## Overview Acute renal failure (also called acute kidney injury when milder) is a sudden decline in kidney function that reduces the kidneys’ ability to filter waste, regulate fluid and electrolytes, and maintain acid-base balance. In horses it is most often secondary to severe systemic illness (hemodynamic causes) or exposure to nephrotoxic drugs or pigments. Horses have substantial renal reserve, so clinical signs may appear only after significant damage has already occurred. Early recognition and aggressive fluid therapy improve the chance of recovery. ## Causes The most common causes are reduced renal blood flow from dehydration, hypovolemia, endotoxemia, or shock, and direct nephrotoxicity from aminoglycoside antibiotics, nonsteroidal anti-inflammatory drugs, oxytetracycline, bisphosphonates, or myoglobin/hemoglobin. Leptospira species are the most frequent infectious cause. Prolonged prerenal azotemia can progress to intrinsic acute tubular necrosis. ## Diagnosis History of recent illness or drug exposure, combined with azotemia (elevated creatinine and blood urea nitrogen), is suggestive. Urinalysis may show casts, proteinuria, or isosthenuria. Ultrasound can reveal enlarged kidneys with increased echogenicity. Fractional excretion of electrolytes and response to fluid therapy help distinguish prerenal from intrinsic renal failure. Renal biopsy is rarely performed. ## Treatment The cornerstone is intravenous fluid therapy to restore circulating volume, blood pressure, and renal perfusion, plus elimination of any nephrotoxic agents and treatment of the underlying disease. Electrolyte and acid-base abnormalities are corrected. Diuretics such as furosemide are sometimes used if oliguria persists after volume restoration, but they are not consistently effective. Supportive care addresses secondary complications such as laminitis or thrombophlebitis. ## Recovery and Prognosis Horses with polyuric acute renal failure that respond quickly to fluids often have a good prognosis. Oliguric or anuric cases carry a guarded to poor prognosis. Duration of renal failure before treatment is a major determinant of outcome. Many horses that survive the acute phase regain sufficient function for a normal quality of life, although some develop chronic kidney disease. ## Prevention Avoid unnecessary or prolonged use of nephrotoxic drugs, maintain hydration during illness or transport, and monitor renal values in critically ill horses. Prompt treatment of endotoxemia and colic reduces risk.
depression; reduced appetite; oliguria or polyuria; elevated heart rate; dehydration; edema in some cases; azotemia on bloodwork
## Overview Acute renal failure (also called acute kidney injury when milder) is a sudden decline in kidney function that reduces the kidneys’ ability to filter waste, regulate fluid and electrolytes, and maintain acid-base balance. In horses it is most often secondary to severe systemic illness (hemodynamic causes) or exposure to nephrotoxic drugs or pigments. Horses have substantial renal reserve, so clinical signs may appear only after significant damage has already occurred. Early recognition and aggressive fluid therapy improve the chance of recovery. ## Causes The most common causes are reduced renal blood flow from dehydration, hypovolemia, endotoxemia, or shock, and direct nephrotoxicity from aminoglycoside antibiotics, nonsteroidal anti-inflammatory drugs, oxytetracycline, bisphosphonates, or myoglobin/hemoglobin. Leptospira species are the most frequent infectious cause. Prolonged prerenal azotemia can progress to intrinsic acute tubular necrosis. ## Diagnosis History of recent illness or drug exposure, combined with azotemia (elevated creatinine and blood urea nitrogen), is suggestive. Urinalysis may show casts, proteinuria, or isosthenuria. Ultrasound can reveal enlarged kidneys with increased echogenicity. Fractional excretion of electrolytes and response to fluid therapy help distinguish prerenal from intrinsic renal failure. Renal biopsy is rarely performed. ## Treatment The cornerstone is intravenous fluid therapy to restore circulating volume, blood pressure, and renal perfusion, plus elimination of any nephrotoxic agents and treatment of the underlying disease. Electrolyte and acid-base abnormalities are corrected. Diuretics such as furosemide are sometimes used if oliguria persists after volume restoration, but they are not consistently effective. Supportive care addresses secondary complications such as laminitis or thrombophlebitis. ## Recovery and Prognosis Horses with polyuric acute renal failure that respond quickly to fluids often have a good prognosis. Oliguric or anuric cases carry a guarded to poor prognosis. Duration of renal failure before treatment is a major determinant of outcome. Many horses that survive the acute phase regain sufficient function for a normal quality of life, although some develop chronic kidney disease. ## Prevention Avoid unnecessary or prolonged use of nephrotoxic drugs, maintain hydration during illness or transport, and monitor renal values in critically ill horses. Prompt treatment of endotoxemia and colic reduces risk.
depression; reduced appetite; oliguria or polyuria; elevated heart rate; dehydration; edema in some cases; azotemia on bloodwork