Limitation of Shock-Wave-Induced Renal Tubular Dysfunction by Nifedipine

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Abstract
In a prospective randomized study, the effects of the calcium entry blocker nifedipine on shock-wave-induced tubular impairment were studied. 24 patients with renal pelvic or calyceal stones undergoing anesthesia-free extracorporeal shock wave lithotropsy (ESWL) without ancillary measures were randomly assigned to the nifedipine group (n = 12) or the control group (n =12). Four doses of nifedipine (10 mg t.i.d.) were given orally, starting the night before ESWL. Controls received no medication. To assess renal tubular function,the urinary excretion of ai-microglobulin (A(i)M), N-acetyl-β-glucosaminidase(NAG) and Tamm-Horsfall protein (THP) were measured before,immediately, 12 and 24 h after ESWL. After lithotripsy, there was a rise in urinary A[M and NAG which was significantly higher in the control than in the nifedipine group. THP, a glycoprotein synthesized by distal tubular cells,fell significantly less in the nifedipine group compared to the controls. Our results indicate that nifedipine exhibits a protective effect on shock-waveinduced tubular damage similar to verapamil. The underlying mechanisms are not clarified yet, direct actions on tubular cells and interference with renal hemodynamics have to be discussed.

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