Diseases of the equine urinary tract
8.1 Evaluation of the urinary system
8.3 Acute renal failure due to renal disease
8.4 Chronic renal failure (CRF)
8.8 Patent and persistent urachus
8.10 Polyuria/polydypsia (PUIPD)
8.11 Diagnosis of diseases of the testis and associated structures
8.15 Inguinal herniation and rupture
8.16 Torsion of the spermatic cord
8.19 Diagnosis of diseases of the penis and prepuce
8.20 Penile and preputial injuries
8.25 Cutaneous habronemiasis (or ‘summer sore’)
8.27 Diagnosis of diseases of the female reproductive tract
8.29 Perineal lacerations and fistulae
8.1 Evaluation of the urinary system
Renal function and water balance in the normal horse
• Water intake: varies greatly depending upon diet, ambient temperature, exercise, lactation, and psychogenic factors. Range: 4 to 6% of body weight daily.
• Urination frequency: 7–11 times daily (foals urinate hourly and usually upon standing).
• Urine volume: 1–3% body weight daily.
• Urine character: pale yellow to brown (may darken upon standing); viscid due to mucus-secreting cells in the renal pelvis; often opaque due to suspension of calcium carbonate crystals. Horses fed legume hay form large amounts of calcium carbonate crystals and thus tend to have more opaque urine than horses fed grass or hay.
Physical examination
Only the caudal pole of the left kidney can be palpated per rectum. Evaluation is highly subjective, but:
Ultrasonographic examination
• Equipment: 3.0–3.5 Mhz transducer for percutaneous examination (5.0 Mhz for foals); 5.0–7.5 Mhz transducer for examination per rectum.
• Location: level of tuber coxae and 15th to 17th intercostal space for right kidney and paralumbar fossa for left kidney.
Distinguishing acute and chronic renal disease. Acute – swollen kidney with decreased echogenicity. Chronic – small, irregular kidney with increased echogenicity. A kidney should be considered to be abnormally small when it measures less than 10 cm.
Diagnosis of renal cysts, urinary calculi, urinary neoplasia, uroperitoneum, etc.
Endoscopic examination
Useful in diagnosis of cystitis, urinary calculi, sources of haematuria, etc. For male horses, a 100 cm, or longer, endoscope with an outside diameter no greater than 12 mm is used. Polyethylene tubing can be passed through the accessory chamber of the endoscope into a ureter for collection of urine (Figure 8.1).
Percutaneous renal biopsy
Usually Vim-Silverman-type or Tru-Cut-type biopsy needles are used.
• Ultrasonically guided – the kidney is located ultrasonographically and the depth for needle penetration is measured, usually 3 cm and 7 cm for the right and left kidney, respectively.
• Assistant-guided – the left kidney is grasped per rectum by an assistant who can feel the needle contact the kidney.
Serious haemorrhage can result, but in general, biopsy is a safe procedure. Biopsy is of most value for assessment of suspected chronic renal failure. There is often poor correlation between severity of histological lesions and severity of renal dysfunction in acute ischaemic renal disease.
Laboratory assessment of urinary tract disease
• Serum urea nitrogen (SUN) (also known as blood urea nitrogen, BUN) – concentration rises when glomerular filtration rate (GFR) decreases. Not a reliable indicator of GFR because it is affected by non-renal factors. Anorexia and liver disease decrease concentration of SUN; increased protein intake increases concentration of SUN.
• Serum creatinine – concentration rises when GFR decreases. Production (from muscle) is fairly constant. Not significantly absorbed or secreted by renal tubules. Therefore, creatinine concentration approximates GFR. Azotaemia (elevated concentration of SUN and/or creatinine) is not necessarily indicative of renal disease or the severity of renal disease.
• Creatinine clearance – a reliable index of GFR in horses – determined by comparing creatinine concentrations in serum (Scr) and urine (Ucr) and the rate of urine production. Clearance cr = Ucr/Scr × mL/min/kg body wt. Reference range is 1.39 to 1.87 mL/min/kg. Concentrations below the reference range indicate decreased GFR.
Tendency toward hyponatraemia, hypochloraemia, and hyperkalaemia in renal failure. Degree of abnormality, if any, depends upon diet, appetite, and duration of renal failure.
