Renal retention of sodium in cirrhosis and fulminant hepatic failure

Abstract

Summary 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. In fulminant hepatic failure the site in the nephron of abnormal sodium retention appears to be predominantly the proximal tubule, but its cause is obscure.

Renin, aldosterone and renal haemodynamics in cirrhosis with ascites

“…Second, renin secretion in cirrhosis may be also mediated by the adrenergic system, since propranolol, a &blocking agent, markedly reduces plasma renin activity in patients with cirrhosis and ascites [24]. Another possibility, already suggested, is that renin release could be induced by a redistribution of blood flow withn the renal cortex [25]. It has been shown that there is more reninin the superficial than in the juxtamedullary nephrons [26-281; a redistribution of renal blood flow to the juxtamedullary nephrons could lead to ischaemia of the outer cortex, stimulating renin release without decreasing the total glomerular filtration rate or the renal plasma flow.…”

Importance of Plasma Aldosterone Concentration on the Natriuretic Effect of Spironolactone in Patients with Liver Cirrhosis and Ascites

“…which promotes per se increased sodium reabsorption at the proximal nephron level through aldosteroneindependent mechanisms [13].…”

Renal Sodium Handling in Cirrhosis: A Reappraisal

“…The traditional viewpoint held is that aldosterone is a major determinant of sodium reten tion [5,42,43]. Thus, several investigators have reported progressive loss of ascites in cirrhotic patients following adrenalectomy [18,29], Wilkinson el al.…”