Erythrocyte calcium influx is related to severity of ventricular arrhythmias in uraemic patients

Background. Myocardial disorders are a remarkable cause of morbidity and mo rtality in chronic haemodialysed patients (HD). They could be favoured by a lteration of cell Ca2+ handling. In previous studies we characterized an er ythrocyte Ca2+ influx, sensitive to membrane potential and inhibited by Ca2 + antagonists. Since its maximal influx rate was decreased in HD patients, this study investigates if Ca2+ influx alterations are related to myocardia l disorders in HD patients. Methods. Voltage-sensitive erythrocyte Ca2+ influx was measured in 30 healt hy controls and in 53 patients (47 HD patients and six patients with left v entricular hypertrophy and normal kidney function), using fura 2. In 29 HD patients and in six healthy subjects Ca2+ influx was also determined in the presence of parathyroid hormone (PTH) in vitro. Patients were classified a ccording to Lown's ventricular arrhythmias classification after 24-h Holter electrocardiograph (ECG) monitoring. Forty-six patients underwent echocard iography. Results. Voltage-sensitive erythrocyte Ca2+ influx was significantly reduce d in HD patients. Maximal influx rate was significantly higher in HD patien ts of Lown's classes 3 and 4 (0.789+/-0.156 nmol/s, n = 8; P < 0.01) than i n patients of classes 1 and 2 (0.499+/-0.055 nmol/s, n=15), or without vent ricular arrhythmias (0.400+/-0.041 nmol/s, n = 24). Maximal influx rate was directly correlated to left ventricular mass index (LVM) (r = 0.353, P < 0 .05). Subjects with left ventricular hypertrophy and normal kidney function displayed erythrocyte Ca2+ influx similar to that of normal subjects. Mult iple regression indicates that LVM and Ca2+ influx were independently relat ed to severity of arrhythmias. When added to the influx assay, PTH increase d the maximal influx rate only in patients with ventricular arrhythmias. Conclusion. Myocardial dysfunction and altered ventricular excitability cou ld be related in uraemic HD patients to alterations of calcium transport, a s found in the erythrocyte model. Reduced resistance to PTH could contribut e to this phenomenon.