[Molecular physiology and pathophysiology of renal phosphate excretion].
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.
Murer
H
H
Physiologisches Institut der Universität Zürich. murer@physiol.unizh.ch
Biber
J
J
D000818:Animals; D001692:Biological Transport; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D007668:Kidney / Q000737:chemistry / Q000378:metabolism / Q000502:physiology* / Q000503:physiopathology*; D050608:Sodium-Phosphate Cotransporter Proteins; D027981:Symporters
D002352:Carrier Proteins; D050608:Sodium-Phosphate Cotransporter Proteins; D027981:Symporters
Molekulare Physiologie und Pathophysiologie der renalen Phosphat-Ausscheidung.