[The calcium-binding properties of the plasma proteins from patients with aseptic necrosis of bone following a cadaveric kidney allograft]. / Kal'tsiisviazyvaiushchie svoistva plazmennykh belkov u bol'nykh s asepticheskimi nekrozami kostei posle allotransplantatsii trupnoi pochki.

Calcium-binding properties of plasma proteins in hypo- and hypercalcaemia, induced in vitro, were studied at late posttransplantation periods in 15 recipients of cadaveric kidney, 8 of whom showed aseptic necrosis (AN) of the femur heard. Immunosuppression included prednisolone and azathioprine with analogous mean monthly doses in all recipients. Langmuir and Scatchard analysis revealed lowering of specific and total buffer capacity of plasma proteins (beta SP., beta pr) in hypercalcemia only in AN recipients at the expense of decreased Na and increased Ka during calcium binding by independent protein sites.

[A method of calculating complexed calcium in patients with in-vitro simulated hypo- and hypercalcemia]. / Metod rascheta kompleksirovannogo kal'tsiia u bol'nykh pri modeliruemoi in vitro gipo- i giperkal'tsiemii.

Assessment of plasma protein calcium-binding capacity in disease involves measurements of Ca fractions in native plasma and its samples after in vitro stimulation of hypo- and hypercalcemia; such measurements include multiple and labor-consuming anaerobic ultrafiltration procedures. Values of Ca bound to plasma complexons and effective constants of their associations with Ca were experimentally assessed in 20 normal subjects, 7 patients before and 20 ones after kidney transplantation with the use of ultrafiltration. A method for estimation of integrated calcium in a sample lot has been developed, based on a single experimental value of integrated calcium in native plasma and the mean association constant in health. Experimental and estimated values of liganded Ca were in good correlation, this confirming the rightfulness of clinical use of the suggested method. This method essentially simplifies assessment of plasma proteins Ca-binding properties and requires lesser blood volumes.

[The mechanisms of the disorder of calcium homeostasis in terminal kidney failure and the allotransplantation of a cadaver kidney]. / Mekhanizmy narusheniia gomeostaza kal'tsiia pri terminal'noi pochechnoi nedostatochnosti i allotransplantatsii trupnoi pochki.

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.

[Use of the equipment for hemodialysis in the diagnosis of calcium metabolism disorders in terminal chronic renal failure]. / Ispol'zovanie apparatury dlia gemodializa v diagnostike narushenii obmena kal'tsiia pri terminal'noi khronicheskoi pochechnoi nedostatochnosti.

As many as 18 patients with terminal chronic renal failure were treated by program hemodialysis. The initial concentration of ionized calcium in those patients' blood plasma amounted to 1.06 +/- 0.22 mmol/l. To assess function of the systems counteracting hypocalcemia, use was made of a session of hemodialysis against calcium-free dialysate. 2/3 of the patients demonstrated satisfactory function of the homeostatic system, maintained by a high secretion of PTH and involvement into regulation processes of the extraplasmic system marked by higher buffer capacities and a large pool of metabolism-capable calcium and apparently localized in the skeleton. In 1/3 of the patients, homeostatic function turned out to be dramatically impaired, which was provoked by inhibition of the secretory capacity of the parathyroid glands and manifested clinically by low tolerance to calcium losses and osteomalacia.

[The calcium-binding properties of plasma proteins following the allograft of a cadaveric kidney]. / Kal'tsiisviazyvaiushchie svoistva plazmennykh belkov posle allotransplantatsii trupnoi pochki.

The kinetics of calcium binding to plasma proteins in hypo- and hypercalcaemia, induced in vitro, were studied in 60 patients after renal transplantation. Langmuir and Scatchard analysis revealed the normal binding of calcium to plasma proteins in 10 patients (cooperative mechanism of calcium-protein interaction in hypocalcaemic state and existence of one or several sets of calcium binding independent sites in hypercalcaemic state). Cooperative binding with the decreased values of effective Ka, effective n. molar binding ratio (CaPr/A) and specific buffer capacity (beta sp.) were observed in 1/3 patients. Cooperative mechanism of calcium-proteins interaction has not been observed in more than 1/2 patients and the values of n. CaPr/A, beta sp, decreased in most of the patients. The observed changes may be caused by a proteins metabolism deterioration and may result in deterioration of calcium homeostasis.