Hypo, normo, or hypercalcaemia can occur in renal failure – depends upon diet, appetite, duration of failure, and age of the horse. Hypercalcaemia in renal failure is unique to the horse and is not understood.
Hypo, normo, or hyperphosphataemia can be seen in equine renal failure.
• Fractional excretion (clearance) of electrolytes – in renal tubular disease, electrolytes may be inappropriately excreted in urine. Because the clearance of creatinine is constant over time, the excretion of electrolytes can be compared to the excretion of creatinine. The formula for determining fractional excretion of an electrolyte (FEe) is:
in which U = urine, S = serum, cr = creatinine, e = electrolyte.
Values greater than reference range indicate increased loss of electrolyte in urine, and may reflect inability of renal tubular cells to reabsorb that electrolyte.
FEsodium is normally ≤ 1%; > 3% indicates abnormal renal excretion.
FEphosphorus is normally ≤ 1%; increases occur not only in renal disease but also in primary or pseudohyperparathyroidism and secondary nutritional hyperparathyroidism.
• Urine to plasma or serum ratios for urea nitrogen (un), creatinine (cr) and osmolality (osm). Useful in distinguishing between renal and prerenal azotaemia, but measurements for renal and prerenal azotaemia may overlap. Based on a small number of azotaemic horses, reported measurements are:
• Urinary enzymology. When renal tubular cells die, enzymes contained within these cells are released into the urine. Abnormally high concentrations of gamma glutamyltranspeptidase (GGT) indicate renal tubular damage. Comparison of UGGT concentration to Ucr concentration corrects for the effect of urine concentration on enzyme concentration.
Elevation indicates that tubular necrosis is occurring. Urinary concentrations of GGT are unaffected by serum concentrations of GGT. Concentration of UGGT is useful in monitoring for aminoglycoside-induced renal tubular necrosis.
• Urinary specific gravity (USG) tends to be between 1.030 and 1.060, but fluctuates widely. Random urine samples may indicate hyposthenuria (USG <1.008), isosthenuria (USG 1.008–1.014) or hypersthenuria (USG >1.015). Foals tend to be hyposthenuric because they have a large fluid intake. Possible explanations for dilute urine in the adult horse are:
A water-deprivation test may distinguish between these causes if the cause is not obvious. For the water-deprivation test, the horse is weighed and held off water for 24 hours, or until it has a 5% weight loss, develops azotaemia or signs of dehydration or a USG >1.020. USG in the isosthenuric range (1.008–1.014) in a dehydrated horse suggests renal disease. The test should not be performed on horses that are azotaemic or dehydrated.
*USG <1.020 in horses with clinical dehydration and/or azotaemia is highly suggestive of renal disease. Azotaemia associated with USG >1.030 indicates prerenal azotaemia.
A modified water-deprivation test is indicated if a horse fails to concentrate urine to SG >1.020 during a water-deprivation test. Water intake is restricted to 40 mL/kg body weight per day for 3 to 4 days. The urine of horses with psychogenic polydypsia and ‘medullary washout’ should concentrate to >1.020 during this test.
• Urinary pH. Normally alkaline (pH is usually between 7.5 and 8.5). Urine may be acidic in cases of:
The urine of foals tends to be acidic.
Casts – presence of granular or cellular casts usually indicates renal disease; casts dissolve quickly in alkaline urine. Leukocyte casts are indicative of bacterial nephritis.
Bacteria – the presence of more than 10 000 colony-forming units per mL of urine indicates urinary infection.
White blood cells – the presence of small numbers (≤ 8/high-power field or 400× on a free catch or ≤5/hpf on catheter collection) is not abnormal.
Crystals – normal urine may contain crystals of calcium carbonate, triple phosphate, and oxalate.
Commercial dipsticks may falsely indicate the presence of protein in alkaline urine. The sodium sulfasalicyclic acid test should be performed to determine whether the horse has proteinuria. Proteinuria without presence of blood or cellular debris is likely of renal origin, and may indicate glomerulonephritis.
