Premium
Impaired free water excretion in child C cirrhosis and ascites: relations to distal tubular function and the vasopressin system
Author(s) -
Krag Aleksander,
Møller Søren,
Pedersen Erling B.,
Henriksen Jens H.,
HolsteinRathlou NielsHenrik,
Bendtsen Flemming
Publication year - 2010
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2010.02319.x
Subject(s) - cirrhosis , ascites , free water clearance , vasopressin , renal function , medicine , endocrinology , excretion , gastroenterology
Background: Water retention in advanced cirrhosis and ascites may involve disturbances in renal distal tubular function and in the vasopressin system. Methods: Twelve patients with Child B cirrhosis and ascites were compared with 11 patients with Child C cirrhosis and ascites. The subjects were studied during a 400 ml/h oral water load. Results: Child C patients had a lower baseline glomerular filtration rate (32 vs 63 ml/min, P <0.001) and a lower urinary flow rate ( V u ) (0.86 vs 1.95 ml/min, P <0.001) than the Child B patients. However, the free water clearance () did not differ (−0.60 vs −0.21 ml/min, P =0.20). After the water loading, plasma vasopressin (AVP) decreased significantly in both the groups ( P <0.05). The Child B patients had increased V u (1.95–3.24 ml/min, P <0.001) and (−0.21–1.21 ml/min, P <0.01) and distal fractional water excretion (10.5 vs 0% in Child C, P =0.01) and aquaporin‐2 (AQP2) ( P <0.058) after water loading. In contrast, the Child C patients did not have increased V u and in response to the water and the decrease in AVP. Furthermore, the markers of distal tubular water regulation, AQP2 excretion and distal fractional water excretion, were unaltered. Conclusion: In Child C cirrhosis, ascites and mild hyponatraemia, there is an impaired ability to excrete solute‐free water. The patients are characterised by a low glomerular filtration rate, a low distal tubular flow and an inability to increase free water clearance during water loading. This may be related to a vasopressin‐independent production of AQP2.