Loss of protein stores, reflected by negative nitrogen balance and accelerated accumulation if nitrogenous breakdown products, is an important factor in the morbidity of chronic renal failure and the high mortality rate of acute renal failure. Low protein intake intensifies the suppressed protein synthesis that results from impaired insulin-stimulated protein anabolism. The metabolic acidosis of uremia contributes to tissue loss, both by increasing muscle protein degradation, and by raising the requirements for essential amino acids. Correcting metabolic acidosis improves the nitrogen balance and reduces tissue wasting. It is important to ensure adequate nutrient intakes, rather than the low protein diet often prescribed to slow loss of renal function.