We studied the actions of nifedipine and the platelet activating factor (PAF) antagonist BN 52021 on renal and tubular function in glycerol-induced acute renal failure (Gly-ARF). The tubular handling of sodium was evaluated through the lithium clearance method in awake rats in metabolic cages. The sequential analysis of tubular function 3, 6, 12, and 24 h after Gly-ARF showed a sharp decrease in fractional proximal Na reabsorption (FPRNa)--control 74.1 +/- 12.5%, 3 h: 79.5 +/- 6.0%; 6 h: 41.8 +/- 15.9%; 12 h: 22.9 +/- 17.9%; and 24 h: 31.1 +/- 16.2% (p < 0.001) while fractional distal Na reabsorption (FDRNa) did not change during the study. The effect of nifedipine (20 mg/kg p.o.) and BN 52021 (1 mg/kg i.p.) were evaluated 24 h after the induction of Gly-ARF. Both drugs attenuated the reduction in creatinine clearance (control 431.8 +/- 108.2, glycerol 96.7 +/- 43.8, glycerol plus nifedipine 264.9 +/- 103.5, and glycerol plus BN 52021 188.9 +/- 69.8 microL/min/100 g, p < 0.001). However, only nifedipine could keep FPRNa higher than untreated rats (58.3 +/- 13.2 vs. 31.1 +/- 16.2%, p < 0.05) and reduced the tubular necrosis on histologic semiquantitative analysis. Our data showed that nifedipine and BN 52021 could protect against filtration failure in Gly-ARF but that only nifedipine reduced the proximal tubular lesion.

This study shows that the frequency of renal stones in patients suffering from Crohns disease is higher than in general population and, also, higher than that described elsewhere for this disease. We identified hypocitraturia and hypomagnesiuria as the main factors which could explain our data. The impact of these metabolic disturbances can be also evaluated by means of the high supersaturation obtained for calcium oxalate and calcium phosphate which suggests the way those factors could be influencing crystal nucleation and, consequently, lead to renal stones formation in this group of patients.

Urinary tract obstruction is a common cause of acute renal failure (ARF). During unilateral ureteral obstruction (UUO) arteriolar vasoconstriction, increase in tubular pressure, and ultrafiltrate retrodiffusion occur. We studied renal function of rats with surgical UUO for 24 hr. After this period of UUO, the contralateral kidney was removed and the right ureter was deobstructed. The control uninephrectomized group consisted of normal rats submitted to left uninephrectomy (UNx). Functional studies were performed 12 and 24 hr, and 7 days after deobstruction and UNx. We measured creatinine clearance, and fractional excretion of sodium and lithium. Using conventional formulas we calculated fractional proximal and distal sodium reabsorption. Initially we observed a reduction in glomerular filtration rate (GFR) after deobstruction (12 and 24 hr). However, after 7 days, the GFR was significantly higher in deobstructed rats than in controls (340.3 +/- 18.3 vs. 286.4 +/- 9.3 microL/min/100 g, p < 0.01). The dry kidney weight was also increased in these rats. The fractional sodium excretion was increased in deobstructed rats, mainly in early studies (12 and 24 hr). Whereas fractional proximal reabsorption was reduced in both groups, the fractional distal reabsorption was significantly decreased in the deobstructed group compared to UNX controls (93.9 +/- 0.9 vs. 98.9 +/- 0.1% after 24 hr, p < 0.01). Our data showed that UUO influenced both glomerular and tubular functions. A salient finding was the overcorrection of GFR 7 days after deobstruction. The renal release of hormones and growth factors could mediate these alterations in renal function through their vascular, tubular, and proliferative actions.

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