Renal disease vs. renal failure
Renal disease tends to be inapparent until renal failure occurs, and renal failure can occur without the presence of renal disease. Renal failure is the inability of the kidneys to excrete nitrogenous wastes and is characterized by azotaemia (elevated concentration of serum urea nitrogen and/or creatinine). Renal failure occurs when about 75% of nephrons becomes temporarily or permanently non-functional. Azotaemia can occur in the absence of renal disease merely from decreased renal blood flow (prerenal azotaemia), or from disease of the urinary tract distal to the kidneys (urolithiasis, uroperitoneum) (postrenal azotaemia). Differentiating prerenal azotaemia from renal failure caused by renal disease (renal azotaemia) is not always straightforward.
8.2 Prerenal azotaemia
Prerenal azotaemia represents a decrease in GFR due to renal hypoperfusion. The condition is rapidly reversible.
Aetiology: Usually caused by intravascular volume depletion caused by haemorrhage, diarrhoea, endotoxaemia, inadequate water consumption, etc.
Pathogenesis: Systemic hypotension stimulates the renin–angiotensin–aldosterone axis, release of antidiuretic hormone, and the sympathetic nervous system. As a result, blood flow is redistributed away from the renal cortex, and water is conserved.
Diagnosis: Based on clinical and clinicopathological signs and rapid response to appropriate therapy.
8.3 Acute renal failure due to renal disease
Aetiology: Acute renal tubular necrosis (RTN) resulting in acute renal failure (ARF) is caused by sustained or severe hypoperfusion, or nephrotoxins, or a combination of both.
• Haemodynamic causes are most often initiated by endotoxaemia associated with some types of colic and acute diarrhoeal syndromes.
1. Plants – include red maple and oak trees, onions, and white snake root. Plants containing oxalates are potentially nephrotoxic, but oxalate-induced nephropathy is rare in horses. Deposition of oxalate crystals in kidneys, however, may occur secondarily to renal disease.
2. Heavy metals – mercury, lead, arsenic, and others.
3. Antibiotics – aminoglycosides (gentamicin, neomycin, amikacin), tetracycline, sulfonamides, cephaloridine, amphotericin B, and others.
4. Non-steroidal anti-inflammatory drugs – (NSAIDS) phenylbutazone and flunixin meglumine. NSAIDS are more likely to cause ARF when there is concurrent dehydration.
5. Pigments – myoglobin and haemoglobin. Haemoglobin and myoglobin are more likely to cause ARF if there is concurrent dehydration.
• Acute pyelonephritis – most likely to occur in septicaemic neonates; Leptospira sp. and other bacteria can cause acute tubular necrosis in adults.
Clinical signs of renal tubular necrosis: Clinical signs of acute renal failure due to renal tubular necrosis are non-specific – anorexia, depression, and weakness. These clinical signs can also be attributed to a precipitating haemodynamic cause such as colic or colitis. Toxins that induce acute renal failure are often not renal specific, and clinical signs associated with organ damage of other systems may predominate.
Diagnosis: Acute renal failure caused by renal tubular necrosis is usually diagnosed on the basis of clinical signs, physical examination, ultrasonography, and laboratory evaluation.
Caudal pole of left kidney may feel enlarged when palpated per rectum, or kidneys may appear enlarged during ultrasonic examination. Horses with renal tubular necrosis, however, often have no ultrasonographic abnormalities of the kidneys.
• Isosthenuria with concurrent dehydration and/or azotaemia.
• Measurement of urinary enzymes. The UGGT/Ucr ratio is most commonly used.
• Fractional excretion of sodium and phosphorus may be increased.
• Glycosuria without hyperglycaemia.
• Urine to plasma ratios of urea, creatinine, or osmolality may help distinguish prerenal from renal azotemia.
Of all the above tests, only isosthenuria with concurrent dehydration or azotemia indicates renal failure. Other tests indicate renal disease.
• Treatment of the predisposing disease process (e.g. endotoxaemia, myositis).
• Removal of suspected nephrotoxins.
• Correction of fluid balance, serum electrolyte concentration, and acid–base abnormality.
Intravenous administration of balanced electrolyte solution if anuric or oliguric. Over-hydration of anuric or oliguric horses can be avoided by:
1. monitoring central venous pressure.
2. monitoring for increases in body weight.
3. auscultating lungs for evidence of oedema.
4. observing for subcutaneous oedema.
