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PubMed1977

Complications of diuresis in the alcoholic patient with ascites: a controlled trial.

Forty-three patients with decompensated alcoholic liver disease and ascites of recent onset were randomized to salt and water restriction alone (control group) or to salt and water restriction plus diuretics (diuresis group). The two treatment groups were comparable in clinical findings and laboratory results. Seven patients in the control group and 5 patients in the diuresis group died during the acute illness. Weight loss was more marked and the disappearance of ascites more common in those given diuretics. A modest decrease in serum sodium and increase in serum potassium, and readily reversible elevations of blood urea nitrogen were noted in the diuresis group. Eight patients in each treatment group developed either the hepatorenal syndrome, marked electrolyte abnormalities, or encephalopathy. Diuresis can be accomplished in these critically ill patients without serious complications that can be attributed to the diuretic treatment.

Alcoholism↗
PubMed1983

Response of the kidney to furosemide. I. Effects of salt intake and renal compensation.

We investigated the effects of varying salt intake on five factors that could affect sodium balance during furosemide (F) administration: the quantity of F reaching the renal tubules; the magnitude of the acute natriuresis; Na+ excretion in the period after the acute diuresis; diuretic tolerance; and changes in plasma aldosterone. Six normal subjects were given F (40 mg day-1) for 3 days after equilibration to Na+ intakes of 20 mmol day-1 (low salt, LS) and 270 mmol day-1 (high salt, HS). Salt intake did not modify F excretion. Salt restriction reduced the short-term natriuretic response to F, led to diuretic tolerance, and potentiated the F-induced rise in plasma aldosterone. There was a progressive diminution in the quantity of Na+ excreted per unit of F excreted during LS. In spite of this, cumulative Na+ balance was negative only during LS because of a compensatory increase in Na+ reabsorption in the period between diuretic doses. During HS, this compensation exactly matched the short-term loss of Na+ produced by F, leading to neutral Na+ balance. During LS, the acute natriuresis exceeded the daily Na+ intake, so that, despite the renal compensation, Na+ balance was negative. In conclusion, salt restriction impairs the short-term natriuretic response to F and leads to diuretic tolerance. However, homeostatic mechanisms activated by the diuretic can maintain Na+ balance even in subjects without a disease causing Na+ retention, unless dietary salt is restricted.

Adult↗
PubMed1950

[Diuretics].

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Diuresis↗