Impaired free water excretion in child C cirrhosis and ascites: relations to distal tubular function and the vasopressin system
Article first published online: 20 AUG 2010
© 2010 John Wiley & Sons A/S
Volume 30, Issue 9, pages 1364–1370, October 2010
How to Cite
Krag, A., Møller, S., Pedersen, E. B., Henriksen, J. H., Holstein-Rathlou, N.-H. and Bendtsen, F. (2010), Impaired free water excretion in child C cirrhosis and ascites: relations to distal tubular function and the vasopressin system. Liver International, 30: 1364–1370. doi: 10.1111/j.1478-3231.2010.02319.x
- Issue published online: 1 SEP 2010
- Article first published online: 20 AUG 2010
- Received 24 May 2010Accepted 23 July 2010
- aquaporin 2;
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 (Vu) (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 Vu (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 Vu 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.