Epithelial Ca2+ and Mg2+ channels in kidney disease.
until further notice
SourceAdvances in Chronic Kidney Disease, 13, 2, (2006), pp. 110-7
Article / Letter to editor
Display more detailsDisplay less details
Advances in Chronic Kidney Disease
SubjectIGMD 9: Renal disorder; NCMLS 5: Membrane transport and intracellular motility; UMCN 5.4: Renal disorders
Many physiological functions rely on the precise maintenance of body calcium (Ca2+) and magnesium (Mg2+) balance, which is tightly regulated by the concerted actions of intestinal absorption, renal reabsorption, and exchange with bone. The kidney plays an important role in the homeostasis of divalent ions. Most Ca2+ and Mg2+ reabsorption occurs in the proximal tubules and the thick ascending limb of Henle's loop via a passive paracellular pathway. At the level of the distal convoluted tubule (DCT) and the connecting tubule (CNT), Ca2+ and Mg2+ are reabsorbed via an active transcellular route. Reabsorption of divalents in these latter segments is regulated in a Ca2+ and Mg2+-specific manner and determines the final excretion in the urine. Importantly, genetic studies, as well as molecular cloning strategies, recently identified epithelial ion channels as the gatekeepers of active Ca2+ and Mg2+ reabsorption. These channels are members of the transient receptor potential (TRP) superfamily. TRP vanilloid 5 (TRPV5) is responsible for the rate-limiting Ca2+ entry, and TRP melastatin 6 (TRPM6) constitutes the apical entry step in Mg2+ reabsorption. Dysregulation or malfunction of these influx pathways has been associated with renal Ca2+ and Mg2+ wasting. This review updates the current knowledge and the recent advances of Ca2+ and Mg2+ reabsorption and related disorders.
Upload full text
Use your RU credentials (u/z-number and password) to log in with SURFconext to upload a file for processing by the repository team.