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Ren Fail ; 44(1): 54-61, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-35174782

RESUMO

INTRODUCTION: Endothelial dysfunction is frequent in patients treated with peritoneal dialysis and may lead to cardiac complications. We evaluated the effect of effluent dialysates and serum on the function of coronary artery endothelial cells (CAEC). METHODS: Human CAEC in in vitro culture were exposed to serum and dialysates from 24 patients treated with continuous ambulatory peritoneal dialysis (CAPD) and secretion of interleukin-6 (IL6), von Willebrand factor (vWF), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) were measured. Modulation of the secretory activity of CAEC by Sulodexide, mixture of glycosaminoglycans: heparin sulfate and dermatan sulfate, was studied. RESULTS: Serum from CAPD patients stimulated synthesis of IL6 (+93%), vWF (+18%), and PAI-1 (+20%) and did not change t-PA secretion in CAEC. Dialysates stimulated secretion of IL6 (+89%), vWF (+29%), and PAI-1 (+31%) and did not change t-PA synthesis. Dialysates collected in 12 patients after 6 months more strongly stimulated synthesis of IL6 (+37%) and PAI-1 (+7%). Sulodexide suppressed the secretory activity of CAEC stimulated by the studied sera: IL6 (-38%), vWF (-19%), t-PA (-13%), and PAI-1 (-12%). CONCLUSIONS: Serum and the dialysate from CAPD patients induce inflammatory and prothrombotic reaction in coronary arterial endothelial cells. The general pattern of the observed effects for serum and dialysates was similar but the intensity of the effects was not identical. Sulodexide reduced these effects.


Assuntos
Vasos Coronários/citologia , Soluções para Diálise/efeitos adversos , Células Endoteliais/metabolismo , Diálise Peritoneal Ambulatorial Contínua/métodos , Adulto , Anticoagulantes/farmacologia , Feminino , Glicosaminoglicanos/farmacologia , Humanos , Interleucina-6/metabolismo , Masculino , Pessoa de Meia-Idade , Inibidor 1 de Ativador de Plasminogênio/metabolismo , Ativador de Plasminogênio Tecidual/metabolismo , Fator de von Willebrand/metabolismo
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