Abstract
Reactive oxygen species can promote the formation of kidney stones, and this process requires the participation of cells associated with the renal papilla. Here, we present a revised interpretation of the characteristics of the different types of renal papillary stones and the possible pathways responsible for their formation. We examined kidney stones from a biobank that contains 15,000 stones and identified five different types of papillary stones. Type I stones are calcium oxalate monohydrate (COM) stones that clearly have Randall's plaque but have no renal tubules near the stone-tissue junction. Type II stones are COM stones that have Randall's plaque and calcified renal tubules around the stone-tissue junction. Type III stones are calcium oxalate dihydrate (COD) stones that have a stone-tissue junction and calcified renal tubules. Type IV stones are COM stones containing important deposits of uric acid and/or Na or K urates that occur around stone-tissue junction, together with apatite phosphate, and may also contain bacterial imprints. Type V stones are small COM calculi that have no hydroxyapatite deposits at the stone-tissue junction. Oxidative stress of papillary tissues can generate heterogeneous nucleants that promote the crystallization of calcium phosphate and calcium oxalate, and urine composition determines the type of papillary stone ultimately develops. An active immune response can limit or prevent the development of these stones by eliminating the intra-tissue hydroxyapatite deposits or promoting the regeneration of the outer uroepithelium.