[Fluid, electrolyte, and acid-base disorders in liver cirrhosis].
The common disorders of fluid, electrolyte and acid-base metabolism observed in patients with liver cirrhosis are hyponatremia, hypokalemia, respiratory alkalosis, and metabolic acidosis, in addition to an excess accumulation of body fluids with edema and ascites formation. It has been suggested that an impaired renal sodium excretion in liver cirrhosis is caused by rather an increase in tubular sodium reabsorption than a decrease in glomerular filtration rate. In order to explain the pathophysiological mechanisms involved in initiating and maintaining sodium retention in cirrhosis, three hypotheses, namely, the "underfilling" hypothesis, the "overflow" hypothesis, and the "pepipheral arterial vasodilation" hypothesis have been proposed. However, neither of them could not fully account for the pathogenesis and pathophysiology of the avid renal sodium retention in cirrhosis. Although it is undoubted that the abnormal renal sodium handling in cirrhosis is mediated mainly by the sympathetic nervous system and the certain humoral agents such as renin-angiotensin-aldosterone system, atrial natriuretic peptide, prostaglandins, kallikein-kinin system, antidiuretic hormone and so on, the precise mechanism of the enhanced tubular sodium reapsorption induced via these factors is not well understood and still remains to be elucidated.
Kinouchi
T
T
Third Department of Medicine, Teikyo University School of Medicine.
D000137:Acid-Base Imbalance / Q000209:etiology*; D009320:Atrial Natriuretic Factor / Q000502:physiology; D006801:Humans; D007610:Kallikreins / Q000502:physiology; D007705:Kinins / Q000502:physiology; D008103:Liver Cirrhosis / Q000150:complications* / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology; D014883:Water-Electrolyte Imbalance / Q000209:etiology*
D007705:Kinins; D009320:Atrial Natriuretic Factor; D007610:Kallikreins