If the horse is anuric or oliguric despite rehydration, convert to polyuria with:
8.4 Chronic renal failure (CRF)
Once thought to be a rare condition in horses, CRF is now considered to account for a significant portion of horses presented for weight-loss and anorexia.
Aetiology and pathogenesis: Chronic glomerulonephritis is the most frequent cause of CRF. Chronic glomerulonephritis does not always cause CRF. In one study 40% of equine kidneys examined at necropsy had microscopic glomerular lesions); there are two types of lesions:
• Antiglomerular basement membrane glomerulonephritis – (anti-GBMG) – is due to antibodies directed against the glomerular basement membrane.
• Immune complex glomerulonephritis (ICG) – (the most common type) – is due to deposition of immune complexes along the glomerular basement membrane. Immune complexes may be associated with upper respiratory infections caused by Streptococcus spp. With either type, the glomeruli become inflamed and the glomerular membrane becomes thickened by fibroblasts.
Tubulointerstitial disease (chronic interstitial nephritis); sequelae to acute renal tubular necrosis (induced by toxins or haemodynamic causes).
Chronic pyelonephritis: an uncommon cause of renal failure in adult horses. The most commonly reported cause is ascending infection of the urinary tract, which is a consequence of urinary stasis caused by urolithiasis, neurological disease affecting the urinary tract (e.g. sorghum cystitis, herpes virus-1 myeloencephalitis), or trauma (e.g. from foaling). Renal infection can also occur by haematogenous spread. In adult horses, left-sided bacterial endocarditis is a cause.
Bilateral renal hypoplasia – probably a congenital lesion; disease becomes evident when the horse is young.
Chronic oxalate nephrosis – thought to be a consequence rather than a cause of CRF.
Renal neoplasia – uncommon in horses. Types reported: adenocarcinoma (most common) and lymphoma.
Polycystic renal disease – very rare; probably a congenital disease that becomes evident in most affected horses before they reach maturity.
Clinical signs: Signs vary depending upon the aetiology
• Peripheral oedema. Seen in horses with chronic glomerulonephritis; caused by extensive loss of plasma proteins through damaged glomerular capillaries. Triad of oedema, hypoproteinaemia, and proteinuria is referred to as the nephrotic syndrome.
• Oral ulceration and dental tartar – occasionally observed.
• Fever – may be seen with pyelonephritis.
• Palpation per rectum and/or ultrasonic examination may reveal shrunken, firm kidney(s) with an irregular surface.
• Ureteral discharge of bloody or purulent urine may be seen endoscopically in horses with pyelonephritis.
Clinicopathological signs: Laboratory findings vary depending on the aetiology, stage of disease, and management factors.
• Anaemia – due to decreased production of renal erythropoietic factor and shortened RBC lifespan.
• Proteinuria – if glomerulonephritis is the cause of CRF, proteinuria is a consistent finding. Tubulointerstitial disease and pyelonephritis cause minimal proteinuria.
• Horses with chronic tubulointerstitial disease are invariably isosthenuric (1.008–1.019). Isosthenuria eventually develops in horses with chronic glomerulonephritis.
• The horse is usually azotaemic.
• Concentrations of serum electrolytes may be abnormal.
Diagnosis: Based on clinical and clinicopathological signs, endoscopic and ultrasonic examination, and renal biopsy.
Treatment: Chronic renal failure is progressive. Clients should be advised that treatment is aimed at prolonging life rather than resolving the condition.
• Supplementation of electrolytes based on periodic evaluation of serum concentrations of sodium, potassium, calcium, and bicarbonate. (If oedema develops, sodium should be restricted from the diet, even if the horse is hyponatraemic.)
• Dietary supplementation with carbohydrates and fat.
• Restriction of dietary protein to less than 10%.
• Forced feeding in cases of anorexia.
• Antimicrobial therapy for pyelonephritis. Selection of drug is based on culture and sensitivity and the ability of the antimicrobial drug to concentrate in renal tissue and urine.
8.5 Cystitis
Clinicopathological findings: Examination of urine sediment for:
• WBCs. More than 8 WBCs per high-power field of urine collected during urination or more than 5 when urine is collected by catheterization is evidence of inflammation.
• RBCs. More than 8 RBCs per high-power field of urine collected during urination or more than 5 when urine is collected by catheterization is evidence of haemorrhage.
