LIMITATION OF SHOCK-WAVE-INDUCED RENAL TUBULAR DYSFUNCTION BY NIFEDIPINE

In a prospective randomized study, the effects of the calcium entry bl ocker nifedipine on shock-wave-induced tubular impairment were studied . 24 patients with renal pelvic or calyceal stones undergoing anesthes ia-free extracorporeal shock wave lithotropsy (ESWL) without ancillary measures were randomly assigned to the nifedipine group (n = 12) or t he control group (n = 12). Four doses of nifedipine (10 mg t.i.d.) wer e given orally, starting the night before ESWL. Controls received no m edication. To assess renal tubular function, the urinary excretion of al-microglobulin (A(1)M), 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 AIM and NA G 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. O ur results indicate that nifedipine exhibits a protective effect on sh ock-wave-induced tubular damage similar to verapamil. The underlying m echanisms are not clarified yet, direct actions on tubular cells and i nterference with renal hemodynamics have to be discussed.