American Journal of Clinical Nutrition, Vol 31, 1615-1626, Copyright © 1978 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

The metabolism of human serum albumin in renal failure on conservative and dialysis therapy

R Bianchi, G Mariani, MG Toni and F Carmassi

The pathophysiology of albumin metabolism in uremia was investigated by turnover measurements in a large series of uremic patients, either on conservative management or on dialysis therapy. A total of 62 turnover studies were performed in patients on dietary treatment, divided into two groups according to the duration of the low protein diet: 35 subjects from 6 to 30 days, 27 subjects from 6 months to 5 years. Albumin catabolism and distribution were measured by the two-tracer technique (131I-albumin and 125I-iodide, simultaneously injected iv), while albumin synthesis was directly determined in 10 patients by the use of 14C-carbonate and 131I-albumin. Sixteen turnover studies were also performed in a group of end-stage uremics on dialysis therapy by a two-tracer procedure especially designed to determine albumin catabolism in the course of a single peritoneal or hemodialytic treatment. The main features of albumin metabolism observed in the patients on dietary management were: normal intravascular albumin mass, marked reduction of the extravascular and total albumin pools, with proportionally reduced catabolism. No significant turnover difference was found between the short-term diet group and the patients on low- protein diet from 6 months to 5 years. As to the uremics on dialysis therapy, catabolic rate of albumin was 3-fold increased in three patients showing clinical features of "hypercatabolism" in the early phase of uremia, or during relapse from it. Albumin turnover rate returned to normal when measured during clinical steady-state conditions. All these findings suggest that a marked body protein depletion exists in chronic uremia, and that dietary treatment per se is not responsible for such a depleted state. Instead, the depletion of protein stores observed in the steady phase of chronic uremia may have been originated by the exaggerated increased catabolism in the early phase of renal failure, not compensated by a proportional increase of the synthetic rate, due to both the state of uremic intoxication and to the reduced dietary protein intake during the early phase.