title: Natriuretic hormone activity in the urine of cirrhotic patients.
abstract: The ability of urine extracts to inhibit sodium and potassium-activated ATPase, cross-react with antidigoxin antibodies and induce natriuresis in rats was investigated in 10 healthy subjects, 10 cirrhotic patients without ascites (compensated cirrhotics), 27 nonazotemic cirrhotic patients with ascites and 10 cirrhotic patients with ascites and functional renal failure to assess whether reduced activity of natriuretic hormone contributes to sodium retention in cirrhosis. No significant differences were seen between healthy subjects and compensated cirrhotic patients in any of these parameters (sodium and potassium-activated ATPase inhibition = 178.5 +/- 19.8 vs. 247.4 +/- 48.7 nmol equivalent of ouabain/day; digoxinlike activity = 43.9 +/- 6.1 vs. 48.0 +/- 5.6 ng equivalent of digoxin/day; natriuretic activity = 0.36 +/- 0.15 vs. 0.63 +/- 0.27 mumol/min). Cirrhotic patients with ascites with and without functional renal failure showed significantly higher values of sodium and potassium-activated ATPase inhibition (708.1 +/- 94.0 and 529.2 +/- 53.9 nmol equivalent of ouabain/day, respectively), digoxinlike activity (136.9 +/- 7.2 and 116.3 +/- 7.9 ng equivalent of digoxin/day) and natriuretic activity (1.78 +/- 0.48 and 1.93 +/- 0.37 mumol/min) than healthy subjects and compensated cirrhotic patients. We saw no significant differences between these two groups of cirrhotic patients with ascites with respect to these parameters. In the cirrhotic patients studied, sodium and potassium-activated ATPase inhibition and antidigoxin antibodies directly correlated with the degree of impairment of hepatic and renal function, plasma renin activity and plasma levels of aldosterone and norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Clinica Medica II, University of Florence School of Medicine, Italy.
authors.forename: G
authors.initials: G
authors.lastname: La Villa
authors.forename: M
authors.initials: M
authors.lastname: Asbert
authors.forename: W
authors.initials: W
authors.lastname: Jiménez
authors.forename: P
authors.initials: P
authors.lastname: Ginés
authors.forename: J
authors.initials: J
authors.lastname: Claria
authors.forename: C
authors.initials: C
authors.lastname: López
authors.forename: R
authors.initials: R
authors.lastname: Planas
authors.forename: J
authors.initials: J
authors.lastname: Llach
authors.forename: J
authors.initials: J
authors.lastname: Gaya
authors.forename: F
authors.initials: F
authors.lastname: Rivera
mesh_terms: D000328:Adult; D000818:Animals; D000906:Antibodies / Q000032:analysis; D001201:Ascites / Q000652:urine; D001681:Biological Assay / Q000379:methods; D004077:Digoxin / Q000276:immunology; D005260:Female; D006801:Humans; D006975:Hypertension, Portal / Q000652:urine; D007668:Kidney / Q000378:metabolism; D008103:Liver Cirrhosis / Q000652:urine*; D008297:Male; D008875:Middle Aged; D009318:Natriuresis / Q000187:drug effects; D045283:Natriuretic Agents / Q000494:pharmacology / Q000652:urine*; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D012982:Sodium, Dietary / Q000008:administration & dosage; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
chemical_list: D000906:Antibodies; D045283:Natriuretic Agents; D012982:Sodium, Dietary; D004077:Digoxin; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase