Urinary Tract Diseases

Chapter 10 Urinary Tract Diseases


Urinary tract diseases are less common in dairy cattle than disorders of the gastrointestinal, respiratory, musculoskeletal, and other systems. For this reason and because signs of renal disease may be subtle, the urinary tract often is overlooked as a cause of illness. Evaluation of urine for abnormal constituents, urinalysis, and serum chemistry may be necessary to confirm urinary tract disease. Additionally, ultrasound examination of the kidneys and/or cystoscopic examination may be warranted in some cases. Percutaneous examination of both kidneys can be achieved easily in adult dairy cows and calves through the paralumbar fossae with a 2.5- to 5-mHz probe, and excellent images of the left kidney, ureter, and bladder can often be obtained during rectal examination using a conventional 5- or 10-mHz reproductive probe. Geographic differences in the incidence of diseases also may affect the relative frequency of urinary tract disease in cattle. Most practitioners utilize the gross appearance of urine, evaluation of abnormal urine constituents based on multiple reagent test strips, and signs found on physical examination as indicators of urinary tract disease. Vague illnesses that originate from the urinary system may require more ancillary data in the form of complete urinalysis, serum electrolytes and chemistry, and complete blood counts (CBCs) for diagnosis. Fortunately urine is obtained routinely during completion of physical examination for evaluation of urinary ketones, and this provides a sample for other routine screening processes when indicated. Abnormal urinary constituents identified by multiple reagent strips seldom are specific but give direction as to other ancillary tests to be performed. The following discussion of abnormal urinary constituents will give examples of diseases to be considered in a differential diagnosis. Although midstream samples are usually sufficient for cultures, on rare occasion it may be necessary to collect a catheterized sample. Catheterization is difficult in the cow because of the urethral diverticulum, and the technique is shown in Figure 10-1.


Because positive values for proteinuria obtained using multiple reagent test strips are relative rather than absolute, a urinalysis including sulfosalicylic acid test (SSA) or urine protein/creatinine ratio evaluation of protein is indicated before attributing much significance to these levels. For example, highly alkaline urine in ruminants may cause a false-positive protein reaction on reagent test strips (tetrabromphenol blue). An even more specific test would be to perform simultaneous protein and creatinine measurements and to calculate the urinary protein/creatinine ratio.

Proteinuria may be normal in ruminants less than 2 days of age that have ingested adequate or large amounts of colostrum. This physiologic phenomenon should correct quickly after this time, and the urine should then be negative for protein. Any insult to the renal glomeruli or tubules could lead to mild or moderate proteinuria. For example, renal infarcts secondary to severe dehydration and reduced renal perfusion could cause mild proteinuria, whereas glomerulonephritis, tubular nephrosis, amyloidosis, pyelonephritis, and other severe renal diseases would lead to more significant proteinuria with eventual hypoalbuminemia. Nonspecific inflammation or irritation of the postrenal urinary tract as found in cystitis, urolithiasis, trauma, or neoplasia also may result in proteinuria. Finally, false-positive proteinuria may occur from admixture of urine with vaginal discharges, preputial discharges, uterine discharges, or fecal material and is therefore particularly common in free-catch samples obtained from normal, healthy postparturient cattle.


Renal Ischemia

A common but often undetected problem, renal ischemia results from decreased renal perfusion with subsequent reduced glomerular filtration in dehydrated patients. Renal failure is more common when both sepsis and dehydration are concurrent. Another possible cause of ischemic renal failure is severe ruminal distention. Cattle with severe dehydration resulting from gastrointestinal obstruction or diarrhea frequently develop renal infarcts that result in some RBCs, WBCs, and protein in the urine.

Finding these abnormal constituents in urine from dehydrated patients should arouse suspicion of renal failure and alert the clinician to the need for rehydration and avoidance of nephrotoxic drugs. If renal failure is present, urine concentration is, 1.022; therefore evaluation of specific gravity is imperative to rule out renal failure. This is especially true when serum chemistry indicates azotemia in dehydrated patients. Further laboratory tests that help distinguish between prerenal and true renal azotemia should be utilized including fractional excretion of electrolytes, particularly sodium. There is considerable variation in urinary fractional excretion of sodium in normal dairy cattle according to diet, stage of lactation, and gestational status, but values for pregnant and periparturient dairy cattle rarely exceed 1%, whereas normal cows in early and peak lactation may occasionally reach 2% to 3%. Neonatal calves typically have urinary fractional sodium excretion values of, 1%. Prerenal azotemia is properly diagnosed only when a dehydrated, azotemic cow possesses the ability to concentrate urine. As in other species, renal prostaglandin levels are cytoprotective to the kidney during reduced perfusion. Therefore prostaglandin inhibitors such as nonsteroidal antiinflammatory drugs (NSAIDs) should be used in reduced dosages or not at all in severely dehydrated cattle, lest further ischemic damage with increased infarction or papillary necrosis occurs. If sepsis is present, the benefits of the NSAID would likely outweigh the negative effects on the kidneys, such as might be the case in individuals with severe gram-negative mastitis or severe metritis.

Treatment should be directed toward the primary disease and the patient rehydrated with IV fluids to improve renal perfusion, urine production, and to correct existing prerenal azotemia. Nephrotoxic drugs such as aminoglycosides, oxytetracycline, and NSAIDs should be avoided if possible. If potentially nephrotoxic drugs must be used, repeated serum creatinine values, serial urinalyses, and fractional excretion ratios should be considered to monitor renal function.

Toxic Nephrosis

Damage to the renal tubules by toxins, certain drugs, and physiologic events linked to hemoconcentration, endotoxemia, and ischemic changes may cause tubular degeneration, inflammation, and in some instances interstitial nephritis. Usually both kidneys are affected equally.


Antibiotics such as aminoglycosides, tetracycline, and sulfa drugs are known to be nephrotoxic. Neomycin, gentamicin, amikacin, and other aminoglycosides can cause renal tubular damage in cattle and other species. Tetracycline, and perhaps the vehicles used in certain injectable forms of tetracycline, may contribute to renal tubular nephrosis. Propylene glycol and polyvinylpyrrolidone vehicles are used in many oxytetracycline hydrochloride preparations, and these vehicles may cause hemodynamically mediated reduced renal perfusion, thereby accentuating any basic nephrotoxicity of the antibiotic itself. Sulfa preparations possess the ability to damage kidney tubules and precipitate in the renal tubules. Most antibiotic nephrotoxicity occurs as a result of two factors that deserve emphasis:

Overuse of calcium salts has also, on rare occasions, caused renal tubular nephrosis. In some instances, recumbent cattle received inordinate amounts of calcium solutions as therapy for suspected hypocalcemia.

Nephrosis also may result from physiologic progression of minor renal ischemia associated with septic conditions, gastrointestinal diseases, and other problems that reduce renal perfusion and glomerular filtration rate (GFR). Early manifestations of renal ischemia include renal infarcts and papillary necrosis. These conditions are much more common in dehydrated cattle than most veterinarians realize but are relatively benign if the cow’s primary disease and dehydration status are treated. When severe renal ischemia occurs, widespread reduction in renal perfusion results in further organic necrosis of tubulointerstitial renal tissue. Acute renal failure is possible in this instance and would be indicated by azotemia and isosthenuria, despite severe dehydration in the patient.

Reduced renal perfusion also is a possible result of overuse of NSAIDs in cattle. Drugs such as phenylbutazone and flunixin meglumine are potent inhibitors of prostaglandin synthesis within many tissues, including the kidney. Renal prostaglandins are “cytoprotective” because they help maintain renal perfusion through small vessels during times of hypotension or dehydration. Loss of this protective effect occurs when NSAIDs have reduced the production of renal prostaglandins. Therefore the kidneys are more susceptible to ischemic damage. Although renal papillary necrosis frequently is associated with the use of NSAIDs, minor (infarction) or major (tubular nephrosis) renal organic disease also may occur. Once again, the use of NSAIDs in dehydrated patients increases the risk of nephrotoxicity. The risk of toxicity can be further exacerbated by hypoalbuminemia such as occurs with acute gastrointestinal diseases because more of the NSAID being administered will be non–protein bound and therefore pharmacologically active drug. Therefore reduction of the dosage or total avoidance of these drugs, unless concomitant fluid therapy restores renal perfusion, should be practiced when devising therapy for a dehydrated patient.

Other nephrotoxins include the heavy metals (i.e., lead, mercury, and arsenic) and plant toxicities, such as oxalates, oak, and pigweed, that occur in some parts of the United States. Toxicities may involve several animals within a group, thus raising an index of suspicion regarding a toxic etiology. Oak poisoning most commonly affects heifers at pasture, with acorns being ingested in the fall and oak buds in the spring.


Therapy must attempt to reestablish renal function and to correct primary disorders that may have contributed to nephrosis. Previous use of nephrotoxic drugs should be discontinued and other potentially nephrotoxic drugs avoided in the therapy.

