Liver metabolism in CRF.

Alteration in liver function are not typically present in patients with uremic syndrome, but varying degrees of liver dysfunction were observed in animals with experimental uremia and, to a lesser degree, in patients with chronic renal failure. This article summarizes the data obtained during the last 2 decades on protein, carbohydrate, and lipid metabolism by the liver in uremia and molecular aspects of regulation of lipids and protein synthesis. Particular attention is given to the role of cytosolic calcium ([Ca(2+)](i)) regulation and calcium signal transduction in hepatocytes in chronic renal failure. It is proposed that the parathyroid hormone (PTH)-mediated increase in the [Ca(2+)](i) of hepatocytes in chronic renal failure is a major signal for the downregulation of hepatic receptors for PTH-PTHrP, vasopressin and angiotensin II as well as as hepatic lipase. It is possible that the mRNA of other hormone receptors and various proteins of the liver cells are affected similarly by the elevated basal levels of [Ca(2+)](i) in CRF.