Reduced renal blood flow in early cisplatin-induced acute renal failure in the rat

Studies were designed to determine the cause of the reduced glomerular filtration rate (GFR) in early cisplatin-induced acute renal failure. Rats were studied 72 h following a single intraperitoneal injection of cisplatin (5 mg/kg) or vehicle (0.9% NaCl). Whole kidney GFR and blood flow were lower in cisplatin-treated animals than in controls (0.30 ± 0.06 vs. 1.17 ± 0.06 ml·min^-1·g kidney wt^-1 and 5.30 ± 0.62 vs. 8.25 ± 0.43 ml·min^-1·g kidney wt^-1, respectively; P<0.001), as were superficial nephron GFR and stop-flow pressure (20.2 ± 2.1 vs. 34.5 ± 2.0 nl·min^-1·g kidney wt^-1 and 29.0 ± 1.9 vs. 39.8 ± 1.3 mmHg, respectively; P < 0.001). After volume expansion, renal plasma flow increased in control rats, whereas whole kidney and single nephron GFR did not change. In experimental animals, whole kidney filtration rate rose to 0.58 ± 0.07 ml·min^-1·g kidney wt^-1, single nephron filtration rate increased to 29.9 ± 3.5 nl·min^-1·g kidney wt^-1 (P < 0.005), and renal plasma flow increased to 5.62 ± 0.60 ml·min^-1·g kidney wt^-1 (P < 0.05). Intratubular hydrostatic pressure was not different in the two groups before or after volume expansion. The results of these studies show that the reduced GFR in early cisplatin-induced renal failure is due, in part, to reversible changes in renal blood flow and renal vascular resistance.