Little is known about the mechanisms and determining factors of shock wave-induced kidney trauma. After classification of the renal lesion in a canine model, we attempted to establish an ex vivo model using the isolated kidney of the pig perfused by Tyrode's solution under physiologic conditions. After shock wave application on the Modulith SL 20, vessel lesions were evaluated by microangiography to determine the size and frequency of dye extravasation in the different areas of the organ. Variation of the focus localization caused different patterns of lesions that characterized the pathway of the shock wave. In particular, constant petechial extravasation in the cortex was observed. The generator voltage correlated with the diameter and the frequency of the lesion area. The number of shock waves primarily affected the incidence of vessel rupture in the regions adjacent to the focal zone. Light microscopy revealed dose-dependent necrosis of tubular cells up to gap-like parenchymal defects. Even after application of the minimal shock wave doses, electron microscopy demonstrated vacuolization of tubular cells in the shock wave focus. Traumatic junctions between capillaries and the tubulur system can explain clinically observed macrohematuria without renal hematomas. With this model, it was possible to evaluate localization and dose dependence of shock wave-induced kidney trauma with high sensitivity and reproducibility. Further advantages of the model were easy availability and the fact that studies on living animals were not necessary. Therefore, standardization and comparison of different lithotripters becomes possible.

The aim of this investigation was the development of an easily reproducible model with which to evaluate shockwave-induced renal tissue damage using light and electron microscopy. Kidneys (n = 45) from freshly slaughtered pigs were perfused under physiologic conditions and treated with shockwaves at different doses (2-250 shockwaves; 12-20 kV) on the Modulith SL 20 lithotripter. The dose-dependent alterations in tissue structure were characterized by disintegration of tubular cells leading to circumscribed gap-like defects resulting from reticular fiber disruptions. Even after low shockwave doses, cellular and subcellular alterations could be observed. Our findings in this ex vivo model verify the development of considerable strictly localized, dose-dependent shockwave-induced damage of the renal parenchyma. On morphologic grounds, we cannot confirm a primary lesion or rupture of blood vessel walls as the cause of the shockwave lesions. The destruction of tubular cells in combination with disruption of peritubular and pericapillary reticular fiber coats results in capillarotubular leaks, which can explain even severe transitory macrohematuria after clinical shockwave lithotripsy without renal hematoma formation.

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