Abstract
Objective:Serum leptin levels of chronic kidney disease patients have been detected higher than normal population. The aim of this study was to investigate the effects of serum leptin levels on thrombocyte aggregation in peritoneal dialysis patients.Methods:Fourty three peritoneal dialysis patients were included in the study. Thrombocyte aggregation was calculated from the whole blood subsequently the effects of different concentrations of human recombinant leptin on thrombocyte aggregations were investigated. Four test cells were used for this process. While leptin was not added into the first test cell, increasing amounts of leptin was added into the second, third and fourth test cells to attain the concentrations of 25, 50 and 100 ng/ml respectively.Results:Thrombocyte aggregation was inhibited by recombinant leptin in peritoneal dialysis patients. Thrombocyte aggregation mean values were found statistically significantly higher in first test cell when compared to leptin groups in peritoneal dialysis patients. For leptin groups we could not find any statistically significant differences for thrombocyte aggregation mean values between any of the groups.Conclusion:Further studies with larger number of peritoneal dialysis patients are required to prove the action of leptin on thrombocyte aggregation.
Highlights
Cardiovascular diseases and their adverse events are the leading cause of morbidity and mortality in chronic kidney disease.[1]
In our study we aimed to investigate the effect of varying concentrations of recombinant human leptin hormone on platelet aggregation in peritoneal dialysis (PD) patients
When mean serum leptin levels of PD patients were compared with platelet aggregation measurements in first test cell (C1), statistically significant difference was not detected for mean AUC, velocity and aggregation mean values (p values were 0.348, 0.186, 0.476 respectively)
Summary
Cardiovascular diseases and their adverse events are the leading cause of morbidity and mortality in chronic kidney disease.[1] In the development of atherothrombosis platelet aggregation and adhesion have critical importance.[2] Leptin is a 16kDa protein hormone synthesized from adipocytes. Its cell membrane receptor (Ob-R), is a member of the class 1 cytokine receptor family.[3] Upon finding Ob-R in a megakaryoblastic cell line the relation between leptin and platelet functions was investigated.[4] By Western blot analysis OB-Rb (the long form of its receptor) could be detected on platelet membrane .[4,5] The studies conducted so far in healthy (normal weight or obese) volunteers with in vitro leptin administration revealed varying results on aggregation of platelets activated by an agonist. While some studies have suggested that leptin increased platelet aggregation.[4,5,6,7] one study reported no effect.[8]
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