Aggressive fluid therapy to ensure adequate renal perfusion and accomplish diuresis is the primary therapeutic goal. IV fluids that are balanced to address associated electrolyte or acid-base abnormalities must be tailored to the individual patient. Because hypochloremia, hypokalemia, and hyponatremia usually are present, physiologic sodium chloride with supplemental KCl added at 20 to 40 mEq/L is frequently used. Unless the patient is anuric, large volumes of IV fluids are required to address existing dehydration, allow for anticipated fluid losses, and establish diuresis. If an adult patient is anuric or oliguric following an initial 20 to 40 L of IV fluids, 250 to 500 mg of furosemide may be administered IV one or more times at 15- to 30-minute intervals in an effort to initiate diuresis. Failure to produce urine in the face of high volume fluid therapy alongside diuretic administration should be taken as a negative prognostic sign. Repeated bladder evaluation by rectal palpation or ultrasonography to confirm urine production and accumulation may be a useful monitoring technique. Patients that are severely hypoproteinemic, produce inadequate urine despite large volume fluid administration, or show evidence of dependent edema may need additional monitoring for an increasing central venous pressure. A 500-kg cow that is azotemic, isosthenuric, and 10% dehydrated requires 50 L of fluids simply to counteract her existing dehydration. Therefore she may require a total of 80 to 100 L during the first 24 hours of therapy to establish adequate diuresis.

Judicious IV calcium or subcutaneous (SQ) calcium borogluconate should be utilized in those patients that are hypocalcemic. A low percentage of dextrose may be added to the basic fluids by adding 1 L of 50% dextrose to each 20 L of saline/KCl if desired.

Although adult cows with renal failure resulting from nephrosis seldom become hyperkalemic, calves that have acute diarrhea and metabolic acidosis may be hyperkalemic. Therefore initial fluid therapy should be formulated based on the individual patient’s acid-base and electrolyte status. Acidotic, hyperkalemic patients should receive IV saline, dextrose (half-strength physiologic saline solution [PSS] mixed equally with 2.5% dextrose), and supplemental NaHCO3. Salmonellosis patients (either calves or cows) with secondary tubular nephrosis may be acidotic and require bicarbonate therapy if balanced crystalloid administration does not correct the acidosis. Oliguric or anuric patients also may require 20 L of 10% dextrose solution in addition to furosemide to instigate osmotic diuresis. Anuria that is unresponsive to fluid diuresis and furosemide therapy may also necessitate dopamine (3 to 5 μg/kg/min) and/or dobutamine (2 to 5 μg/kg/min) in 5% dextrose if all other therapy fails. Other potential treatments include mannitol, norepinephrine, vasopressin, and aminophylline.

Once diuresis is established, fluid therapy is adjusted to maintain diuresis and assist renal excretion of wastes. Serum urea nitrogen and creatinine initially should be monitored each day to establish a trend. The length of treatment varies from a few days to 2 weeks in most cases. The prognosis is guarded until normal renal function is reestablished. The more prolonged the azotemia, the more likely the patient is to develop chronic renal failure. Initially the clinician must proceed with therapy in the hope that nephrosis is acute and reversible. The exact degree of renal damage is impossible to assess initially. Response to therapy and the results of renal biopsies, once available, afford the best means of prognosis.

If a potential nephrotoxic drug must be used to treat a primary condition, reduced dosages and monitoring of blood levels, if available, are essential to continued usage.


Infectious nephritis caused by bacterial infection of the kidney is usually an ascending infection from the lower urinary tract. Pyelonephritis is the most commonly diagnosed disease of the kidney in dairy cattle. Reported incidence in practice settings seems to far outnumber other renal diseases such as nephrosis and glomerulonephritis. This may be a true representation or merely supposed because of the relative ease of diagnosis of pyelonephritis as opposed to other conditions that require more ancillary laboratory data for diagnosis.

Clinical Signs

Acute primary pyelonephritis causes fever of 103.5 to 105.5° F (39.72 to 40.83° C), anorexia, and a precipitous decrease in milk production. Some cows with acute pyelonephritis have colic manifested by kicking at the abdomen, restlessness, and treading. Signs of colic usually are associated with renal or ureteral inflammation and pain, but urinary obstruction caused by blood clots blocking urine outflow from a kidney (ureter) or bladder (urethral) also may contribute to colic (Figure 10-4). Further agitation, such as swishing of the tail, may be observed if the affected cow also has cystitis as a precursor lesion of pyelonephritis. Stranguria, polyuria, an arched stance, gross hematuria (Figures 10-4 and 10-5), blood clots, fibrin, or pyuria also are observed in some patients with C. renale infection. Acute pyelonephritis should be considered as a differential for acute colic in postparturient cattle. Consequently left kidney and ureter palpation per rectum should be mandatory components of the physical examination of any sick cow with signs of colic.

