Shock wave induced kidney injury promotes calcium oxalate deposition

Extracorporeal shock wave lithotripsy is the preferred treatment for upper urinary tract renal calculi. However, this treatment is associated with a high rate of recurrent renal calculi. Shock wave therapy can result in renal epithelial cell injury, which in turn is a most important factor in calculus formation. We investigated the influence of kidney damage secondary to shock waves on Ca oxalate crystal retention in the kidney.

A total of 32 rats were randomly divided into 4 groups, including group 1--controls, group 2--sham treated rats given 25 ml 0.75% ethylene glycol per day for 14 days, group 3--rats given 15 kV 1 Hz shock waves 500 times to the left kidney, followed by 25 ml 0.75% ethylene glycol daily for 14 days, and group 4--rats with the same treatment as group 3 except the number of impacts was increased to 1,000. The 2 kidneys were removed at the end of the experiment. Ca oxalate crystals were observed by surgical microscopy in kidney sections stained with hematoxylin and eosin. Crystal morphology was determined using polarizing microscopy. Acidified kidney tissue homogenate was examined for Ca and oxalate content by colorimetry (Sigma).

Kidney sections showed that kidneys that did not receive shock waves had fewer crystals than kidneys with shock waves, which had crystals in major areas. In the left kidney in groups 2 to 4 the mean +/- SD quantity of Ca was 16.88 +/- 6.41, 28.58 +/- 7.54 and 40.81 +/- 15.29 micromol/gm wet kidney and the mean quantity of oxalate was 8.44 +/- 6.80, 20.52 +/- 7.70, 31.76 +/- 14.14 micromol/gm wet kidney, respectively. Ca oxalate density increased with the number of shock wave impacts.

Kidney damage caused by shock wave treatment can increase Ca oxalate crystal retention in the kidneys of rats in this stone model.