Skip to main content
Article thumbnail
Location of Repository

Renal retention of sodium in cirrhosis and fulminant hepatic failure

By S. P. Wilkinson, A. Alam, Helen Moodie and Roger Williams

Abstract

Abnormal renal retention of sodium is a characteristic finding in both cirrhosis and fulminant hepatic failure. In cirrhosis the pathogenesis varies according to the level of renal perfusion. When this is normal, hyperaldosteronism is probably the most important factor and this results from an increased release of renin by the kidney. The stimulus to the latter may be a shunting of blood from the outer cortical to juxtamedullary nephrons, although there is no direct relationship between the changes in intrarenal blood flow distribution and sodium excretion. The patients with hyperaldosteronism fail to escape from its sodium retaining effects because of impaired production of natriuretic hormone, which in turn is the result of a failure to expand the ‘effective’ extracellular fluid volume, because of ascites formation

Topics: Renal and Electrolyte Disorders in Liver Disease
OAI identifier: oai:pubmedcentral.nih.gov:2496257
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)
  • Suggested articles


    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.