Chronic pyelonephritis is associated with weight loss, poor hair coat, anorexia, poor production, diarrhea, polyuria, anemia, stranguria and gross urine abnormalities. Lordosis and stretching out may be apparent in some cows affected with chronic pyelonephritis because of renal pain.

Latent or subclinical pyelonephritis may exist in cattle with multiple medical problems, especially during the first few months of lactation. Cattle with concurrent abomasal displacement, metritis, mastitis, or cattle that had dystocia may develop pyelonephritis that is “masked” by more obvious signs in other systems. Only through screening urine and subsequent urinalysis will the condition be confirmed. Specific physical signs of pyelonephritis in these instances are minimal unless, on rectal palpation, the left kidney is large, painful, and has indistinct lobulations, thereby increasing the possibility of pyelonephritis.


Diagnosis of pyelonephritis is made by combining the clinical signs, rectal palpation findings, vaginal palpation findings, and urinalysis. Fever usually is present in acute pyelonephritis but may be absent in chronic pyelonephritis. Urinalysis abnormalities such as RBCs, WBCs, protein, and bacteria may be present in both cystitis and pyelonephritis. However, cystitis does not usually lead to systemic illness, and the ureters would not be enlarged (as one or both are in pyelonephritis) as determined by palpation per vagina or per rectum. Vaginal palpation remains an essential aid to diagnosis because it allows detection of unilateral or bilateral ureteral enlargement that is too subtle to be detected per rectum.

Rectal palpation may reveal enlargement of the left kidney in unilateral left kidney infection or bilateral infections. Normal lobations of the kidney may be lost; the kidney may feel “mushy”; and there may be a pronounced arterial pulsation. Rectal palpation is not helpful to diagnosis in right kidney infections unless the infection is very chronic with massive enlargement of the right kidney. Ultrasonography is another helpful ancillary aid to diagnosis and may reveal valuable prognostic information (see video clips 20 and 21).

Other laboratory tests may be performed in valuable cattle or when a diagnosis is not definitive. Hypoalbuminemia is present in most pyelonephritis patients and is more severe in chronic pyelonephritis. Proteinuria appears to be very significant in pyelonephritis and occurs in most cases. Serum globulin values may be higher (.5.0 g/dl) if infection has been chronic. Generally a period of 10 to 14 days of renal infection is necessary to elevate globulin values, and adult cattle tend to have higher globulin levels than calves with chronic infection.

Gross examination of the urine may be diagnostic in acute cases in which fibrin, blood clots, and pus are apparent in voided urine. Some cows with acute pyelonephritis will suffer severe renal hemorrhage that may obstruct the ureter or urethra, thus leading to intermittent or continuous urinary blockage. On occasion blood clots may be so substantial as to fill and occlude the bladder and urethra. Cattle with less obvious urinary abnormalities will have positive blood and protein reactions on reagent test strips, and urinalysis will confirm the presence of RBCs, WBCs, protein, and bacteria. Routine use of multiple test reagent strips to screen urine during the routine physical examination is an excellent means to detect pyelonephritis and other urinary tract diseases.

Urine culture is the most important laboratory aid because it allows identification of the causative organisms and more importantly the sensitivity of the causative organism to antibiotics. Previous treatment with antibiotics by the owner may interfere with in vitro growth. Therefore antibiotics should be discontinued for 24 to 48 hours before culture of the urine. Urine for culture should be obtained using catheterization or a midstream voided sample to avoid contamination, and a colony count should be requested. Colony counts (.103/ml on a catheterized sample or .104/ml on a midstream voided sample) are often necessary to determine the infectious organism(s).

Azotemia is cause for prognostic concern and may indicate prerenal conditions such as dehydration, bilateral pyelonephritis with subsequent renal failure, or postrenal urinary obstruction. Postrenal obstruction usually is obvious following the physical examination and rectal examination. Prerenal azotemia should be suspected if the animal is very dehydrated but is capable of concentrating urine to a specific gravity .1.022. Prerenal azotemia also should respond to rehydration using oral or IV fluids. Most cattle with pyelonephritis that also are azotemic have bilateral disease and renal failure (Figure 10-6). These usually are chronic infections and also have elevated globulin levels, hypoalbuminemia, inability to concentrate urine, and may have electrolyte abnormalities such as hypochloremia, hyponatremia, hypokalemia, and hypocalcemia. Therefore cattle with bilateral pyelonephritis and azotemia have a guarded prognosis.

Apr 26, 2017 | Posted by in GENERAL | Comments Off on Urinary Tract Diseases
Premium Wordpress Themes by UFO Themes