Renal failure in the horse is the loss of adequate kidney function — the kidneys can no longer filter nitrogenous waste, regulate electrolytes, or maintain fluid balance at levels sufficient to sustain normal physiology. It presents in two forms: acute renal failure (ARF), which develops over hours to days and is potentially reversible if the underlying cause is removed promptly, and chronic renal failure (CRF), which is a slow, progressive, and irreversible loss of functional nephrons that typically goes undetected until more than 70 percent of renal mass is already compromised.
Horses are susceptible to several specific precipitating causes. ARF is most commonly triggered by nephrotoxic drugs — non-steroidal anti-inflammatory drugs (NSAIDs) such as phenylbutazone and flunixin meglumine are the leading culprits when given at high doses or during dehydration, as are aminoglycoside antibiotics (gentamicin in particular). Severe systemic illness, particularly endotoxemia from colitis or sepsis, reduces renal perfusion and can precipitate ischemic ARF. Pigment nephropathy following myositis (tying-up) or hemolysis is a recognized acute presentation. CRF in horses most often results from immune-mediated glomerulonephritis, chronic interstitial nephritis, or congenital anomalies; oxalate nephrolithiasis from high-oxalate tropical grasses is documented in geographic clusters.
Clinical signs reflect the degree of azotemia and the disruption of electrolyte homeostasis. Affected horses show weight loss, ventral edema, polydipsia and polyuria (classic in CRF; oliguria or anuria in severe ARF), oral ulceration from uremic mucositis, and inappetence. Hypercalcemia is a distinctive finding in equine CRF — horses, unlike other large animals, are calcium-excreting species, and failing kidneys accumulate it; serum calcium above 14 mg/dL with concurrent azotemia is diagnostically significant. Diagnosis is confirmed by elevated blood urea nitrogen, creatinine, and fractional excretion of electrolytes; renal ultrasonography and biopsy characterize the lesion type and guide prognosis.
Treatment of ARF centers on aggressive IV fluid diuresis to clear nephrotoxins and restore perfusion, removal of the offending drug or cause, and supportive care. CRF is managed palliatively — low-protein, low-calcium diet (reducing alfalfa in favor of grass hay), adequate water access, and monitoring. Prognosis for ARF caught early is guarded-to-fair; CRF carries a poor long-term prognosis in working horses, though some cases are managed in a reduced role for months to years.