THE RENAL LESIONS OF ELECTROLYTE IMBALANCE

TLDR

Nephrolithiasis in the kidney reproduces the classic sequence of calculus formation, migration, lodging, obstruction, and resultant localized hydronephrotic changes within the nephron. The study proposes adding a third form of urinary lithiasis—intranephric calculosis—to the classic bladder and renal pelvis categories. Magnesium depletion in rats produces PAS‑positive, calcium‑phosphate microliths in the thin limb of Henle that accrete into intranephric calculi with a Liesegang‑ring pattern.

Abstract

A dietary depletion of magnesium in rats leads to the production in the thin limb of Henle's loop of the nephrons of spherical microliths composed of a matrix of PAS-positive substances and calcium phosphate (3). These microliths grow by accretion to form intranephronic calculi. The classical pathological syndrome of clinical nephrolithiasis is thus reproduced within the nephron; to wit, the origin of the calculus at a certain level, local traumatic damage at the site of its origin, passage with the fluid flow down the urinary passages, lodgment of the calculus at some restricting point, obstruction of fluid flow and the usual consequent localized intrarenal "hydronephrotic" alterations of regressive atrophic cellular dysplasias within the nephron. To the classical description of the two forms of urinary lithiases occurring in the bladder and in the renal pelvis must therefore be added a third form, intranephronic calculosis. From the first origin of a microlith to its ultimate form as a calculus its organized structure is characterized by its matrix (PAS-positive materials) in which the periodic precipitation of crystalline mineral (Ca(++), PO(3) (---)) occurs in a pattern simulating Liesegang rings.