidence of oxalate uroliths in dogs include demographic and dietary changes in dog housing that have occurred in given period. These factors may include feeding on an acidifying diet (wide 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 stone.
A breed predisposition to urolithiasis with the formation of oxalates has been 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 is noted in castrated males of small breeds, as well. Urolithiasis against the background of the formation of oxalate stones is more often noted in middle-aged and elderly animals (average age 8-9 years).
In general, the formation of uroliths has more to do with the acid-base balance of the animal's body than with the specific pH and composition of the 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 struvite, urinary tract infection in oxalate uroliths develops as a complication of urolithiasis, and not as the root cause. Also, with the oxalate form of urolithiasis in dogs, there is a high percentage of recurrence after the extraction of stones (about 25% -48%).
Risk Factors for Canine Urolithiasis with Struvite Formation
According to some data, the percentage of struc- tural urinary stones to 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 (see above). Struvites are composed of ammonium, magnesium and phosphate ions, the shape is rounded (spherical, ellipsoidal and tetrahedral), the surface is often smooth. With struvite urolithiasis, both single uroliths and multiple ones with different diameters can be formed. Struvites in the urinary tract of dogs are most often localized in the bladder, but can also occur in the kidneys and ureter.
The vast majority of struvite urinary stones in dogs are induced by urinary tract infection (more often Staphylococcus intermedius, but may also play a role Proteus mirabilis.). The bacteria have the ability to hydrolyze urea to ammonia and carbon dioxide, which is accompanied by an increase in urine pH and contributes to the formation of struvite urinary stones. In rare cases, the urine of dogs can be supersaturated with the minerals that make up struvite, and then, urolithiasis develops without infection. Based possible causes struvite urolithiasis in dogs, even with a negative urine culture, the search for infection continues and it is preferable to culture the bladder wall and/or stone.
In urolithiasis of dogs with the formation of struvite uroliths, a breed predisposition has been noted in such representatives as the Miniature Schnauzer, Bichon Frise, Cocker Spaniel, Shih Tzu, Miniature Poodle and Lhasa Apso. An age predisposition was noted in middle-aged animals, a sexual predisposition in females (presumably due to an increased incidence of urinary tract infection). The American Cocker Spaniel may have a predisposition to form sterile struvites.
Risk Factors for the Development of Urolithiasis in Dogs with Urate Formation
Urate urinary stones make up 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 (may be green). Urate stones usually crumble easily, concentric layering is determined on the fault. In urate urolithiasis, a certain predisposition to urolithiasis in male dogs has been noted, presumably due to the smaller lumen of the urethra. Also, in urolithiasis of dogs with the formation of urates, a high percentage of relapses after the 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 have the formation of urates, despite the congenital elevated level uric acid in the urine of an animal, a clinically significant disease is determined in animals in 26% -34% of cases. Some other breeds (English Bulldog and Black Russian Terrier) may also have a hereditary predisposition to impaired purine metabolism (similar to Dalmatians) and a tendency to urate urolithiasis.
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 disorders of the liver, a mixed form of urolithiasis is more often noted, in addition to urates, struvites are also formed. Breed predisposition to the formation of this type of urolithiasis was noted in breeds predisposed to the formation (ex. Yorkshire terrier, miniature schnauzer, Pekingese).
Risk factors for the development of urolithiasis in dogs with the formation of silicate stones
Silicate uroliths are also rare and cause urolithiasis in dogs (about 6.6% of total urinary stones), they are mostly silica (quartz) and 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 fed a diet high in gluten grains (gluten) or soy skins. The recurrence rate after stone removal is quite low. As with oxalate urolithiasis, urinary tract infection is considered to be a complicating rather than a causal factor in the disease.
Risk Factors for the Development of Cystine Urolithiasis in Dogs
Cystine uroliths are rare in dogs (about 1.3% of the total number of urinary stones), consist entirely 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 as 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. In cystine urolithiasis in dogs, an exceptional sexual predisposition has been noted in males, with the exception of the Newfoundland. The average age of onset of the disease is 4-6 years. When extracting stones, a very high percentage of relapses of their formation was noted, it is about 47%–75%. As with oxalate urolithiasis, urinary tract infection is considered to be a complicating rather than a causal factor in the disease.
Risk factors for the development of urolithiasis in dogs with the formation of hydroxyapatite (calcium phosphate)
This type of urolith is extremely rare in dogs, and apatite (calcium phosphate or calcium hydroxyl phosphate) often appears as a component of other urinary stones (usually struvite). Alkaline urine and hyperparathyroidism predispose to the precipitation of hydroxyapatitis in the urine. The following breeds have a predisposition to the formation of urinary stones of this type - Miniature Schnauzer, Bichon Frise, Shih Tzu and Yorkshire Terrier.
Clinical signs
Struvite urinary stones are more commonly found in females due to their increased susceptibility to urinary tract infection, 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 dogs. Urinary stones in dogs under 1 year of age are most often struvite and develop due to 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 Miniature Schnauzer, Shih Tzu, Pomeranian, Yorkshire Terrier and Maltese. Also, oxalate urolithiasis in dogs occurs at an older age compared to the struvite type of urolithiasis. Urates are more likely to form in Dalmatians and English Bulldogs, as well as 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. Breed, sex and age predispositions for the formation of urinary stones in dogs.
