[Cinacalcet in the management of normocalcaemic secondary hyperparathyroidism after kidney transplantation: one-year follow-up multicentre study]. / Cinacalcet en el manejo del hiperparatiroidismo secundario normocalcémico tras el trasplante renal: estudio multicéntrico de un año de seguimiento.

BACKGROUND: The effect of cinacalcet in patients with persistent secondary hyperparathyroidism (SHPT) after kidney transplantation (RT) has mainly been reported in patients with secondary hypercalcaemia. OBJECTIVES: Our objective was to assess the long-term effect of cinacalcet on patients with a RT and normocalcaemic SHPT. METHODS: A one-year multicentre, observational, retrospective study that included kidney recipients with SHPT (intact parathyroid hormone [iPTH] >120 pg/ml) and calcium levels within the normal range (8.4-10.2 mg/dl). Patients began treatment with cinacalcet in clinical practice. RESULTS: 32 patients with a mean age (standard deviation [SD]) of 54 (11) years, 56% male, were included in the study. Treatment with cinacalcet began a median of 16 months after RT (median dose of 30 mg/day). Levels of iPTH decreased from a median (P25, P75) of 364 (220, 531) pg/ml at the start of the study to 187 (98, 320) after 6 months (48.6% reduction, P=.001) and to 145 (91, 195) after 12 months (60.2% reduction, P=.001), without there being changes in calcium and phosphorus levels (P=.214 and P=.216, respectively). No changes were observed in kidney function or anti-calcineuric drug levels. 3.1% of patients discontinued cinacalcet due to intolerance and 6.2% due to a lack of efficacy. CONCLUSIONS: In patients with normocalcaemic SHPT after RT, cinacalcet improves the control of serum PTH values without causing changes to calcaemia, phosphataemia or kidney function. Cinacalcet showed good tolerability.

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

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.