Cumulative renal damage in dogs by repeated treatment with extracorporeal shock waves.
BACKGROUND
Extracorporeal shock wave lithotripsy (ESWL) has become a routine method for the treatment of renal and ureteral calculi. Occasionally, multisequential ESWL treatments and high energy shock waves are required to treat large calculi. The purpose of the study was to compare renal histopathologic damage caused by varying the application of shock waves.


METHODS
Six groups of dogs were defined by the frequency of shocks, application time and numbers of sessions. Bilateral nephrectomies were performed immediately, 3, 7 and 60 days after the application of shock waves. Histopathologic features of the kidneys were assessed by both light and electron microscopy.


RESULTS
Irreversible damage was observed in all exposed kidneys. After a single session of low application frequency, damage by shock waves occurred with progressive deterioration of the nephron. At any frequency rate, the damage was caused by tissue hypoxia due to rupturing of the interstitial capillaries. As the application frequency increased, capillary rupture became more severe, and consequently, morphological damage tended to be more intense. Repeated sessions at any application frequency made the damage more intense, suggesting that an accumulation of damage had occurred.


CONCLUSIONS
Minimal doses of shock waves cause renal damage and repeated ESWL sessions may result in an accumulation of damage. Considering that the damage is dose-dependent, divided ESWL treatments at a low frequency rate are advisable in a clinical setting.
Koga
H
H
Department of Urology, Kurume University School of Medicine, Japan.
Matsuoka
K
K
Noda
S
S
Yamashita
T
T
D000818:Animals; D001485:Basement Membrane / Q000473:pathology / Q000648:ultrastructure; D004285:Dogs; D004487:Edema / Q000209:etiology; D004727:Endothelium / Q000473:pathology / Q000648:ultrastructure; D004848:Epithelium / Q000473:pathology / Q000648:ultrastructure; D005355:Fibrosis / Q000209:etiology; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology / Q000473:pathology; D006470:Hemorrhage / Q000209:etiology; D007249:Inflammation; D007668:Kidney / Q000098:blood supply / Q000473:pathology* / Q000648:ultrastructure; D007683:Kidney Tubular Necrosis, Acute / Q000209:etiology; D008096:Lithotripsy / Q000009:adverse effects*; D008297:Male; D008854:Microscopy, Electron; D015388:Organelles / Q000473:pathology / Q000648:ultrastructure; D013997:Time Factors