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Biomedical subjects

I A Pronchenko

Publications and source records attributed to I A Pronchenko.

At least 19 recordsLinked to original sources
PubMed2006

[The peculiarities of bone exchange disorder and its regulation in men after long terms following orthotopic heart transplantation and cadaveric kidney transplantation].

The study found bone exchange disorder manifested by accelerated bone resorption, retarded bone formation, and the loss of the bone mineral density (BMD) of the axial and peripheral skeleton in 19 men (39 observations) 66 +/- 44 months following orthotopic heart transplantation (OTHT) and in 92 men 45 +/- 28 months after cadaveric kidney transplantation. An accelerated bone resorption, more pronounced in cadaveric kidney (CK) recipients, is associated with hyperparathyroidism (HPT) and renal dysfunction, while bone formation retardation is associated with a decrease in insulin-like growth factor-1 level. An increase in osteoprotegerin level is of compensatory character. The prominence of HPT depends on the degree of renal dysfunction; in CK recipients it also depends on the degree of the reduction in the levels of biologically active testosterone and estradiol. Reduction in BMD of the peripheral skeleton after OTHT are associated with the degree of renal dysfunction and a decrease in free testosterone index; after CK transplantation it is associated with HPT, the cumulative dose of glucocorticoids, reduction in the levels of biologically active testosterone and estradiol, as well as sex-hormone binding globulin (SHBG); reduction in spine BMD is only associated with SHBG.

Adult↗
PubMed2006

[Biochemical markers of bone formation in hemodialysis and after allotransplantation of cadaveric kidney].

AIM: To ascertain informative value of estimation of bone forming markers in patients on chronic hemodyalisis (CHD) and recipients of cadaveric kidney (CK). MATERIAL AND METHODS: Parathyroid hormone (PTH), beta-crosslaps (CTX), osteocalcin (OC), amino-terminal procollagen propeptide 1 (PINP), bone alkaline phosphatase (BAP), bone mineral density (BMD) were determined in 152 patients on CHD (89 males and 63 females aged 49 +/- 13 years) and 195 CK recipients (106 males and 89 females aged 42 +/- 12 years) 30 +/- 38 months after kidney transplantation. RESULTS: PTH, CTX and BAP determination specifies skeletal disease (secondary hyperparathyroidism or adynamic bone disease) in CHD patients. In patients with CK recipients osteoporosis differed from osteopenia by higher levels of PTH, CTX, OC in the absence of any differences in BAP, PINP. All bone forming markers were lower than CTX showing suppression of bone forming. Bone fractures in CK recipients' anamnesis were associated with OC and BAP decrease in men and low border of normal OC in women. Determination of bone formation and resorption markers in patients on CHD and CK recipients is of great clinical importance.

Biomarkers↗
PubMed2005

[Biochemical markers of bone metabolism and bone tissue losses after allotransplantation of the cadaveric kidney: a cross-sectional].

The biochemical markers of bone metabolism (osteocalcin (OC), C- and N-terminal procollagen I propeptides (PICP) and PINP), bone alkaline phosphatase (BALP), deoxypyridinoline (DPD), beta-crosslaps (beta-CL), bone acid phosphatase (BAP), osteoprotegerin (OPG), insulin-like growth factor I (IGF-I), and parathyroid hormone (PTH)), daily urinary calcium excretion (DUCE) (intestinal calcium absorption), and lumbar and hip bone mineral density (BMD) were determined in 195 patients (78 females and 74 males with normal function of the grafted kidney and 11 females and 31 males with chronic renal failure (CRF) 40 +/- 33 months after renal transplantation (RT). All RT recipients received triple immunosuppressive therapy (cyclosporin, prednisolone, and azathioprine). All groups showed a significant increase in resorption markers and a moderate increase in bone formation markers (except BALP), which suggested bone remodeling dissociation, as well as elevated levels of PTH and OPG and decreased DUCE and BMD in the vertebral column and hip. Increased bone metabolism and decreased intestinal calcium absorption were largely pronounced in CRF. In the majority of recipients, the BMD reduction in the vertebral column and hip was moderate (osteopenia) and only in male recipients with CRF, axial osteopenia was concurrent with peripheral osteoporosis. The main predictor of accelerated bone metabolism and BMD losses following RT was hyperparathyroidism mainly caused by decreased renal graft function. Decreased IGF-I may be a cause of bone remodeling dissociation after RT/ and the increase in OPG seems to be compensatory, which suppresses bone resorption and reduces bone losses.

Biomarkers↗
PubMed1993

[The calcium-binding properties of the plasma proteins from patients with aseptic necrosis of bone following a cadaveric kidney allograft].

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.

Adolescent↗
PubMed1991

[Calcium-binding properties of tissue proteins after kidney allotransplantation].

The kinetics of calcium binding to tissue substrates in hypercalcaemia, induced by intravenous constant rate infusion of calcium gluconate were studied in 19 patients after renal transplantation and in 14 healthy volunteers. Langmuir, Scatchard and Hill analysis revealed the positive cooperative mechanism of calcium binding to tissue in all patients and in healthy volunteers. These results provide indirect evidence of binding of calcium to tissue proteins. The significant decrease of the values of specific buffer capacity of tissue proteins, pool of exchangeable calcium and also the effective Ka were observed in 37% of patients. These changes are proposed to play a role in the pathological calcification of vessels and soft tissues in patients after renal transplantation.

Calcium↗
PubMed1991

[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.

Buffers↗
PubMed1990

[The calcium-binding properties of plasma proteins following the allograft of a cadaveric kidney].

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.

Adolescent↗
PubMed1984

[Radioimmunoassay in the testing of new pharmacological agents].

The activity of Parathorm, a pharmaceutical obtained from parathyroid hormone (PTH), was studied. Human blood plasma proteins as well as bivalent anions have been shown to produce a negative effect on the antigen-antibody interaction. The proportion of the PTH-protein complexes with the elevation of the pharmaceutical dose is constant in many concentrations whereas with the elevation of the PTH dose the PTH-low molecular complexes account for ever increasing proportion of the radioactive complexes.

Blood Proteins↗