• Large number of bacteria. Recovery of more than 10 000 colony-forming units per mL of urine collected by catheterization is diagnostic of urinary tract infection.
Diagnosis: Clinicopathological findings confirm the presence or urinary tract infection, and physical examination (thickened bladder palpated per rectum) and/or cystoscopic examination (thickened, hyperaemic, or ulcerated mucosa) localize the infection to the bladder.
• Correction of a predisposing cause if possible, such as removal of cystic calculi.
• Antimicrobial therapy based on culture and sensitivity and ability of antimicrobial drug to concentrate in urine (such as aminoglycosides, trimethoprim/sulfadiazine, fluoroquinolones, penicillin and cephalosporins).
8.6 Urolithiasis
Uroliths or calculi can form in the kidney (nephrolithiasis), ureters (ureterolithiasis), bladder (cystic urolithiasis) or urethra. If small, may be voided on urination or cause urethral obstruction. Most uroliths are composed of calcium carbonate and are spiculated and fragment easily (see Figure 8.2); those that also contain phosphate are smooth and hard and uncommon.
• Mineralization of a nidus – renal disease may provide the nidus for nephro- and ureterolithiasis. NSAID-induced nephropathy has been speculated to be a cause of nidus formation in horses with nephro- and ureterolithiasis. Urolithiasis also may be the consequence of disease of the upper portion of the urinary tract such as pyelonephritis.
• Abnormally low concentrations of natural inhibitors of mineral complexes in urine. High content of mucus produced by glands in the renal pelvis may prevent crystal aggregation.
Clinical signs of nephrolithiasis and ureterolithiasis: Clinical signs of chronic renal failure (cachexia, anorexia, depression, dental tartar, oral ulcers, etc.). Calculi may cause or be the result of renal disease.
• Surgical removal of a cystic calculus:
• Urethrotomy at any site (for removal of urethral calculi).
• Electrohydraulic or laser lithotripsy via ischial uretrotomy.
Renal function of both kidneys should be assessed before nephro- or ureterolithiasis is treated surgically (nephrectomy, nephrotomy) because bilateral renal failure is a common finding.
Prevention of recurrence: Insuring complete removal of all fragments is important in preventing recurrence. Because urolithiasis may be the consequence of disease of the upper portion of the urinary tract, horses presented for urolithiasis should be examined for disease of the upper urinary tract. Treatment for pyleonephritis, if present, may prevent recurrence. Other preventive measures include:
8.7 Uroperitoneum (see also Chapter 20)
2. Foals – bladder rupture and urachal tears, ureteral defects.
• Prenatal distension of the bladder (perhaps caused by partial torsion of the umbilical cord) coupled with pressure on the full bladder during parturition leads to rupture of bladder or urachus. Affected foals are usually male.
• Congenital bladder defects may be responsible for uroperitoneum of some foals.
• Bladder and urachal rupture may occur due to lesions caused by urinary tract infections.
• Tenesmus associated with g.i. disease may cause urachal tears.
• Concentration of creatinine in peritoneal fluid containing urine is usually double that of serum creatinine (exception is foals evaluated early after bladder rupture).
• Hypochloraemia, hyponatraemia, and hyperkalaemia in foals. These electrolyte abnormalities may not be seen in the adult.
• Foals are usually, but not necessarily, azotaemic.
• Calcium carbonate crystals may be seen in peritoneal fluid.
• Clinical signs and clinicopathological findings.
• Dye (methylene blue or fluorescein) placed into the bladder and subsequently recovered in peritoneal fluid.
• Positive contrast cystography (do not use barium).
• For diagnosis of suspected ureteral defects, exploratory laparotomy and cystotomy are performed. The ureters are infused with dye such as methylene blue, and examined for leakage. Intravenous pyelography is not very useful.
Treatment: Cystorrhaphy and/or resection of urachus. Preoperative therapy might involve:
1. Measures to lower the potential for cardiac arrythmia caused by high serum concentration of potassium.
• isotonic or hypertonic saline solution, IV.
• 5% dextrose, IV and insulin.
• enemas of sodium polystyrene sulfonate (a potassium-removing resin).
• mask induction and anaesthesia with isoflurane or sevoflurane, which are less arrythmogenic than halothane.
Full access? Get Clinical Tree
