Equine Urinary Tract Disease Study Guide

Overview and Clinical Importance

Urinary tract disease in horses is relatively uncommon compared to other species, with a reported prevalence of kidney disease at approximately 0.12%. However, horses possess unique urinary tract physiology that creates specific vulnerabilities to certain conditions. Understanding these diseases is critical for the NAVLE because when urinary problems do occur, they often represent serious, potentially life-threatening conditions that require prompt recognition and intervention.

Equine urine is uniquely alkaline (pH 7.0-9.0), high in calcium carbonate crystals, and contains mucoproteins from glands in the renal pelvis that give it a characteristic viscous, frothy appearance. This physiology predisposes horses to calcium carbonate urolithiasis and makes urinalysis interpretation different from other species.

Equine Urinary Tract Anatomy

The equine urinary tract has several unique anatomical features relevant to disease. The right kidney is heart-shaped (approximately 650g, 15cm long) and located retroperitoneally below the last 2-3 ribs and first lumbar transverse process, embedded against the liver. The left kidney is bean-shaped (approximately 600g, 18cm long), more caudal, and can be palpated rectally.

The equine kidney has a unilobar configuration with a single renal crest (fused papillae) and terminal recesses extending toward each pole. This is important because the renal papilla is sensitive to NSAID toxicity (papillary necrosis), particularly phenylbutazone.

Normal Equine Urinalysis Parameters

Acute Kidney Injury (AKI)

AKI in horses is relatively uncommon but carries a serious prognosis if not recognized early. It represents a continuum of kidney damage from mild, clinically inapparent nephron loss to severe acute kidney failure.

Etiology

Clinical Signs

Clinical signs of AKI are often non-specific and may be overshadowed by the primary disease. Key findings include: oliguria or anuria (often manifested as dry bedding within 6-12 hours of starting fluids), depression and anorexia disproportionate to the primary disease, inappropriate weight gain (fluid retention) 1-2 days before visible edema, and progression to polyuria during recovery phase.

Diagnosis

Serum creatinine (sCr) remains the recommended biochemical test to estimate GFR. BUN is unreliable in horses because it can be affected by diet, GI bleeding, and other factors. Remember that creatinine only increases when 60-75% of nephron function is lost, so a normal creatinine does not rule out early AKI. Ultrasound findings in acute AKI include: enlarged kidneys with decreased echogenicity (swelling/edema) and loss of corticomedullary distinction.

Treatment

Treatment priorities: 1) Eliminate nephrotoxic drugs, 2) Correct underlying disorders, 3) IV fluid therapy to promote diuresis (typically crystalloids at 2-4 L/hour initially), 4) Monitor central venous pressure and body weight to prevent overhydration, 5) If oliguria persists, furosemide or dopamine may be attempted but are inconsistently effective.

Chronic Kidney Disease (CKD)

CKD is rare in horses (0.12% prevalence) but is irreversible and progressive. There is often a continuum from AKI to CKD, and horses with CKD are predisposed to acute exacerbations. Common causes include chronic tubulointerstitial nephritis, glomerulonephritis (associated with Streptococcus equi, EIA), pyelonephritis, and nephrolithiasis.

Clinical Signs

Clinical signs are non-specific: weight loss (most common), polyuria/polydipsia, and ventral edema. Less common signs include poor appetite and performance, dull hair coat, oral ulcerations, gingivitis, dental tartar, and diarrhea. Rarely, horses may develop forebrain signs due to uremic encephalopathy.

Diagnosis

Urolithiasis

Urolithiasis in horses is relatively uncommon despite the fact that equine urine is supersaturated with calcium and carbonate ions and has an alkaline pH that favors crystal formation. The most common stone type is calcium carbonate (greater than 90%), and stones are most frequently found in the bladder (60%) followed by urethra (24%), kidney (12%), and ureter (4%).

Stone Types

Risk Factors

• Male horses (especially geldings) - narrower urethra makes obstruction more likely
• High calcium diets (alfalfa, legumes) - increases urinary calcium excretion
• Dehydration - concentrates minerals in urine
• Chronic NSAID use - renal papillary necrosis may provide nidus
• Bladder dysfunction - urine stasis allows crystal deposition

Clinical Signs

Cystic calculi: Hematuria (especially after exercise and at end of urination), stranguria, pollakiuria, urine scalding of perineum/hind limbs. Horses often maintain a stretched-out urination posture for prolonged periods. Geldings may protrude penis and dribble urine. Urethral obstruction causes acute distress, colic, sweating, frequent attempts to urinate, and palpably distended bladder.

Diagnosis

Rectal palpation: Bladder stones often palpable as grating masses. Cystoscopy: Confirms diagnosis and estimates size. Ultrasound: Useful for nephroliths and cystoliths. Always ultrasound kidneys to check for nephrolithiasis if bladder stones are found.

Treatment

Uroperitoneum in Foals

Uroperitoneum is a medical emergency characterized by leakage of urine into the peritoneal cavity. It occurs in approximately 0.2-2.5% of hospitalized foals, most commonly from rupture of the dorsocranial bladder wall during parturition. The dorsal bladder lacks the outer longitudinal muscle layer, making it the weakest point. Male foals are overrepresented due to longer, narrower urethra.

