Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle

TLDR

Our purpose is to test the hypothesis that Randall’s plaques arise in unique anatomical regions of the kidney, conditioned by specific stone‑forming pathophysiologies. We tested this hypothesis by performing intraoperative biopsies of plaques in kidneys of idiopathic‑calcium‑stone formers, patients with obesity‑related bypass‑procedure stones, and non‑stone formers, and found that plaque is specific to certain stone‑forming patients, initiating in thin‑limb basement membranes via mechanisms yet to be elucidated. Plaque originates in the basement membranes of thin loops of Henle and spreads through the interstitium to beneath the urothelium; bypass‑surgery patients form intratubular hydroxyapatite crystals in collecting ducts instead of plaque, and non‑stone formers do not form plaque.

Abstract

Our purpose here is to test the hypothesis that Randall’s plaques, calcium phosphate deposits in kidneys of patients with calcium renal stones, arise in unique anatomical regions of the kidney, their formation conditioned by specific stone-forming pathophysiologies. To test this hypothesis, we performed intraoperative biopsies of plaques in kidneys of idiopathic-calcium-stone formers and patients with stones due to obesity-related bypass procedures and obtained papillary specimens from non–stone formers after nephrectomy. Plaque originates in the basement membranes of the thin loops of Henle and spreads from there through the interstitium to beneath the urothelium. Patients who have undergone bypass surgery do not produce such plaque but instead form intratubular hydroxyapatite crystals in collecting ducts. Non–stone formers also do not form plaque. Plaque is specific to certain kinds of stone-forming patients and is initiated specifically in thin-limb basement membranes by mechanisms that remain to be elucidated.