Calcium as a Mediator of Renal Tubule Cell Injury

Abstract

T HE POTENTIAL for alterations in cellular calcium metabolism to play a role in cell injury and death has long been recognized because of the occurrence of elevated levels of calcium in tissues containing necrotic cells; however. understanding of the pathogenetic role of calcium in cell injury has increased substantially with improved understanding of the cellular physiology of intracellular calcium metabolism during the past three decades. Despite wide recognition of the occurrence of nephrocalcinosis in a number of clinical settings and of renal calcification after renal cortical necrosis, experimental investigation of the pathogenetic role of calcium in cell injury in the kidney has lagged somewhat behind similar studies of cell injury in the heart and liver. However, information is becoming increasingly available. This review will concentrate on several major areas pertaining to the role of calcium as a mediator of cell injury in the kidney: (1) a quantitative summary of the distribution of calcium within the intracellular compartments of the renal tubular cell, and the relationships between these compartments and the extracellular space, (2) mechanisms and sites of action of calcium to promote cell injury at the subcellular level, and (3) the major focus of this review, the available data on the role of calcium during in vivo models of injury in the kidney. Several other recent reviews of the role of calcium in cell injury may also be of interest to the reader. 1-3