The kidneys excrete the end-products of tissue metabolism and maintain fluid, electrolyte and acid-base balance. Renal failure is the result of impaired renal excretory and homeostatic functions and the clinical syndrome of uremia will be present. The pathophysiology of uremia, however, is difficult to study in humans because of the type of experimentation required. The aim of this study was to induce experimental model of chronic renal failure in sheep for further research. Uremic state was created by two stages surgery in eight adult male sheep. Initially, in the left kidney, the posterior branch of the renal artery was completely ligated. At least 3 weeks after the animal had recuperated from the renal infarction, the right kidney was removed. All sheep became uremic and mildly anemic. Four weeks after right nephrectomy (second stage of surgery) mean urea, creatinine, potassium, and sodium levels in the serum of sheep were significantly elevated and were 110.4 ± 11.69 mg/dl, 3.09 ± 0.84 mg/dl, 4.86 ± 0.40 mmol/L and 130.5 ± 8.02mmol/L, respectively. Mean PCV of sheep at same time was 25.2 percent. Acute renal failure developed in one sheep so that serum biochemical parameters including urea, creatinine, potassium, and sodium levels increased to 250 mg/dl, 7.3 mg/dl, 7.4 mmol/L and 123 mmol/L, respectively. This study suggested that two stages subtotal nephrectomy can be used for experimentally induction of chronic renal failure and uremia in sheep.