|
Type of stones |
Incidence |
|
Struvites |
Breed Predisposition - Miniature Schnatsuer, Bichon Frize, Cocker Spaniel, Shih Tzu, Miniature Poodle, Lhasa Apso. Sexual predisposition in females Age predisposition - average age The main predisposing factor for the development of struvite is an infection of the urinary tract with urease-producing bacteria (eg. Proteus, Staphylococcus). |
|
Oxalates |
Breed Predisposition – Miniature Schnauzer, Shih Tzu, Pomeranian, Yorkshire Terrier, Maltese, Lhasa Apso, Bichon Frise, Cairn Terrier, Miniature Poodle Sexual predisposition - in castrated males more often than in non-castrated. Age predisposition - middle and old age. One of the predisposing factors is obesity. |
|
Breed Predisposition - Dalmatian and English Bulldog The main factor predisposing to the development of urates is a portosystemic shunt, and, accordingly, is more common in predisposed breeds (ex. Yorkshire terrier, miniature schnauzer, Pekingese) |
|
|
silicates |
Breed predisposition - German Shepherd, old english sheepdog Sex and age predisposition - middle-aged males |
|
Breed Predisposition - Dachshund, Basset Hound, English Bulldog, Newfoundland, Chihuahua, Miniature Pinscher, Welsh Corgi, Mastiff, Australian Cow Dog Sex and age predisposition - middle-aged males |
|
|
calcium phosphate |
Breed Predisposition - Yorkshire Terrier |
The clinical history of canine urolithiasis depends on the specific location of the stone, how long it has been present, various complications, and conditions predisposing to stone development (eg).
When a urinary stone is found in the kidneys, animals are characterized by a long asymptomatic course of urolithiasis, blood in the urine (hematuria) and signs of pain in the kidney area may be noted. With the development of pyelonephritis in an animal, fever, polydipsia / polyuria and general depression may be noted. Ureteric stones in dogs are diagnosed quite rarely, dogs may have various signs pain in the lumbar region, most animals more often develop unilateral lesions without systemic involvement, and the stone can be detected as an incidental finding against the background of hydronephrosis of the kidney.
Canine bladder stones represent the vast majority of cases of canine urolithiasis, owner complaints on presentation may be signs of difficulty and frequent urination, sometimes with hematuria. The displacement of stones into the urethra in male dogs 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, complete obstruction of the outflow of urine may develop complete break bladder with signs of uroabdomen. It should be remembered that urinary tract stones in dogs may be asymptomatic and are found as an incidental finding on plain radiography.
Physical examination data for urolithiasis sin with a weak specificity of signs. With unilateral hydronephrosis in dogs, an enlarged kidney (renomegaly) may be detected during a palpation examination. With obstruction of the ureters or urethra, pain in the abdominal cavity can be determined, with a rupture of the urinary tract, signs of the uroabdomen and general oppression develop. Bladder stones during physical examination can be detected only if they are a significant number or volume, crepitus sounds can be determined by palpation or a significant urolith can be felt. With obstruction of the urethra, palpation of the abdomen can reveal an enlarged bladder, rectal palpation can reveal a stone localized in the pelvic part of the urethra, with localization of the 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 doctor veterinary clinic may reveal mechanical resistance to catheter travel.
The most radiopaque urinary stones are calcium-containing uroliths (calcium oxalates and calcium phosphates), struvites are also well defined on plain radiographic examination. The size and number of radiopaque stones is best determined by x-ray examination. Double contrast cystography and/or retrograde urethrography can be used to identify radiolucent stones. Ultrasound diagnostic methods are able to identify radiolucent stones in the ureter of the bladder and urethra, in addition - ultrasound can help in the evaluation of the kidneys and ureter of the animal. When examining a dog with urolithiasis, a combination of radiographic and ultrasonic methods studies, 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 general analysis blood, biochemical profile of the animal, urinalysis and urine culture. In canine urolithiasis, even in the absence of overt pyuia, hematuria, and proteinuria, there is still a high chance of urinary tract infection and it is preferable to use additional methods research (ex. cytological examination urine, urine culture). Biochemical research blood can detect signs of liver failure (ex. high level blood urea nitrogen, hypoalbuminemia) in dogs with .
Diagnosis and differential diagnosis
Urinary stones should be suspected in all dogs with evidence of urinary tract infection (eg, hematuria, stranguria, pollakiuria, urinary outflow obstruction). List differential diagnoses includes any form of bladder inflammation, urinary tract neoplasms, and granulomatous inflammation. Detection of uroliths as such is carried out by means of visual methods of examination (radiography, ultrasound), in rare cases, identification of urolith is possible only intraoperatively. Determination of a specific type of urolith requires its study in a specialized veterinary laboratory.
It should be remembered that the identification of most crystals in the urine does not always indicate pathology (with the exception of cystine crystals), in many dogs with urolithiasis, the type of crystals found in the urine may differ in composition from the urinary stone, crystals may not be detected at all, or multiple crystals may be determined without the risk of urinary stones.
Treatment
Finding urinary stones in the urinary tract of dogs is not always associated with development clinical signs, in many cases, the presence of uroliths is not accompanied by any symptoms from the animal. In the presence of uroliths, there may be several scenarios for the development of events: their asymptomatic presence; evacuation of small uroliths into the spring environment through the urethra; spontaneous dissolution of urinary stones; stop growth or its continuation; accession of a secondary urinary tract infection (); partial or complete obstruction of the ureter or urethra (if the ureter is blocked, unilateral hydronephrosis may develop); 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 an emergency, and if it develops, a number of conservative measures can be taken to move 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 method can return the urinary stone 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, descending urohydropopulsion can be used, when a sterile saline solution is injected into the bladder of an anesthetized animal, followed by manual emptying in an attempt to bring the stones down (the procedure can be performed several times).
Once the stone has been displaced into the bladder, it can be removed by cytostomy, endoscopic laser lithotripsy, endoscopic basket retrieval, 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 necessary equipment and the qualifications of the veterinarian. If it is impossible to move the stone from the urethra, in males, urethrotomy can be used, followed by removal of the stone.
