Derangements of renal water handling in liver disease.
It is apparent that renal water retention in patients with advanced liver disease constitutes a fascinating clinical constellation with numerous and diverse causes and an elusive pathophysiology. The dissociation between elevated AVP levels and the attendant changes in renal water handling under diverse experimental conditions, and the demonstration of an impairment in renal water excretion in response to prostaglandin synthetase inhibition, underscore the multifactorial nature of the derangement. It is likely that the development of impaired renal water handling is attributable to a panoply of several hormonal or neural mediators, or both, acting in concert. Additional insight into this fascinating problem must await further characterization of some of the mediators and a delineation of their pathophysiologic role.
D001834:Body Water / Q000378:metabolism; D002395:Catecholamines / Q000097:blood; D005919:Glomerular Filtration Rate; D006801:Humans; D007010:Hyponatremia / Q000209:etiology; D007668:Kidney / Q000294:innervation / Q000378:metabolism / Q000503:physiopathology*; D008103:Liver Cirrhosis / Q000503:physiopathology; D008107:Liver Diseases / Q000150:complications / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D011453:Prostaglandins / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014667:Vasopressins / Q000378:metabolism; D014883:Water-Electrolyte Imbalance / Q000209:etiology*
D002395:Catecholamines; D011453:Prostaglandins; D014667:Vasopressins