Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: the effect of acute plasma expansion.
Twenty cirrhotic patients with ascites, divided into two groups of 10 each, according to their daily urinary sodium excretion (sodium retainers and sodium excretors) and given a diet of 75 mEq of sodium daily, underwent acute plasma volume expansion with 1,000 ml of 10% dextran in saline, infused through a catheter located in the right atrium. Even if a significant increase in sodium excretion was observed in both groups (p less than 0.001 in sodium excretors and p less than 0.05 in sodium retainers), plasma expansion did not reverse sodium retention in sodium retainers. A significant increase in creatinine clearance was found only in sodium retainers (p less than 0.02). Basal plasma renin activity and plasma aldosterone were elevated only in a few patients of both groups. The renin-angiotensin-aldosterone system was highly responsive to plasma expansion. Sodium retainers, who showed an ineffective natriuretic response after expansion, were able to suppress both plasma renin activity and plasma aldosterone in an analogous manner to the sodium-excreting group. This result lends strong support to the concept that the elevated aldosterone level in cirrhosis is not the major determinant of sodium retention. The kallikrein-kinin system was responsive to volume stimulus, since a decrease in kallikrein excretion was noted. It was significant in sodium retainers (p less than 0.05). Plasma PGE1,2 levels were significantly higher in sodium retainers than in controls. This may suggest that there is an activation of the intrarenal prostaglandin system, which could play a protective role against renal ischaemia. After volume expansion, PGE1,2 increased, but not significantly. Octopamine appeared unrelated to sodium excretion and unresponsive to volume stimulus. Endotoxins did not seem to be involved in renal sodium handling. Plasma volume expansion seemed effective in inducing a reduction of vasoconstrictor and sodium-retaining factors, such as the renin-angiotensin-aldosterone system. It is possible to suggest that volume expansion could increase PGE1,2. Plasma volume expansion produced different rates of sodium excretion in the two groups of patients and this suggests that impaired sodium handling in cirrhosis could, to some extent, be independent of effective plasma volume.
D005260:Female; D006801:Humans; D007610:Kallikreins / Q000652:urine; D007677:Kidney Function Tests; D008103:Liver Cirrhosis / Q000503:physiopathology* / Q000628:therapy / Q000652:urine; D008297:Male; D008875:Middle Aged; D009655:Octopamine / Q000097:blood; D010952:Plasma Substitutes / Q000008:administration & dosage*; D010953:Plasma Volume; D011188:Potassium / Q000652:urine; D011458:Prostaglandins E / Q000097:blood; D012084:Renin-Angiotensin System; D012964:Sodium / Q000652:urine*
D010952:Plasma Substitutes; D011458:Prostaglandins E; D009655:Octopamine; D012964:Sodium; D007610:Kallikreins; D011188:Potassium