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Aquaporin‐1 and aquaporin‐2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome
Author(s) -
EstevaFont Christina,
Baccaro Maria E.,
FernándezLlama Patricia,
Sans Laia,
Guevara Monica,
Ars Elisabet,
Jiménez Wladimiro,
Arroyo Vicente,
Ballarín Jose A.,
Ginès Pere
Publication year - 2006
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.21414
Subject(s) - cirrhosis , ascites , hepatorenal syndrome , hyponatremia , medicine , endocrinology , excretion , urinary system , gastroenterology
Several experimental models of cirrhosis have shown dysregulation of renal aquaporins in different phases of liver disease. We investigated the urinary excretion of both aquaporin‐1 and aquaporin‐2 in patients with cirrhosis at different stages of the disease. Twenty‐four‐hour urine was collected from 11 healthy volunteers, 13 patients with compensated cirrhosis (without ascites), and 20 patients with decompensated cirrhosis (11 with ascites without renal failure and 9 with hepatorenal syndrome). Aquaporin‐1 and aquaporin‐2 excretion was analyzed by immunoblotting. Urinary aquaporin‐2 excretion was reduced in patients with cirrhosis compared to healthy subjects. A progressive decrease in urinary aquaporin‐2 excretion was observed as the severity of cirrhosis increased, from compensated cirrhosis to cirrhosis with ascites and hepatorenal syndrome. Patients with hyponatremia had lower urinary aquaporin‐2 excretion than patients without hyponatremia. Vasopressin plasma level did not correlate with aquaporin‐2 excretion. There were no differences between healthy subjects and patients with cirrhosis with or without ascites in urinary excretion of aquaporin‐1, but urinary aquaporin‐1 excretion of those with hepatorenal syndrome was extremely low. In conclusion , patients with cirrhosis appear to exhibit a decreased abundance of renal aquaporin‐2 and therefore lower water permeability in the collecting tubules. This may represent an adaptive renal response to sodium retention, with expansion of extracellular fluid volume and dilutional hyponatremia observed in those who have cirrhosis with ascites. Finally, aquaporin‐1 does not appear to play a role in the progressive dysregulation of extracellular fluid volume in cirrhosis. (H EPATOLOGY 2006;44:1555–1563.)