Indications for surgical treatment of urolithiasis in dogs are such indicators as obstruction of the urethra and ureter; multiple recurrent episodes of urolithiasis; lack of effect from attempts at conservative dissolution of stones within 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 extracorporeal shock wave lithotripsy. If urinary stones are found in the ureters and localized in the proximal areas, ureteretomy can be used; if localized in the distal sections, resection of the ureter can be used, followed by the creation of a new connection with the bladder (ureteroneocystostomy).
Indications for conservative treatment of urolithiasis in dogs are the presence of soluble uroliths (struvites, urates, cystines and possibly xanthines) as well as animals with comorbidities increasing operational risk. Regardless of the composition of the urolith, general measures are taken in the form of increased water intake (hence increased urine output), treatment of any underlying diseases (eg Cushing's disease) and 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 supporting mechanism. The effectiveness of the conservative dissolution of urinary stones in dogs is usually monitored by visual examination methods (usually radiographically).
In struvite urolithiasis, the main cause of 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 the sterile form of struvite urolithiasis in dogs, 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 the stones may not be necessary, and regression of stones occurs only with appropriate antibiotic therapy and increased water intake.
In dogs with urate urolithiasis, allopurinol at a dose of 10-15 mg/kg PO x 2 times a day can be used in an attempt to conservatively dissolve stones, as well as urine alkalinization through dietary changes. The efficiency of conservative dissolution of urates is less than 50% and takes an average of 4 weeks. It should be remembered that significant reason urate formation in dogs is, and the dissolution of stones can be noted only after the surgical resolution of this problem.
In cystine uroliths in dogs, 2-mercatopropionol glycine (2-MPG) 15-20mg/kg PO x 2 times daily and feeding an alkalizing, low-protein diet may be used in an attempt to conservatively treat urolithiasis. The dissolution of cystine stones in dogs takes about 4-12 weeks.
Xanthine uroliths are treated with reduced allopurinol and a low purine diet and are likely to regress. With oxalate uroliths, there are no proven methods for their dissolution and it is considered that they are not subject to reverse development despite all the measures taken.
Valery Shubin, veterinarian, Balakovo
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 that reflect the state of protein, carbohydrate, lipid and mineral metabolism, as well as the activity of some key blood serum enzymes.
For research, blood is taken strictly on an empty stomach in a test tube with a coagulation activator, blood serum is examined.
- General biochemical parameters.
total protein.
Total protein is the total concentration of all blood proteins. Exist various classifications plasma proteins. They are most commonly divided into albumin, globulins (all other plasma proteins), and fibrinogen. Concentration total protein and albumin is determined using biochemical analysis, and the concentration of globulins by subtracting the concentration of albumin from the total protein.
Boost:
- dehydration,
- inflammatory processes
- tissue damage
- diseases accompanied by activation of the immune system (autoimmune and allergic diseases, chronic infections, etc.),
- pregnancy.
A false increase in protein can occur with lipemia (chylosis), hyperbilirubinemia, significant hemoglobinemia (hemolysis).
Downgrade:
- hyperhydration,
- bleeding
– nephropathy
- enteropathy,
- strong exudation
- ascites, pleurisy,
- lack of protein in food,
- long-term chronic diseases characterized by depletion of the immune system (infections, neoplasms),
- treatment with cytostatics, immunosuppressants, glucocorticosteroids, etc.
During bleeding, the concentration of albumin and globulins falls in parallel, however, in some disorders accompanied by loss of protein, the content of albumin decreases mainly, since the size of its molecules is smaller compared to other plasma proteins.
Normal value
Dog 55-75 g/l
Cat 54-79 g/l
Albumen
Homogeneous plasma protein containing a small amount of carbohydrates. An important biological function of albumin in plasma is to maintain intravascular colloid osmotic pressure, thereby preventing the release of plasma from the capillaries. Therefore, a significant decrease in the level of albumin 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.
Boost:
- dehydration
Disorders that would be accompanied by an increase in albumin synthesis are not known.
Downgrade:
- hyperhydration;
- bleeding
- nephropathy and enteropathy,
- severe exudation (for example, burns);
— chronic insufficiency liver,
- 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" red blood cells. Dead "old" erythrocytes are destroyed by reticuloendothelial cells. When heme is oxidized, biliverdin is formed, which is metabolized to bilirubin. The remainder of circulating bilirubin (about 20%) is formed from other sources (destruction of mature erythrocytes in bone marrow containing heme, muscle myoglobin, enzymes). The bilirubin formed in this way 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 glucuronyltransferases. Associated bilirubin includes bilirubin monoglucuronide, which is predominant in the liver, and bilirubin diglucuronide, which is predominant in bile. Bound bilirubin is transported to the bile capillaries, from where it enters the bile ducts 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 being 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. Level up direct bilirubin in blood serum is associated with reduced excretion of conjugated pigment from the liver and biliary tract and manifests itself as 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 the urine, the presence of bilirubin in the urine highlights the increase in serum levels of conjugated bilirubin.
indirect bilirubin
The serum concentration of unconjugated bilirubin is determined by the rate at which newly synthesized bilirubin enters the blood plasma and the rate of elimination of bilirubin by the liver (hepatic clearance of bilirubin).
Indirect bilirubin is calculated by calculation:
indirect bilirubin = total bilirubin - direct bilirubin.
Raise
- accelerated destruction of red blood cells (hemolytic jaundice),
- hepatocellular disease (hepatic and extrahepatic origin).
