Review: Revisiting Randall’s plaque

Abstract

Kidney stones have probably affected mankind for ages with early reports in an Egyptian mummy. While prevalence of stone disease is increasing, its pathogenesis remains elusive. Randall, after his study on more than 1100 cadaver kidneys, gave hypothesis of subepithelial plaque acting as a nucleation site for kidney stones. His plaque hypothesis met with criticism because he proposed a unified theory for all types of stones. However, recently Randall’s plaque has been reinvestigated. This review discusses their role in stone formation and current understanding about their pathogenesis. Randall’s plaques begin in the basement membrane of thin segment of loop of Henle. Low urine volume, hypercalciuria, low urine pH are now implicated as important urinary risk factors. Plaque–stone association is best described in the idiopathic calcium oxalate stone formers. Pathogenesis of plaque itself involves interaction of multiple factors including gene polymorphism, oxidative stress, inflammatory mediators, matrix proteins, and urinary solute supersaturation.