Evaluation of some platelet functions and platelet membrane glycoproteins in uremic, hemodialysis and renal transplant patients

The hemostatic defect of chronic renal failure [CRF] is well recognized. Increased bleeding has been attributed to platelet dysfunction. However, the available reports are controversial. To study platelet aggregation and glycoprotein receptors' [GP] expression in a well identified population with CRF. 25 patients with advanced CRF on conservative treatment [CRF group], 25 patients on regular hemodialysis [HD group], 25 renal transplant patients [Tx group], and 20 age-, race- and sex-matched healthy controls [control group] were subjected to complete physical examination, complete blood count, bleeding time [BT], renal functional parameters and other necessary laboratory tests, in addition to estimation of platelet aggregation in response to adenosine 5-diphosphate [ADP] and ristocetin as well as GPIb, GPIIb, and GPIIIa receptors' expression using fluorescein isothiocyanate-conjugated monoclonal antibodies CD42b, CD41 and CD62, respectively and a flow cytometer. BT was prolonged in both CRF and HD groups [P<0.001], and was not attributed to a decrease in platelet count. Both CRF and HD patients had similar, but significantly decreased maximum percentage of platelet aggregation induced by either ADP or ristocetin compared with Tx and healthy control groups [P<0.001]. GPIb expression was significantly decreased in the CRF group than the Tx and healthy control groups [P<0.05], while HD group showed non significant difference when compared with CRF, Tx or control groups. GPIIb and GPIIIa showed a highly significant decreased expression in both CRF and HD groups compared with Tx and healthy control groups [P<0.001], with no significant difference in between both uremic groups. An inverse correlation was observed between serum creatinine and GPIIb [r=-0.641, P=0.023] and GPIIIa [r=-0.545, P=0.031] receptors' expression in CRF patients versus no correlation in HD patients. The results of the studied parameters in Tx group were comparable to healthy controls. Uremic patients have decreased platelet aggregability and decreased GP receptors' expression [mainly GPIIb and GPIIIa], denoting that platelet dysfunction is at least partially contributing to their hemorrhagic problem. The observed defects were not corrected by regular HD. Renal transplantation seemed to be a better choice

Effect of different hormonal treatment modalities on biochemical markers of bone remodling in postmenopausal women

Is to measure some of the biochemical markers of bone formation and bone resorption in postmenopausal women before and after hormone replacement therapy. Thirty postmenopausal women and fifteen healthy pre-menopausal women were included in this work. Postmenopausal women were allocated into two groups. Group I: receiving Estrogen replacement therapy. Group II: receiving Combined hormone replacement therapy. The following serum markers were evaluated before the start and two weeks after the end of the study; total and ionized calcium, inorganic phosphorus, alkaline phosphataseiso enzyme, osteocalcin. Also urinary deoxypyridinoline cross links were assessed. Bone densitometry using quantitative computed tomography was done. In postmenopausal women of this study, there was an increase in both bone formation markers as well as bone resorption markers but in favour of bone resorption with diminished bone mass. There was significant reduction of both serum alkaline phosphatase and osteocalcin in both groups following treatment. This reduction was also noticed in both groups in urinary deoxypyridinoline / creatinine after hormonal therapy. However, bone mineral density showed no obvious changes in both groups after three months of replacement therapy. Changes in biochemical markers of bone turnover preceded changes in bone density observed by densitometry. These effects were similar in both groups receiving two different forms of hormone replacement therapy