[The mechanisms of the disorder of calcium homeostasis in terminal kidney failure and the allotransplantation of a cadaver kidney].

Overall 34 patients with terminal renal failure (TRF) and 81 recipients of the allotransplanted cadaveric kidney (ACK) were examined. It has been established in in-vitro experiments with modulated by additions of EDTA to the plasma and CaCl2 hypo- and hypercalcemia that the magnitude of bound calcium (standardized at the concentration of ionized calcium-Ca++1 mmol/l) decreased in the blood plasma in 65 and 61% of cases. Besides protein-bound calcium dropped in 94 and 91% of cases; the total buffer capacity of the plasma and buffer capacity of proteins fell in 59 and 87% of cases in TRF and ACK, respectively. The rise of the Ca++ content on an empty stomach seen in 21 out of 99 patients with TRF and in 42 out of 98 recipients of the ACK was caused by a decrease of calcium binding in the blood plasma, not made for by the fall of calcium supply to the blood because of "tertiary" hyperparathyroidism. Hypocalcemia detected in 38% of TRF patients was consequence to the rise of calcium binding not made for by the increased calcium supply to the blood provoked by bone resistance to parathyroid hormone.