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Impaired free water excretion in child C cirrhosis and ascites: relations to distal tubular function and the vasopressin system

Authors

  • Aleksander Krag,

    1. Department of Gastroenterology, Copenhagen University Hospital Hvidovre, Faculty of Health Sciences, University of Copenhagen, Denmark
    2. Department of Clinical Physiology, Copenhagen University Hospital Hvidovre, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
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  • Søren Møller,

    1. Department of Clinical Physiology, Copenhagen University Hospital Hvidovre, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
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  • Erling B. Pedersen,

    1. Department of Medical Research, Holstebro Hospital, Holstebro, Denmark
    2. Department of Medicine, Holstebro Hospital, Holstebro, Denmark
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  • Jens H. Henriksen,

    1. Department of Clinical Physiology, Copenhagen University Hospital Hvidovre, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
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  • Niels-Henrik Holstein-Rathlou,

    1. Department of Biomedical Sciences,Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
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  • Flemming Bendtsen

    1. Department of Gastroenterology, Copenhagen University Hospital Hvidovre, Faculty of Health Sciences, University of Copenhagen, Denmark
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Correspondence
Aleksander Krag, MD, PhD Department of Gastroenterology 439, Copenhagen University Hospital Hvidovre DK-2650 Hvidovre, Denmark Tel:+45 3632 3182
Fax:+45 3632 3750
e-mail: aleksanderkrag@hotmail.com

Abstract

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 (inline image) 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 inline image (−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 inline image 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.

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