Mg2+ transport in the kidney

Jun Ichi Satoh, Michael F Romero

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Magnesium is abundant in biological systems and an important divalent cation in the human body. Mg2+ helps mediate cellular energy metabolism, ribosomal and membrane integrity. Additionally Mg2+ modulates the activity of several membrane transport and signal transduction systems. Despite its importance however, little is known about the molecular mechanisms of Mg2+ transport and homeostasis in mammals. In mammals the amount of Mg2+ absorption is about the same as the amount of M2+ excretion in urine. Additionally, when total M2+ intake is deficient, the kidney is capable of reabsorbing all filtered Mg2+. This balance between intake and excretion indicates that the kidney plays a principal role in maintenance of total body Mg2+ homeostasis. Within the kidney, Mg2+ filtered by the glomerulus is handled in different ways along the nephron. About 10-20% of Mg2+ is reabsorbed by the proximal tubule, the bulk of Mg2+ (about 50-70%) is reabsorbed by the cortical thick ascending limb of the loop of Henle. In this region, Mg2+ moves across the epithelium through the paracellular pathway, driven by the positive lumenal transepithelial voltage. A recently cloned human gene, paracellin-1 was shown to encode a protein localized to the tight junctions of the cortical thick ascending limb and is thought to mediate Mg2+ transport via the paracellular space of this epithelium. The distal convoluted tubule reabsorbs the remaining 5-10% of filtered Mg2+. This segment seems to play an important role in determining final urinary excretion, since there is no evidence for significant Mg2+ absorption beyond the distal tubule. Although many renal Mg2+ transport activities have been characterized, no Mg2+ transporter cDNAs have been cloned from mammalian tissues. Recent research has certainly expanded our knowledge of Mg2+ transport in kidney; but details of the transport processes and the mechanisms by which they control Mg2+ excretion must await cloning of renal Mg2+ transporters and/or channels. Such information would provide new concepts in our understanding of renal Mg2+ handling.

Original languageEnglish (US)
Pages (from-to)285-295
Number of pages11
JournalBioMetals
Volume15
Issue number3
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

Mammals
kidneys
Membranes
Kidney
Signal transduction
Cloning
Divalent Cations
Biological systems
Magnesium
excretion
Complementary DNA
Genes
Positive ions
Tissue
Proteins
limbs (animal)
Electric potential
transporters
homeostasis
Homeostasis

Keywords

  • Cortical thick ascending limb of the loop of Henle
  • Distal convoluted tubule
  • Homeostasis
  • Kidney
  • Magnesium (Mg)
  • Mg transport
  • Paracellin-1 (PCLN-1)
  • Proximal tubule

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Mg2+ transport in the kidney. / Satoh, Jun Ichi; Romero, Michael F.

In: BioMetals, Vol. 15, No. 3, 2002, p. 285-295.

Research output: Contribution to journalArticle

Satoh, Jun Ichi ; Romero, Michael F. / Mg2+ transport in the kidney. In: BioMetals. 2002 ; Vol. 15, No. 3. pp. 285-295.
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