Mechanisms of malnutrition in uremia

Loss of lean body mass is common in chronic renal failure and may adversely affect morbidity and mortality of patients. The pathogenesis of protein wasting in chronic renal failure is multifactorial and is reviewed by the authors. When protein kinetics are determined in patients with uncomplicated uremic on conservative treatment by isotopically labeled amino acids, the results indicate that the rates of both protein synthesis and degradation are decreased both at whole body and skeletal muscle levels. On the other hand, if a complication is superimposed (ie, acidosis or infection), protein turnover accelerates, primarily because of proteolysis increase. Therapeutical implications are analyzed in this article. Recently, a cytokine-induced chronic inflammatory response has been proposed to explain the progressive protein loss often observed in these patients even in the absence of complications. Cytokine concentrations often have been found to be increased in both dialyzed and undialyzed chronically uremic patients. Tumor necrosis factor (TNF)-alpha clearance is reduced in uremia because this cytokine is catabolized and excreted mainly by the kidneys. In addition, we found that gene expression for TNF-alpha in circulating blood cells is enhanced in chronically uremic patients, suggesting that an activation of the systemic inflammatory response may contribute to the metabolic, vascular, and immune complications of this disease.