Pathogenesis of renal sodium handling in cirrhosis. A reappraisal.
In summary, it is apparent that renal sodium retention in patients with advanced liver disease constitutes a fascinating constellation with numerous and diverse causes and an elusive pathophysiology. The dissociation between hyperaldosteronism and the attendant changes in renal sodium handling and the demonstration of an impairment in natriuretic hormone release despite the absence of overt signs of sodium retention underscore the complete nature of the derangement. It is likely that the development of sodium retention necessitates the participation of several hormonal and/or neural effectors, acting in concert. Additional insight into this fascinating problem must await further biochemical characterization of some of the mediators and a delineation of their pathophysiological role.
D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications; D007610:Kallikreins / Q000502:physiology; D007668:Kidney / Q000503:physiopathology*; D007705:Kinins / Q000502:physiology; D008103:Liver Cirrhosis / Q000503:physiopathology*; D009318:Natriuresis; D011388:Prolactin / Q000502:physiology; D011458:Prostaglandins E / Q000502:physiology; D012964:Sodium / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000503:physiopathology
D007705:Kinins; D011458:Prostaglandins E; D011388:Prolactin; D012964:Sodium; D007610:Kallikreins