Equine Renal Failure and Urogenital Injuries Study Guide

Overview and Clinical Importance

Renal failure in horses represents a significant clinical challenge and important NAVLE topic. Unlike companion animals, kidney disease is rare in horses (prevalence 0.12%). The large renal reserve means clinical signs often do not appear until 75% of nephron function is lost.

Urogenital injuries, particularly uroperitoneum from bladder rupture, are life-threatening emergencies requiring rapid diagnosis and intervention. These conditions are commonly tested due to distinct presentations and critical treatment decisions.

Equine Renal Anatomy Review

Understanding equine renal anatomy is essential for interpreting diagnostic findings. Equine kidneys have smooth surfaces with less distinct corticomedullary junction than other species.

Acute Kidney Injury (AKI)

Acute kidney injury (AKI) represents a continuum from inapparent nephron injury to acute renal failure (ARF). Serum creatinine does not increase above reference limits until GFR is reduced by nearly 75%.

Classification of Azotemia

Common Nephrotoxins in Horses

Clinical Signs of AKI

• Depression and anorexia (often more severe than expected)
• Oliguria or anuria (dry bedding within 6-12 hours of fluid therapy is concerning)
• Inappropriate weight gain despite fluid therapy
• Ventral and conjunctival edema

Diagnostic Findings

Treatment of AKI

• Discontinue all nephrotoxic drugs
• Correct predisposing disorders (address primary disease)
• Aggressive IV fluid therapy: Balanced crystalloids; monitor CVP and body weight
• Monitor urine output: Goal is 1-2 mL/kg/hr

If oliguric after 10-12 hours: Consider furosemide 1-2 mg/kg IV or CRI 0.12 mg/kg/hr

Prognosis for AKI

• Polyuric ARF: Good prognosis
• Oliguric/Anuric ARF: Guarded to poor prognosis
• No urine for 24 hours despite treatment: Grave indicator

Chronic Kidney Disease (CKD)

Chronic kidney disease is rare in horses (0.12% prevalence) but irreversible and progressive. CKD is defined as kidney disease present for greater than 3 months with creatinine greater than 2.0 mg/dL.

Causes of CKD

• Tubulointerstitial disease: Most common; consequence of previous AKI
• Glomerulonephritis: Immune-mediated; associated with Streptococcus equi, EIA
• Pyelonephritis: Ascending or hematogenous infection
• Nephrolithiasis: Calcium carbonate stones; often secondary to CKD

Clinical Signs of CKD

• Weight loss (most common presenting complaint)
• Polyuria/polydipsia
• Ventral edema
• Oral ulcerations, dental tartar (uremia)
• Dull hair coat, poor performance

Diagnostic Findings in CKD

• Azotemia: Creatinine greater than 2.0 mg/dL persistently
• Isosthenuria: USG 1.008-1.014 (hallmark of CKD)
• Hypercalcemia: UNIQUE to horses with CKD; diet dependent
• Hypophosphatemia: Common; NOT from secondary hyperparathyroidism

Management of CKD

• Dietary: Switch from alfalfa to grass hay (reduces calcium)
• Water: Free access; add 50-75g salt daily to encourage drinking
• Monitoring: Regular creatinine, electrolytes monthly or longer

Prognosis: Many horses maintain fair quality of life for months to years if creatinine stays less than 4-5 mg/dL. Once exceeded, progression accelerates.

Urogenital Injuries: Uroperitoneum

Uroperitoneum is urine leakage into the peritoneal space - a medical emergency. Most common in neonatal foals but can occur in adults post-foaling or with urolithiasis.

Etiology

In Foals:

• Bladder rupture: 73% of cases; usually dorsal wall; colts at higher risk
• Urachal rupture: 22% of cases; from umbilical cord trauma

In Adults:

• Post-foaling trauma in mares
• Urolithiasis with urethral obstruction leading to bladder rupture

Clinical Signs (Foals 2-5 days post-partum)

• Progressive depression and lethargy
• Abdominal distension with fluid wave
• Stranguria (often mistaken for meconium impaction)
• Tachycardia and tachypnea
• Note: Foals may continue to urinate normally despite bladder rupture

Diagnosis: Classic Electrolyte Triad

Abdominocentesis: Peritoneal:Plasma Creatinine Ratio greater than 2:1 confirms diagnosis (classic ratio is greater than 4:1)

Treatment - Medical Stabilization FIRST

• IV Fluid Therapy: 0.9% NaCl preferred (sodium-rich, potassium-free)
• Abdominal Drainage: Drain urine via teat cannula or peritoneal catheter
• Urinary Catheter: Indwelling catheter to decompress bladder
• Correct Hyperkalemia: If K greater than 6.0 mEq/L, consider dextrose/insulin, calcium gluconate
• Antibiotics: Broad-spectrum; many foals have concurrent infection

Surgical Repair: ONLY after electrolyte stabilization. Ventral midline celiotomy; cystorrhaphy with absorbable suture.

Prognosis

• Foals with uncomplicated bladder rupture: approximately 60-64% survival
• Most common complication: recurrence (16-20%)

Urolithiasis

Urolithiasis is uncommon (0.11%) but important as urethral obstruction can cause bladder rupture. Most common in bladder (60%) and urethra (24%). Males more commonly affected.

Urolith Types

• Type 1 (most common): Yellow-green; spiculated; calcium carbonate; crumbles easily
• Type 2: White-gray; smooth; harder composition; difficult to fragment

Clinical Signs

• Cystic calculi: hematuria (worse after exercise), dysuria, pollakiuria, urine scalding
• Urethral: complete obstruction signs; can lead to bladder rupture
• Nephroliths: often incidental; weight loss if symptomatic (CKD)

Treatment

• Mares: Manual removal transurethrally; laser lithotripsy
• Geldings: Perineal urethrotomy; stone fragmentation

Prevention

• Dietary modification: reduce calcium (avoid alfalfa)
• Increase water intake: add 50-75g salt daily
• Urine acidification may help prevent CaCO3 crystal formation

Memory Aids for NAVLE

"URINE" for Uroperitoneum

U - Ultrasound shows free fluid, R - Ratio peritoneal:plasma Cr greater than 2:1, I - Ions abnormal (hyperK, hypoNa, hypoCl), N - Nitrogenous waste elevated, E - Electrolyte correction before surgery!

CKD Quick Facts

Hypercalcemia + Azotemia + Isosthenuria = CKD in horses (unique to equines!)