Metabolic acidosis and protein catabolism: mechanisms and clinical implications.
Metabolic acidosis increases protein degradation resulting in muscle wasting and a negative nitrogen balance. The branched-chain amino acids serve as useful markers of these changes and their catabolism is increased in acidosis, particularly for the spontaneous acidosis associated with renal failure. As a result, the neutral nitrogen balance is compromised and malnutrition results. Glucocorticoids mediate these changes through the recently discovered ATP-dependent ubiquitin-proteasome pathway. Therapy necessitates correction of the underlying acidosis either through adjustment of the alkalinity of the dialysate for the patient on dialysis or through dietary protein restriction and sodium bicarbonate supplements for the predialysis patient.
Bailey
J L
JL
Renal Division, Emory University School of Medicine, Atlanta, GA 30322, USA.
D000138:Acidosis / Q000209:etiology / Q000378:metabolism* / Q000628:therapy; D000597:Amino Acids, Branched-Chain / Q000378:metabolism; D004044:Dietary Proteins / Q000008:administration & dosage; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications; D009124:Muscle Proteins / Q000378:metabolism; D011506:Proteins / Q000378:metabolism*; D017693:Sodium Bicarbonate / Q000627:therapeutic use; D014452:Ubiquitins / Q000502:physiology
D000597:Amino Acids, Branched-Chain; D004044:Dietary Proteins; D009124:Muscle Proteins; D011506:Proteins; D014452:Ubiquitins; D017693:Sodium Bicarbonate