Factors influencing serum albumin in dialysis patients

Abstract

Hypoalbuminemia is a major risk factor for morbidity and mortality in dialysis patients. The proximate cause of hypoalbuminemia is probably responsible for these events, and not the hypoalbuminemia itself. Because protein-calorie malnutrition decreases albumin synthesis, hypoalbuminemia has been attributed to poor nutritional intake resulting from underdialysis. However, serum albumin (Salb) level is determined by several other factors: plasma volume expansion, albumin redistribution, exogenous loss, increased fractional catabolic rate (FCR), and decreased synthesis. Decreased albumin synthesis is primarily responsible for hypoalbuminemia in hemodialysis (HD) patients. Studies of a smaller number of peritoneal dialysis (PD) patients suggest exogenous albumin loss and volume expansion as contributing mechanisms. However, both malnutrition and inflammation suppress albumin synthesis. As the adequacy of dialysis has improved, recent studies are unable to show any relation between dialysis adequacy and Salb level. Further, Salb level appears to be a poor marker of nutritional status in dialysis patients when compared with other measures of nutrition, such as subjective global assessment score, anthropometry, and dietary intake. Instead, cytokines and positive acute-phase reactants, produced in response to inflammation, have been identified as important contributors to hypoalbuminemia in dialysis patients. These markers correlate with hypoalbuminemia and supercede Salb level in predicting mortality. Multivariate analysis identifies markers of inflammation and nutritional status as independent predictors of hypoalbuminemia in HD patients and markers of inflammation and peritoneal albumin loss as independent predictors in PD patients. However, the acute-phase response and malnutrition are closely interrelated, because inflammatory mediators also suppress appetite, increase muscle catabolism, and result in progressive cachexia. Future studies should focus on elucidating the inflammatory stimuli and the complex interaction between the acute-phase response and nutritional status. (Am J Kidney Dis 1998 Dec;32(6 Suppl 4):S118-25)