ABSTRACT
Using an in vitro model with Madin-Darby canine kidney (MDCK) cells, we showed that shock wave-induced renal injury could be ameliorated by selenium. We examined the influence of selenium, a free radical scavenger, in shock wave-induced tubular cell injury in vivo. Male rats were randomly assigned to three groups: 1 control (n= 18), 2 selenium (n = 18), 3 sham treatment (n = 4). Groups 1 and 2 were treated with 500 shock waves on each kidney. Animals assigned to group 3 (sham treatment) received only anesthetics. Selenium (80 microg/kg per 24 h intraperitoneally) was given to the animals in group 2 for 5 days, starting 1 day before shock wave exposure. Urine was collected for 8 h on the day before and immediately, 1, 7 and 28 days after shock wave exposure (SWE) for the measurement of urine volume, N-acetyl-beta-glucosaminidase (NAG), beta-2-microglobulin (beta2 M), and creatinine. Blood was taken from these rats on day 1 after SWE for the determination of creatinine and the calculation of the creatinine clearance (CCr). After SWE, there was a significantly increased diuresis in group 1 and 2. The excretion of NAG and beta2 M was also increased in both groups. These changes were significantly less pronounced in the selenium treated rats. CCr was higher in the selenium group than in the controls. No changes were observed in the sham treated group. These results demonstrate that selenium is able to ameliorate the damaging effects of high energy shock waves on renal tissue not only in vitro, but also in vivo.