Causes

• Bladder rupture (most common) - parturient trauma, prolonged recumbency
• Urachal rupture - parturition trauma, umbilical abscessation
• Ureteral defects - congenital or traumatic (rare)
• Predisposing factors: prematurity, neonatal encephalopathy, sepsis, failure of passive transfer

Clinical Signs

Foals typically appear normal at birth but develop signs over 24-72 hours: progressive lethargy, tachycardia, tachypnea, abdominal distension with fluid wave on ballottement. Stranguria is common but often misinterpreted as straining to defecate. Importantly, many foals continue to urinate normally. Scrotal swelling may occur in colts. Neurological signs (seizures) can occur due to severe hyponatremia.

Classic Electrolyte Abnormalities

Hyperkalemia, hyponatremia, hypochloremia, metabolic acidosis, azotemia. These develop because urine equilibrates with plasma across the peritoneal membrane. High potassium and low sodium in mare's milk exacerbate the electrolyte abnormalities.

Diagnosis

Ultrasound: Large volume of anechoic free fluid, small/collapsed/irregular bladder. Abdominocentesis: Key finding is peritoneal fluid creatinine greater than 2x serum creatinine. Blood work confirms electrolyte abnormalities.

Treatment

Initial stabilization is critical before surgery: Peritoneal drainage to relieve respiratory compromise and correct electrolytes, IV fluids (0.9% NaCl - do NOT use potassium-containing fluids!). Surgical repair: Cystorrhaphy for bladder rupture via ventral midline approach. Small tears may respond to conservative management with urinary catheter and peritoneal drainage.

Bladder Paralysis and Sabulous Cystitis

Sabulous cystitis refers to accumulation of large amounts of crystalloid urinary sediment (primarily calcium carbonate) in the ventral bladder. It occurs secondary to bladder dysfunction that prevents complete emptying. Geldings (92%) and Warmbloods (46%) are overrepresented.

Causes of Bladder Paralysis

Clinical Signs

Urinary incontinence (69% presenting complaint) with constant or intermittent urine dribbling, perineal/hindlimb urine scalding, dysuria, pollakiuria. LMN lesions often accompanied by loss of anal sphincter tone, reduced perineal reflex, tail paralysis, and hindlimb ataxia. Rectal exam reveals distended bladder that is easily expressed.

Diagnosis

Rectal palpation: Distended bladder with sandy/gritty material. Transrectal ultrasound: Hyperechoic sediment in ventral bladder. Cystoscopy: Definitive diagnosis; reveals yellow sediment accumulation with possible mucosal erosion and ulceration.

Treatment

Bladder lavage: High-volume saline lavage to remove sediment (standing or under GA). Pharmacological support: Bethanechol (parasympathomimetic, 0.25-0.75 mg/kg SQ TID) to increase detrusor tone, Phenoxybenzamine (alpha-blocker, 0.7 mg/kg PO q6h) to reduce urethral resistance. Antibiotics: Based on culture. Dietary modification: Avoid high-calcium feeds (alfalfa, beet pulp).

Hematuria in Horses

Common Causes

• Urolithiasis - most common cause, hematuria at end of urination
• Urinary tract infection/cystitis - often with dysuria
• Idiopathic renal hematuria (IRH) - Arabian breed predisposition
• Neoplasia - renal cell carcinoma, bladder squamous cell carcinoma
• Proximal urethral tears - stock-type horses, hematuria at beginning of urination
• Exercise-associated hematuria - microscopic, resolves with rest

Timing of Hematuria - Localizing the Source

Idiopathic Renal Hematuria (IRH)

IRH is characterized by sudden onset of gross, often life-threatening hematuria with passage of large blood clots. Arabian or part-Arabian horses are overrepresented, suggesting genetic predisposition. Hemorrhage originates from one or both kidneys. Cystoscopy confirms blood clots exiting from one or both ureteral orifices. Diagnosis is by exclusion of other causes. Hematuria may resolve spontaneously but recur months to years later. Treatment is supportive; unilateral nephrectomy may be considered for severe unilateral hemorrhage, but contralateral hemorrhage can develop post-procedure.

Pyelonephritis

Pyelonephritis is uncommon in horses and represents ascending or hematogenous bacterial infection of the renal pelvis and parenchyma. Predisposing factors include urolithiasis, recurrent cystitis, bladder paralysis, ectopic ureter, and foaling injury. Common organisms: E. coli, Proteus, Klebsiella, Streptococcus, Staphylococcus, Pseudomonas.

Clinical signs: Fever, weight loss, inappetence, lethargy, flank pain, polyuria/polydipsia. Pyuria and bacteriuria on urinalysis; urine culture confirms diagnosis. Ultrasound may show enlarged kidney with fluid distension or increased echogenicity. Treatment: prolonged appropriate antimicrobials (4-6 weeks minimum). Unilateral nephrectomy may be considered if disease is confined to one kidney and refractory to medical treatment.

Key Summary Points

• Normal equine urine is alkaline (pH 7.0-9.0), turbid, and contains calcium carbonate crystals - this is NORMAL, not pathology
• Creatinine is the preferred biomarker for GFR; BUN is unreliable in horses. Creatinine only increases when 60-75% of nephron function is lost
• AKI vs CKD: AKI = enlarged, hypoechoic kidneys; CKD = small, hyperechoic, irregular kidneys with hypercalcemia
• Uroperitoneum in foals: Classic findings are hyperkalemia, hyponatremia, hypochloremia. Peritoneal creatinine greater than 2x serum creatinine confirms diagnosis
• Urolithiasis: Calcium carbonate stones (Type I) predominate. Surgical removal required; dietary dissolution ineffective
• Sabulous cystitis: Secondary to bladder dysfunction; guarded prognosis for full recovery
• Idiopathic renal hematuria: Arabian breed predisposition; sudden severe hematuria with blood clots