Pathogenesis of renal calculi

Kidney stones are a common entity, affecting approximately 5% of American women and 12% of American men. Recent reports have suggested that the prevalence of kidney stone disease is increasing [1]. Considerable advances have been made over the last 3 decades in the diagnosis and management of kidney stone disease, such as helical CT imaging, enhanced metabolic evaluation, and minimally invasive surgical therapies-shock wave lithotripsy (SWL), percutaneous nephrolithotomy (PNL), and ureteroscopy (URS). Advances in our understanding of the pathogenesis of renal calculi have not paralleled this progression in diagnosis and treatment, however. Although much is understood about the physical chemistry involved in nephrolithiasis, the inciting factor and sequence of events that lead to the formation of a kidney stone remains elusive. Significant research has been performed using animal models and cell culture experiments; however, it is unclear whether these outcomes are transferable to human kidney stone formers. Recent efforts to understand the pathogenesis of nephrolithiasis in humans have led to a delineation of the human surgical anatomy, histopathology, and metabolic factors in a variety of kidney stone formers [2-5]. This work has suggested that there are distinct stone phenotypes; and the cascade of events leading to kidney stone formation may be different, depending on this phenotype. This article reviews the current theories on the pathogenesis of renal calculi.