Abstract

Urinary supersaturation is important for crystallization and likely cause of stone formation on ductal plugs. Formation of idiopathic stones that develop on Randall’s plaques in the presence of low supersaturation is, however, dependent upon immunological responses of the kidneys. Experimental data suggests osteogenic and inflammatory processes playing pivotal role in plaque formation and its exposure to the pelvic urine which is necessary for stone development. Inflammatory and crystallization modulating molecules are released into the urine, becoming incorporated within the crystals and stones as organic matrix. Many of these molecules play roles in both inflammation and crystallization.

Highlights

  • Most idiopathic kidney stones are composed of an organic matrix and crystals of calcium oxalate (CaOx) mixed with small amounts of apatitic calcium phosphate (CaP)

  • We performed a number of light and electron microscopic studies of decalcified CaOx crystals and stones, both from stone patients and those produced experimentally in rats, to localize various matrix components

  • Ultrastructural studies of kidney stones, crystal deposits induced in experimental hyperoxaluric rats, as well as those produced in human urine in vitro, showed the presence of proteins, membranes and lipids in their matrices [37]

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Summary

Introduction

Most idiopathic kidney stones are composed of an organic matrix and crystals of calcium oxalate (CaOx) mixed with small amounts of apatitic calcium phosphate (CaP). Consensus is that these CaOx stones are formed in association with Randall’s plaques (RP) or Randall’s plugs (RPg) on the renal papillae [1,2,3]. The plaques are suburothelial deposits of hydroxyapatite and originate deep inside the papillary tissue, suggested to start in the basement membrane of the loops of Henle. This article explores the role of inflammation and injury in the pathogenesis of CaOx kidney stones with emphasis on the development of RPs and production of stone matrix contents

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