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Experimental model of 5/6 nephrectomy or the remnant kidney model represents one of the most used animal models of progressive renal failure by reduced nephron number, best-characterized in rats. The reduction of renal mass is achieved by either infarction or surgical excision of both poles, with removal of the contralateral kidney. It enables to investigate the influence of pharmacological, nutritive and other factors on functional and morphological renal parameters. 5/6 nephrectomy produced by infarction is characterised by high plasma renin levels. By contrast, reduction of an equivalent amount of renal parenchyma by surgical excision does not result in the development of hypertension and plasma renin activity is normal to low. The initially normal remnant nephrons undergo compensatory functional and structural adaptations. Simultaneous glomerular hypertension is one of the main factors responsible for the development of renal injury. Morphologicaly progressive focal segmental to global glomerulosclerosis is present, accompanied clinically by increasing proteinuria and deteriorating renal function.

In 19 patients with chronic renal failure and still preserved residual diuresis the inulin clearance (Cin) and renal potassium excretion were assessed before and 12 hours after haemodialysis (HD), combined with conventional ultrafiltration. The mean value of Cin after HD declined significantly (p less than 0.001). As a result of HD a significant decline of the plasma potassium concentration occurred (p less than 0.005) and of the urinary excretion (p less than 0.01). The mean value of the fractional potassium excretion (FEK) did not change significantly as a result of HD. The reduced urinary K excretion after HD correlated significantly (p less than 0.05) with the decline of Cin. The findings suggest that the decline of the urinary potassium excretion after HD is above all due to a decline of the glomerular filtration rate. The tubular potassium secretion does not change significantly under these conditions. These findings support indirectly the idea that the increased tubular potassium secretion in residual nephrons in patients with chronic renal failure is not conditioned by retention of low-molecular dialysable substances.