Reabsorption of sodium in the proximal renal tubule in cirrhosis of the liver.
Proximal tubular reabsorption was examined in patients with liver cirrhosis and ascites by a variety of indirect methods. Maximal diluting ability, urine flow rate, and free water clearance were reduced. During frusemide administration V/ GFR was lower than in normal control subjects, indicating that proximal fractional reabsorption is enhanced in liver cirrhosis. This, by reducing Na delivery to the loop of Henle, impairs maximal urine osmolality. Mannitol, by reducing proximal reabsorption, restores availability of Na to the loop and urine concentrating ability during osmotic diuresis, whereas volume expansion with dextran was ineffective. This could be due to a persistent increase in renal vascular resistance preventing the rise in interstitial pressure responsible for driving fluid back into the proximal tubular lumen.[1]References
- Reabsorption of sodium in the proximal renal tubule in cirrhosis of the liver. Chiandussi, L., Bartoli, E., Arras, S. Gut (1978) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
