Lithotripter SWs rupture blood vessels in the kidney. This acute trauma, accompanied by a fall in renal function, can lead to significant long‐term effects such as profound scarring of the kidney cortex and renal papillaea permanent loss of functional renal mass. SWL has been linked to new‐onset hypertension in some patients, and recent studies suggest that multiple lithotripsies can actually alter a patient’s stone disease leading to formation of stones (brushite) that are harder to break. Cavitation and shear appear to play a role in stone breakage and tissue damage. Progress in understanding these mechanisms, and the renal response to SWs, has led to practical strategies to improve treatment. Slowing the SW‐rate, or initiating treatment at low kV/power both improve stone breakage and reduce the number of potentially tissue‐damaging SWs needed to achieve comminution. The observation that SWs cause transient vasoconstriction in the kidney has led to studies in pigs showing that a pre‐conditioning dose of low‐energy SWs significantly reduces trauma from subsequent high‐energy SWs. Thus, SWs can induce adverse effects in the kidney, but what we have learned about the mechanisms of SW action suggests strategies that could make lithotripsy safer and more effective. [Work supported by NIH‐DK43881, DK55674.]