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An Overview of Divalent Cation and Citrate Handling by the Kidney

An Overview of Divalent Cation and Citrate Handling by the Kidney Urinary calcium, magnesium and citrate levels are important in promoting or inhibiting renal stone formation. Here we review current information on the tubular handling of these ions. Most filtered calcium is reabsorbed in the proximal tubule and the thick ascending limb (TAL) of the loop of Henle, largely paracellularly; most of the remainder is reabsorbed in the distal tubule, transcellularly. Calcium reabsorption in the TAL and distal tubule is stimulated by parathyroid hormone and vitamin D; other factors influencing its renal handling include extracellular volume status and acid-base balance. Little filtered magnesium is reabsorbed in the proximal tubule; the bulk is reabsorbed paracellularly in the TAL, while most of the remainder is reabsorbed transcellularly in the distal tubule. Dietary intake, peptide hormones and chronic potassium depletion can all influence magnesium reabsorption in the TAL and distal tubule. Most filtered citrate is taken up across the apical membrane of the proximal tubule via a sodium-dicarboxylate co-transporter (NaDC-1). It also enters proximal tubular cells across the basolateral membrane; citrate contributes to the cells’ oxidative metabolism. Citrate excretion is affected by acid-base balance, acetazolamide treatment, chronic potassium depletion and urinary excretion of calcium and magnesium. Where possible, we have indicated the mechanisms of these complex interactions. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nephron Physiology Karger

An Overview of Divalent Cation and Citrate Handling by the Kidney

Unwin, R.J.; Capasso, G.; Shirley, D.G.
Nephron Physiology , Volume 98 (2): 6 – Oct 1, 2004
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References (25)

Publisher
Karger
Copyright
© 2004 S. Karger AG, Basel
eISSN
1660-2137
DOI
10.1159/000080259
Publisher site
See Article on Publisher Site

Abstract

Urinary calcium, magnesium and citrate levels are important in promoting or inhibiting renal stone formation. Here we review current information on the tubular handling of these ions. Most filtered calcium is reabsorbed in the proximal tubule and the thick ascending limb (TAL) of the loop of Henle, largely paracellularly; most of the remainder is reabsorbed in the distal tubule, transcellularly. Calcium reabsorption in the TAL and distal tubule is stimulated by parathyroid hormone and vitamin D; other factors influencing its renal handling include extracellular volume status and acid-base balance. Little filtered magnesium is reabsorbed in the proximal tubule; the bulk is reabsorbed paracellularly in the TAL, while most of the remainder is reabsorbed transcellularly in the distal tubule. Dietary intake, peptide hormones and chronic potassium depletion can all influence magnesium reabsorption in the TAL and distal tubule. Most filtered citrate is taken up across the apical membrane of the proximal tubule via a sodium-dicarboxylate co-transporter (NaDC-1). It also enters proximal tubular cells across the basolateral membrane; citrate contributes to the cells’ oxidative metabolism. Citrate excretion is affected by acid-base balance, acetazolamide treatment, chronic potassium depletion and urinary excretion of calcium and magnesium. Where possible, we have indicated the mechanisms of these complex interactions.

Journal

Nephron Physiology – Karger

Published: Oct 1, 2004

Keywords: Renal stones; Calcium; Magnesium; Citrate

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