Chilez can cause a falsely high bilirubin value, which should be considered if a high bilirubin level is determined in a patient in the absence of jaundice. "Chileous" blood serum acquires White color, which is associated with an increased concentration of chylomicrons and / or very low density lipoproteins. Most often, chylosis is the result of a recent meal, but in dogs it can be caused by diseases such as diabetes, pancreatitis, hypothyroidism.
downgrade
Has no clinical significance.
Normal value:
Bilirubin total
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 the 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 impaired by infectious factors (for example, viral hepatitis) or toxic, this leads to an increase in the permeability of cell membranes with the passage of cytoplasmic components into the serum (cytolysis). ALT is an indicator of cytolysis, the most studied and the most indicative even for detecting minimal liver lesions. ALT is more specific for liver disorders than AST. Absolute ALT values still do not directly correlate with the severity of liver damage and with the prognosis of development pathological process, and therefore the most appropriate are serial determinations of ALT over time.
Enhanced:
- liver damage
- use of hepatotoxic drugs
Downgraded:
- pyridoxine deficiency
- repeated hemodialysis
- sometimes during pregnancy
Normal value:
Dog 10-58 units/l
Cat 18-79 u/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 isoenzymes are found both in the cytosol and in mitochondria.
Enhanced:
– Toxic and viral hepatitis
- Necrosis of liver tissue
- Acute myocardial infarction
– Administration of opioids to patients with medical conditions biliary tract
An increase and a rapid decrease suggest obstruction of the extrahepatic biliary tract.
Downgraded:
– Azotemia
Normal value:
Dog - 8-42 units / l
Cat - 9-45 units / l
An increase in ALT greater than an increase in AST is indicative of liver damage; if the AST index rises more than the ALT rises, then this, as a rule, indicates problems with myocardial cells (heart muscle).
γ - glutamyl transferase (GGT)
GGT is an enzyme localized on the cell membrane of various tissues, catalyzing the 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 high secretory and absorptive capacity: hepatic tubules, biliary tract epithelium, nephron tubules, villus epithelium small intestine, pancreatic exocrine cells.
Since GGT is associated with epithelial cells of the system bile ducts, she has diagnostic value with impaired liver function.
Enhanced:
- cholelithiasis
- in dogs with an increase in the concentration of glucocorticosteroids
- hyperthyroidism
hepatitis of extra- or intrahepatic origin, liver neoplasia,
- acute pancreatitis, pancreatic cancer
- exacerbation of chronic glomerulonephritis and pyelonephritis,
Downgraded:
Normal value
Dog 0-8 u/l
Cat 0-8 u/l
Unlike ALT, which is contained in the cytosol of hepatocytes and therefore is a sensitive marker of cell integrity disturbance, GGT is found exclusively in mitochondria and is released only when tissue is significantly damaged. Unlike humans, anticonvulsant drugs used in dogs do not cause an increase in GGT activity or it is minimal. In cats with liver lipidosis, ALP activity increases in more than GGT. Colostrum and breast milk in early dates feeding contain high activity GGT, therefore, in newborns, the level of GGT is increased.
Alkaline phosphatase.
This enzyme is found mainly in the liver (bile tubules and bile duct epithelium), renal tubules, small intestine, bones, and placenta. This is an enzyme associated with the cell membrane that catalyzes the alkaline hydrolysis of a wide variety of substances, during which the phosphoric acid residue is cleaved from its organic compounds.
The total activity of alkaline phosphatase in the circulating blood of healthy animals consists of the activity of liver and bone isoenzymes. The proportion of activity of bone isoenzymes is highest in growing animals, while in adults their activity may increase with bone tumors.
Boost:
- violation of the flow of bile (cholestatic hepatobiliary disease),
- nodular hyperplasia of the liver (develops with aging),
- cholestasis,
- increased activity of osteoblasts (in young age),
– diseases 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.
Downgrade:
- hypothyroidism,
- hypovitaminosis C.
Normal value
Dog 10-70 units/l
Cat 0-55 u/l
alpha-amylase
Amylase is a hydrolytic enzyme involved in the breakdown of carbohydrates. Amylase is formed in salivary glands and pancreas, then enters the oral cavity or lumen duodenum respectively. Significantly lower amylase activity is also possessed by such organs as the ovaries, fallopian tubes, small and large intestines, and liver. 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 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 the serum increases, and normal amylase activity is observed in the urine.
Enhanced:
- Pancreatitis (acute, chronic, reactive).
- Neoplasms of the pancreas.
- Blockage of the pancreatic duct (tumor, stone, adhesions).
- Acute peritonitis.
- Diabetes mellitus (ketoacidosis).
- Diseases of the biliary tract (cholelithiasis, cholecystitis).
- Kidney failure.
- Traumatic lesions of the abdominal cavity.
Downgraded:
- Acute and chronic hepatitis.
- Pancreatic necrosis.
- Thyrotoxicosis.
- Myocardial infarction.
Normal values:
Dog - 300-1500 units / l
Cat - 500-1200 units / l
pancreatic amylase.
Amylase is an enzyme that catalyzes the breakdown (hydrolysis) of complex carbohydrates (starch, glycogen, and some others) to disaccharides and oligosaccharides (maltose, glucose). In animals, a significant part of the amylase activity is due to the mucosa. small intestine and other extrapancreatic sources. With the participation of amylase in the small intestine, the process of digestion of carbohydrates is completed. A variety of disturbances in the processes in the acinar cells of the exocrine pancreas, increased permeability of the pancreatic duct and premature activation of enzymes lead to "leakage" of enzymes inside the organ.
Boost:
- heavy inflammatory diseases intestines (perforation of the small intestine, volvulus),
- long-term treatment with glucocorticosteroids.
downgrade :
- inflammation,
Necrosis or tumor of the pancreas.
Normal value
Dog 243.6-866.2 units/l
Cat 150.0-503.5 units/l
Glucose.
