Limitation of shock-wave-induced renal tubular dysfunction by nifedipine

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 extra-corporeal shock wave lithotripsy (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 alpha 1-microglobulin (A1M), N-acetyl-beta-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 A1M 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-wave-induced 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.