Cytokine signature in end stage renal disease patients on hemodialysis

• Autor(a) principal: Danyelle Romana Alves Rios
• Data de Publicação: 2017
• Outros Autores: Melina de Barros Pinheiro, Wander Valadares de Oliveira Junior, Karina Braga Gomes Borges, Andréa Teixeira de Carvalho, Olindo Assis Martins Filho, Ana Cristina Simões e Silva, Luci Maria SantAna Dusse
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFMG
• Texto Completo: https://doi.org/10.1155/2017/9678391; http://hdl.handle.net/1843/59249
• topic: Hemodialysis; Vascular access thrombosis; Inflammation; Cytokine signature; Diálise renal; Nefropatias; Trombose; Inflamação; Citocinas

Hemodialysis is a modality of blood filtration in which accumulated toxins and water are removed from the body. This treatment is indicated for patients at the end stage of renal disease. Vascular access complications are responsible for 20–25% of all hospitalizations in dialyzed patients. The occurrence of thrombosis in the vascular access is a serious problem that may severely compromise or even make the hemodialysis impossible, which is vital for the patient. The aim of this study was to investigate inflammatory profile in patients undergoing hemodialysis as well as the association between these alterations and vascular access thrombosis. A total of 195 patients undergoing hemodialysis have been evaluated; of which, 149 patients had not experienced vascular access thrombosis (group I) and 46 patients had previously presented this complication (group II). Plasma levels of cytokines including interleukin (IL-) 2, IL-4, IL-5, IL-10, TNF-α, and IFN-γ were measured by cytometric bead array. Our results showed that patients with previous thrombotic events (group II) had higher levels of the IL-2, IL-4, IL-5, and IFN-γ when compared to those in group I. Furthermore, a different cytokine signature was detected in dialyzed patients according to previous occurrences or not of thrombotic events, suggesting that elevated levels of T-helper 1 and T-helper 2 cytokines might, at least in part, contribute to this complication.