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PO2-Dependent Glomerular Ultrafiltration of Middle-Weight Protein is Modified by Protective Amino Acids

  • Gernot Gronow
  • Miklós Mályusz
  • Norbert Klause
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 411)

Abstract

In vivo, hypoxia may reduce tubular transport activity in the kidney, leading to an increased diuresis and the urinary excretion of filtered protein (Maack, 1992). Whether hypoxic proteinuria originates exclusively from a reduced tubular reabsorption or, at least in part, from an altered glomerular permeability for plasma proteins remains unclear. Investigations on glomerular permeability at low oxygen tension are complicated in vivo by an increased sympathetic neuronal activity, accompanied by renal arterial vasoconstriction and a reduction of renal blood flow as well as of glomerular filtration rate (Bursaux et al., 1976). An isolated kidney preparation offers the advantage of a maintained perfusion flow rate even at extreme low oxygen tension (Gronow & Kossmann, 1985; Gronow et al., 1986; Mályusz & Gronow, 1987). An additional advantage of this preparation appears to be the observation that at extreme low oxygen tension lack of metabolic energy prevents tubular reabsorption of filtered protein (Park & Maack, 1984). Thus, under experimental conditions of extreme hypoxia, GFR-corrected alterations in urinary excretion of perfusate protein may represent changes in glomerular permeability.

Keywords

Glomerular Filtration Rate Tubular Reabsorption Amino Acid Mixture Filtration Fraction Brush Border Enzyme 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1997

Authors and Affiliations

  • Gernot Gronow
    • 1
  • Miklós Mályusz
    • 1
  • Norbert Klause
    • 2
  1. 1.Department of PhysiologyUniversity of KielKielGermany
  2. 2.Clinic of NephrologyUniversity of KielKielGermany

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