Skeletal muscle mitochondrial function is preserved in young patients with chronic renal failure.

Abstract

Patients with chronic renal failure (CRF) show limited exercise tolerance, classically attributed to anemia. However, persistence of abnormally low peak oxygen consumption, even after restoration of hemoglobin concentration with recombinant erythropoietin therapy and studies of muscle bioenergetics, suggests that the problem is located beyond hemoglobin oxygen transport. The present study is designed to assess mitochondrial respiratory chain (MRC) function from skeletal muscle of patients with CRF to determine whether there is impairment in mitochondrial oxidative capacity. We studied six young patients with CRF on regular hemodialysis and erythropoietin therapy and six healthy controls matched by age, sex, anthropometric characteristics, and physical activity. Muscle biopsy of the quadriceps was performed, and mitochondria were isolated. Mitochondrial content was estimated by means of mitochondrial yield and citrate synthase activity. Maximal capacity for oxygen consumption was measured polarographically using complex I, II, III, and IV substrates of the MRC. Individual enzyme activities of MRC complexes I to V were determined spectrophotometrically. Membrane lipid peroxidation was estimated by cis-parinaric fluorescence. Compared with controls, patients with CRF showed preserved mitochondrial content, conserved respiratory activity, intact enzyme activity of MRC complexes, and no increase in lipid peroxidation. We therefore conclude that mitochondrial function is preserved in young patients with CRF.