Cyclosporine-treated renal allograft recipients frequently suffer CsA-related nephrotoxicity and hypertension. This study demonstrates that glomerular filtration rate is reduced acutely by 13% (P< 0.02) and renal vascular resistance increased by 30% (P< 0.05), immediately after patients take their CsA dose. The reduction in GFR is directly related to their trough CsA level (r = 0.82; P<0.01). The lower the trough CsA level the greater the fall in GFR after the CsA dose. Plasma renin activity does not increase after the CsA dose (pre-CsA 0.6±0.2 ng/L/sec vs. post-CsA 0.4±0.1 ng/L/sec; P = NS), and therefore cannot be responsible for the reduction in renal function.Short-term nifedipine treatment is effective in pre venting the acute reduction in GFR (P< 0.05). This occurred despite no apparent effect of nifedipine in altering trough or post-dose CsA levels. Furthermore nifedipine was effective in lowering both the mean arterial blood pressure (109 mmHg to 94 mmHg;P< 0.01) and the elevated renal vascular resistance (25% reduction;P< 0.02) observed in these patients.These results suggest that nifedipine may be a suitable agent for limiting acute CsA nephrotoxicity and for treating CsA-associated hypertension in renal allograft recipients.