Glucose is the main source of energy in the body. As part of carbohydrates, glucose enters the body with food and is absorbed into the blood from the jejunum. It can also be synthesized by the body mainly in the liver and kidneys from non-carbohydrate components. All organs have a need for glucose, but especially a lot of glucose is used by brain tissues and red blood cells. The liver regulates blood glucose levels through glycogenesis, glycolysis, and gluconeogenesis. In the liver and muscles, glucose is stored in the form of glycogen, which is used to maintain the physiological concentration of glucose in the blood, especially in the intervals between meals. Glucose is the only source of energy for skeletal muscle work under anaerobic conditions. The main hormones that affect glucose homeostasis are insulin and the deregulating hormones glucagon, catecholamines, and cortisol.
Boost:
insulin deficiency or tissue resistance to insulin,
pituitary tumors (found in cats),
- acute pancreatitis,
- kidney failure
- receiving some medicines(glucocorticosteroids, thiazide diuretics, intravenous administration of liquids containing glucose, progestins, etc.),
- severe hypothermia.
Short-term hyperglycemia is possible with head injuries and CNS lesions.
Downgrade:
- tumor of the pancreas (insulinoma),
- hypofunction of the endocrine organs (hypocorticism);
- cirrhosis of the liver;
- prolonged fasting and anorexia;
- congenital portosystemic shunts;
- idiopathic juvenile hypoglycemia in dogs of small and hunting breeds,
- an overdose of insulin,
- 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. The glucose content in uncentrifuged blood decreases by approximately 10% per hour.
Normal value
Dog 4.3-7.3 mmol/l
Cat 3.3-6.3 mmol/l
Creatinine
Creatine is synthesized in the liver, and after release enters the 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 needed for metabolic processes, phosphocreatine is broken down to creatinine. Creatinine is a persistent nitrogenous component of the blood, independent of most food products, loads or other biological constants, and is related to muscle metabolism.
Impaired renal function reduces creatinine excretion, causing an increase in serum creatinine. Thus, creatinine concentrations approximately characterize the level glomerular filtration. The main value of determining serum creatinine is the diagnosis of renal failure.
Serum creatinine is a more specific and more sensitive indicator of kidney function than urea.
Boost:
- acute or chronic renal failure.
Due to prerenal causes that cause a decrease in glomerular filtration rate (dehydration, cardiovascular disease, septic and traumatic shock, hypovolemia, etc.), renal associated with severe diseases of the kidney parenchyma (pyelonephritis, leptospirosis, poisoning, neoplasia, congenital disorders, trauma, ischemia) and postrenal - obstructive disorders that prevent the release of creatinine in the urine (obstruction of the urethra, ureter or rupture of the urinary ways).
downgrade :
- age-related decrease in muscle mass.
Normal value
Dog 26-130 µmol/l
Cat 70-165 µmol/l
Urea
Urea is formed as a result of the catabolism of amino acids from ammonia. Ammonia formed from amino acids is toxic and is converted by liver enzymes into non-toxic urea. The main part of the urea entering after that in circulatory system 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 diuretics), the lower the level of urea in the blood.
Boost:
- renal failure (may be due to prerenal, renal and postrenal disorders).
downgrade
- low intake of protein in the body,
- liver diseases.
Normal value
Dog 3.5-9.2 mmol/l
Cat 5.4-12.1 mmol/l
Uric acid
Uric acid is the end product of purine catabolism.
Uric acid is absorbed in the intestine, circulates in the blood as ionized urate, and is excreted in the urine. In most mammals, elimination is carried out by the liver. Hepatocytes oxidize uric acid with the help of urease to form water-soluble allantoin, which is excreted by the kidneys. The decrease in uric acid metabolism combined with the decrease in ammonia metabolism in portosystemic shunting leads to the formation of urate crystals with the formation of urate stones (urolithiasis).
In portosystemic shunting (PSSh), uric acid generated from purine metabolism practically does not pass through the liver, as PSShs represent a direct vascular connection from the portal vein to the systemic circulation, bypassing the liver.
The predisposition of dogs with PSS to urate urolithiasis is associated with concomitant hyperuricemia, hyperammonemia, hyperuricuria, and hyperammoniuria. Since uric acid does not reach the liver in PSS, it is not completely converted to allantoin, which leads to an abnormal increase in serum uric acid concentration. At the same time, 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 the urine is partly determined by its concentration in the serum.
Dalmatian dogs are predisposed to the formation of urate crystals due to a particular metabolic disorder of the liver, leading to incomplete oxidation of uric acid.
Raise
- uric acid diathesis
- leukemia, lymphoma
anemia caused by vitamin B12 deficiency
- some acute infections (pneumonia, tuberculosis)
- diseases of the liver and biliary tract
- diabetes
- kidney disease
- acidosis
Downgrade:
- diet, poor 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 catalyzes 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.
Raise :
- 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 levels characterizes lipid status and metabolic disorders.
Cholesterol (cholesterol) is a secondary monohydric alcohol. Free cholesterol is a component of cellular plasma membranes. Its esters predominate in blood serum. Cholesterol is a precursor of sex hormones, corticosteroids, bile acids and vitamin D. Most 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 decrease and androgens increase total cholesterol levels.
Enhanced:
- hyperlipoproteinemia
- obstruction of the biliary tract: cholestasis, biliary cirrhosis;
- nephrosis;
- diseases of the pancreas;
- hypothyroidism, diabetes mellitus;
- obesity.
Downgraded:
- severe hepatocellular damage;
- hyperthyroidism;
- myeloproliferative diseases;
- steatorrhea with malabsorption;
- starvation;
- chronic anemia (megaloblastic / sideroblastic);
- Inflammation, infection.
