[Molecular physiology and pathophysiology of renal phosphate excretion]

Schweiz Med Wochenschr. 1998 Aug 22;128(34):1247-52.
[Article in German]

Abstract

The kidney is a key organ in phosphate homeostasis. Phosphate excretion is largely determined by free glomerular filtration and by regulated reabsorption in the proximal tubule. The cellular/molecular mechanisms involved in phosphate reabsorption have been elucidated in great detail over the past few years. A brush border membrane protein with most probably 8 membrane-spanning regions represents the rate-limiting and physiologically/pathophysiologically modified transport mechanism. Altered phosphate reabsorption correlates with an altered brush border membrane transporter protein content, altered either by new synthesis/membrane insertion or by membrane retrieval/degradation. Current knowledge on the molecular/cellular level is a prerequisite for an understanding of kidney based alterations in phosphate homoeostasis.

Publication types

  • Review

MeSH terms

  • Animals
  • Biological Transport
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Carrier Proteins / physiology*
  • Humans
  • Kidney / chemistry
  • Kidney / metabolism
  • Kidney / physiology*
  • Kidney / physiopathology*
  • Sodium-Phosphate Cotransporter Proteins
  • Symporters*

Substances

  • Carrier Proteins
  • Sodium-Phosphate Cotransporter Proteins
  • Symporters