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Eicosanoids of Platelets and Vascular Wall in Chronic Renal Insufficiency
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1987
Year
Arachidonic Acid MetabolismThrombosisMetabolic SyndromeRenal FunctionHematologyChronic Kidney DiseaseAtherosclerosisHealth SciencesBiochemistryPeritoneal DialysisKidney FailureVascular BiologyPharmacologyRetention ProductsThrombopoiesisUrologyBlood PlateletPhysiologyChronic Renal InsufficiencyMetabolismMedicineNephrologyKidney Research
There is good evidence that retention products accumulating in chronic renal insufficiency influence prostaglandin (PG) synthesis, thus affecting platelet-vascular wall interaction. The vascular PGI2 synthesis is increased and prolonged in vitro, the plasma factor activity enhanced. A defective platelet function is frequently observed; it is completely restored by peritoneal dialysis, but only partially by hemodialysis. The sensitivity of platelets to PGI2 and its plasmatic degradation are unchanged. There is evidence of a shift of arachidonic acid metabolism from cyclooxygenase to lipoxygenase. These changes may be attributed to undialyzable plasma constituents, the 'middle molecules'.