Normal value:
Dog - 3.8-7.0 mmol / l
Cat - 1.6-3.9 mmol / l
Creatine phosphokinase (CPK)
Creatine phosphokinase is an enzyme in the cytoplasm of skeletal muscle and myocardial cells that catalyzes the reversible reaction of the conversion of creatine phosphate to creatinine in the presence of ADP, which is then converted to ATP, which is the energy source for muscle contraction.
The active form of CPK is a dimer consisting of subunits M and B, respectively, there are 3 isoenzymes of CPK: BB (contained in the brain), MB (in the myocardium), and MM (in skeletal muscles and myocardium). The degree of increase depends on the nature of the damage and the initial level of the enzyme in the tissue. In cats, the content of CPK in tissues is relatively lower than in animals of other species, so they should pay attention to even a slight excess of the upper limit of the standard range.
Often in anorexic cats, CPK levels may rise and fall several days after an appropriate maintenance diet.
Raise
- damage to skeletal muscles (trauma, surgery, muscular dystrophy, 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, the level decreases by 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.
Downgrade:
- decrease in muscle mass
Normal value
Dog 32-220 units/l
Cat 150-350 units/l
Lactate dehydrogenase LDH
Cytosolic enzyme catalyzing the reversible conversion of lactate to pyruvate with the participation of NADH during glycolysis. With a full supply of oxygen, lactate in the blood does not accumulate, 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 present 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 activity of the enzyme is high in tissues, even relatively small tissue damage or mild hemolysis leads to a significant increase in LDH activity in the circulating blood. It follows from this that any diseases accompanied by the destruction of cells that contain LDH isoenzymes are accompanied by an increase in its activity in the blood serum.
Raise
- myocardial infarction
- damage and dystrophy of skeletal muscles,
- necrotic damage to the kidneys and liver,
- cholestatic liver diseases,
- pancreatitis,
- pneumonia,
- hemolytic anemia, etc.
downgrade
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 damage to the heart muscle and can only serve as an indicative factor for the prognosis of the disease. In general, being a non-specific laboratory marker, changes in LDH levels should only be assessed in combination with the values of other laboratory parameters (CPK, AST, etc.), as well as data from instrumental diagnostic methods. It is also important not to forget that even 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, catalyzing the breakdown 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 (pseudocholineserase) - serum, present in the liver and pancreas, muscles, heart, brain . ChE performs a protective function in the body, in particular, it prevents the inactivation of acetylcholinesterase by hydrolyzing the inhibitor of this enzyme, butyrylcholine.
Acetylcholineserase is a strictly specific enzyme that hydrolyzes acetylcholine, which takes part in the transmission of signals through the endings of nerve cells and is one of the most important neurotransmitters in the brain. With a decrease in the activity of ChE, acetylcholine accumulates, which leads first 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 severe poisoning can lead to death.
Measurement of the level of ChE in the blood serum can be useful in case of poisoning with insecticides or various toxic compounds that inhibit the enzyme (organophosphorus, phenothiazines, fluorides, various alkaloids, etc.)
Raise
- diabetes;
- mammary cancer;
- nephrosis;
- hypertension;
- obesity;
downgrade
- Liver damage (cirrhosis, liver metastases)
- muscular dystrophies, dermatomyositis
Normal value
Dog 2200-6500 U/l
Cat 2000-4000 U/l
Calcium. Ionized calcium.
Calcium is present in plasma in three forms:
1) in combination with organic and inorganic acids (a very small percentage),
2) in protein-bound form,
3) in the ionized form of Ca2+.
Total calcium includes the total concentration of all three forms. Of the total calcium, 50% is ionized calcium and 50% is bound to albumin. Physiological changes rapidly alter calcium binding. In a biochemical blood test, both the level of total calcium in the blood serum and separately the concentration of ionized calcium are measured. Ionized calcium is determined in cases where it is necessary to determine the content of calcium, regardless of the level of albumin.
Ionized Ca2+ calcium 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 are involved in the regulation of the most important physiological and biochemical processes: neuromuscular excitation, blood coagulation, secretion processes, maintenance of membrane integrity and transport through membranes, many enzymatic reactions, release of hormones and neurotransmitters, intracellular action of a number of hormones, participates in the process of bone mineralization. Thus, they ensure the functioning of the cardiovascular and neuromuscular systems. The normal course of these processes is ensured by the fact that the concentration of Ca2+ in the blood plasma is maintained within very narrow limits. Therefore, a violation of 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 blood plasma. The binding of calcium to plasma proteins depends on pH: acidosis promotes the transition of calcium to an ionized form, and alkalosis increases protein binding, i.e. reduces the concentration of Ca2+.
Calcium homeostasis involves three hormones: parathyroid (PTH), calcitriol (vitamin D), and calcitonin, which act on three organs: bones, kidneys, and intestines. All of them work on a feedback mechanism. Calcium metabolism is influenced by estrogens, corticosteroids, growth hormone, glucagon, and T4. PTH is the main physiological regulator of calcium concentration in the blood. The main signal that affects the intensity of 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 the concentration of Ca2+, while it disrupts the release of Ca2+ from the labile calcium depot in the bones. When Ca2+ falls, the reverse process occurs. PTH is secreted by the cells of the parathyroid glands and when the calcium concentration falls, PTH secretion increases. PTH stimulates calcium release from bones and Ca reabsorption in the renal tubules.
