Urinary prostaglandin E2 excretion, sodium retention, and diuretic responsiveness in patients with chronic liver disease.
It has been postulated that diminished renal prostaglandin E2 (PGE2) production, whether basal or in response to stimulation by diuretic treatment, determines the intensity of sodium retention in cirrhosis. Urinary PGE2 excretion (as an index of renal PGE2 production) as well as urine volume, urinary sodium and potassium excretion, and creatinine clearance were examined in 19 patients with cirrhosis and either no ascites, diuretic-responsive ascites, or diuretic-resistant ascites. Measurements were made both before (all patients) and after (ascitic patients) stimulation of renal PGE2 synthesis by 80 mg of furosemide intravenously. Urinary PGE2 excretion was similar in the three groups both before and after furosemide. Baseline urine volume and creatinine clearance were similar in all groups but were significantly less after furosemide in patients with diuretic-resistant ascites as compared to the other two groups. The natriuretic response to intravenous furosemide was significantly less in patients with diuretic-resistant ascites. Insertion of the peritoneovenous shunt to aid in the management of diuretic-resistant ascites resulted in a marked, immediate increase in urine volume and urinary PGE2 excretion in the four patients who were serially evaluated, but natriuresis occurred in only two. Overall, urinary PGE2 excretion correlated with urine volume but not with sodium excretion or creatinine clearance. Diminished renal PGE2 production, as reflected by urinary PGE2 excretion, does not appear to be a determinant of the severity of renal sodium retention in cirrhosis.[1]References
- Urinary prostaglandin E2 excretion, sodium retention, and diuretic responsiveness in patients with chronic liver disease. Rector, W.G. Am. J. Gastroenterol. (1987) [Pubmed]
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