Boost:
- hyperalbuminemia
- malignant tumors
- primary hyperparathyroidism;
- hypocorticism;
- osteolytic bone lesions (ostomyelitis, myeloma);
- idiopathic hypercalcemia (cats);
Downgrade:
- hypoalbuminemia;
- alkalosis;
- primary hypoparathyroidism;
- chronic or acute renal failure;
- secondary renal hyperparathyroidism;
- pancreatitis;
- unbalanced diet, vitamin D deficiency;
- eclampsia or postpartum paresis;
- malabsorption 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, is part of hemoglobin, cytochromes and other biologically important compounds. Iron is an essential element for the formation of red blood cells, participates in the transfer of oxygen and tissue respiration. It is also involved in a number of redox reactions, the immune system, collagen synthesis. Developing erythroid cells take from 70 to 95% of the iron circulating in 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 gastric hydrochloric acid, iron oxides ingested with food pass 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 environment of the small intestine. Under normal conditions, only a small percentage of dietary iron enters the bloodstream. Iron absorption increases with its deficiency in the body, increased erythropoiesis or hypoxia and decreases with its high total content in the body. More than half of all iron is part of hemoglobin.
It is desirable to examine 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.
Enhanced:
- hemolytic anemia,
- folic deficiency hyperchromic anemia,
- liver diseases,
- administration of corticosteroids
- lead intoxication
Downgraded:
- avitaminosis 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 in extracellular fluids, present in gastric juice, pancreatic and intestinal secretions, 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 administration of chlorine, occurs with vomiting and administration of diuretics as a result of the loss of H+ and Cl- ions;
chlorine-resistant type, not corrected by the introduction of chlorine, is observed in patients with primary or secondary hyperaldosteronism.
Enhanced:
- dehydration,
- chronic hyperventilation with respiratory acidosis,
- metabolic acidosis with prolonged diarrhea,
- hyperparathyroidism,
- acidosis of the renal tubules,
- traumatic brain injury with damage to the hypothalamus,
- eclampsia.
Downgraded:
- general hyperhydration,
- intractable 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 the bones and blood. Potassium is concentrated mainly in skeletal muscles, liver and myocardium. From damaged cells, potassium is released into the blood. All potassium that enters the body with food is absorbed in the small intestine. Normally, up to 80% of potassium is excreted in the urine, and the rest in the feces. Regardless of the amount of incoming potassium from outside, it is excreted daily by the kidneys, resulting in severe hypokalemia quickly.
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 the level of potassium in the blood serum are caused by disturbances in the internal and external balance of potassium. The external balance factor is: dietary potassium intake, acid-base balance, mineralocorticoid function. The 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 indirectly by increasing the glomerular filtration rate and urinary excretion, as well as increasing sodium levels in the distal tubules.
Enhanced:
- massive muscle injury
- tumor destruction
- hemolysis, DIC,
- metabolic acidosis,
- decompensated diabetes mellitus,
- kidney failure
- prescription of non-steroidal anti-inflammatory drugs,
- prescribing K-sparing diuretics,
Downgraded:
- administration of non-potassium-sparing diuretics.
- diarrhea, vomiting,
- taking laxatives
- profuse sweating
- Severe burns.
Hypokalemia associated with decreased urinary K+ excretion, but without metabolic acidosis or alkalosis:
- parenteral therapy without additional intake of potassium,
starvation, 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 (RTA),
- diabetic ketoacidosis.
Hypokalemia associated with increased K+ excretion and normal pH (usually of renal origin):
- recovery after 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 the 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 of the intracellular space. The predominance of sodium over other cations is also preserved in other body fluids, such as gastric juice, pancreatic juice, bile, intestinal juice, sweat, CSF. Relatively large amounts of sodium are found in cartilage and slightly less in bones. The total amount of sodium in the bones increases with age, and the proportion of reserves decreases. This lobe is clinically important because it represents the reservoir for sodium loss and acidosis.
Sodium is the main component of the osmotic pressure of a liquid. All movements of sodium cause the movement of certain amounts of water. The volume of extracellular fluid is directly related to the total amount of sodium in the body. Plasma sodium concentration is identical to the interstitial fluid concentration.
Enhanced:
- the use of diuretics,
- diarrhea (in young animals)
- Cushing's syndrome
Downgraded:
A decrease in the volume of extracellular fluid is observed when:
- jade with loss of salt,
- deficiency of glucocorticoids,
- 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 the level of total sodium is observed with:
- congestive heart failure (serum sodium level is a predictor of mortality),
- nephrotic syndrome, renal failure,
- cirrhosis of the liver,
- cachexia,
- hypoproteinemia.
Normal value:
Dog - 140-154 mmol / l
Cat - 144-158 mmol / l
Phosphorus
After calcium, phosphorus is the most abundant mineral in the body, being present in every tissue.
In the cell, phosphorus mainly takes part in the metabolism of carbohydrates and fats or is associated with proteins, and only a small part is in the form of a phosphate ion. Phosphorus is part of bones and teeth, is one of the constituents of nucleic acids, phospholipids of cell membranes, is also involved in maintaining acid-base balance, in energy storage and transfer, in enzymatic processes, stimulates muscle contraction and is necessary to maintain neuron activity. The kidneys are the main regulators of phosphorus homeostasis.
Enhanced:
— Osteoporosis.
- The use of cytostatics (cytolysis of cells and the release of phosphates into the blood).
- Acute and chronic renal failure.
- Disintegration of bone tissue (with malignant tumors)
– Hypoparathyroidism,
– Acidosis
- Hypervitaminosis D.
- Portal cirrhosis.
- Healing of bone fractures (formation of bone "callus").
Downgraded:
- Osteomalacia.
- Malabsorption syndrome.
- Severe diarrhea, vomiting.
- Hyperparathyroidism primary and ectopic synthesis of hormones by malignant tumors.
- Hyperinsulinemia (in the treatment of diabetes mellitus).
- Pregnancy (physiological deficiency of phosphorus).
- Deficiency of somatotropic hormone (growth hormone).
Normal value:
Dog - 1.1-2.0 mmol / l
Cat - 1.1-2.3 mmol / l
Magnesium
Magnesium is an element that, although found in small amounts in the body, is of great importance. About 70% of the total amount of magnesium is in the bones, and the rest is distributed in soft tissues (especially in 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 the nucleus. In addition to its plastic role as a component of bones and soft tissues, Mg has many functions. Together with sodium, potassium and calcium ions, magnesium regulates neuromuscular excitability and the blood coagulation mechanism. The actions of calcium and magnesium are closely related, 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.
Magnesium deficiency leads to mobilization of calcium from the bones, so it is recommended that calcium levels be taken into account when assessing magnesium levels. From a clinical point of view, magnesium deficiency causes neuromuscular diseases (muscle weakness, tremors, tetany and convulsions), and can cause cardiac arrhythmias.
Enhanced:
- iatrogenic causes
- kidney failure
- dehydration;
- diabetic coma
- hypothyroidism;
Downgraded:
- diseases of the digestive system: malabsorption or excessive loss of fluids through the gastrointestinal tract;
- renal diseases: chronic glomerulonephritis, chronic pyelonephritis, renal tubular acidosis, diuretic phase of acute tubular necrosis,
- 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's disease of the bones
- acute and chronic pancreatitis,
- severe burns
- septic conditions,
- hypothermia.
Normal value:
Dog - 0.8-1.4 mmol / l
Cat - 0.9-1.6 mmol / l
Bile acids
Determination of the total content of bile acids (FA) in the circulating blood is a functional test of the liver due to a special process of recycling of fatty acids, called enterohepatic circulation. The main components involved in the recycling of bile acids are the hepatobiliary system, the terminal ileum, and the portal vein system.
Circulatory disorders in the portal venous system in most animals are associated with portosystemic shunting. A portsystemic shunt is an anastomosis between the veins of the gastrointestinal tract and the caudal vena cava, due to which the blood flowing from the intestine does not undergo purification in the liver, but immediately enters the body. As a result, toxic compounds for 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 stored in the gallbladder. Eating stimulates the release of cholecystokinin from the intestinal wall, which causes the gallbladder to contract. There is individual physiological variability in the amount of bile retained and in 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 close to the standard range, such physiological fluctuations can cause postprandial bile acid levels to become similar to, or even less than, fasting levels. In dogs, it can also occur when there is an overgrowth of bacteria in the small intestine.
An increase in blood bile acids secondary to liver disease or portosystemic shunting is accompanied by increased urinary excretion. In dogs and cats, determination of the urinary bile acid/creatinine ratio is a sensitive test in 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.
Enhanced:
- 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);
- end-stage cirrhosis of the liver;
- microvascular dysplasia of the liver;
- violation of the ability of hepatocytes to absorb fatty acids, characteristic of many liver diseases.
Normal value:
Dog 0-5 µmol/l
In dogs, urea is 4 - 6 mmol/liter (24 - 36 mg/dL).
In cats, urea is 6 - 12 mmol/liter (36 - 72 mg/dL).
Norms vary slightly in different laboratories.
To recalculate:
mmol/liter divided by 0.166 gives mg/dl. Multiply mg/dl by 0.166 to get mmol/litre.
Increase in renal failure
With renal failure, urea increases.
Usually, an increase to 20 mmol / liter may not be outwardly noticeable.
If urea is more than 30 mmol / liter, then appetite worsens or disappears.
With urea above 60 mmol / liter, there is usually frequent vomiting, then vomiting with blood.
Rare cases
Some animals with CRF can feel quite well and maintain their appetite even with urea 90 mmol / liter.
In our practice, there was a live animal with urea 160 mmol/liter.
Origin of urea
Approximately half of urea is formed in the liver during biochemical protein reactions. The second half is also formed in the liver, but with the neutralization of ammonia from the intestines.
During starvation, a state of hypercatabolism develops and the formation of urea as a result of metabolic processes increases.
With a delay in defecation, especially with micro or macro bleeding in the intestine, the formation of ammonia sharply increases as a result of putrefactive processes, and as a result, urea in the blood increases.
Other cases of increased urea in the blood
High protein diet.
Putrefactive processes in the intestines as a result of dysbacteriosis, lack of bile, eating non-fresh foods.
Bleeding in the stomach or intestines.
With normally functioning kidneys, in all of the above cases, urea rarely exceeds 30 mmol / liter, while creatinine remains within the normal range, and in renal failure, creatinine is also elevated.
Cases of a decrease in urea in the blood
Prolonged protein starvation.
Cirrhotic changes in the liver. In this case, ammonia from the intestine is not completely converted into urea.
Polyuria, polydipsia. Together with more fluid, more urea is removed from the body. With PN, even with polyuria, urea in the blood remains elevated.
Toxicity of urea to the body
Urea is neutralized ammonia, so urea itself is not toxic.
But very high urea increases the osmolarity of blood plasma, and this can have a harmful effect on the body.
When a lot of urea is released from the blood into the stomach, the urea turns into ammonia, which irritates the walls of the stomach and intestines and increases the ulcerative lesion of the mucous membrane.
Urea is a marker of toxicosis
In general, urea is used in analyzes as a marker of the amount of toxic metabolic products, approximately the same molecular weight.
The formation and excretion of urea are not constant values, depending on many factors, therefore, with the same numbers in the analyzes, the general condition of the animals may be different.
How to take blood tests for urea with PN
Urea tests can be done in whole blood, plasma or serum, depending on the capabilities of the instruments.
You can take blood at any time, in any condition, because with kidney failure, fluctuations in indicators decrease.
Treatment of renal failure in animals