Vascular Calcification Markers and Hemodialysis Vascular Access Complications

Abstract

Background: Arteriovenous (AV) access dysfunction is a common complication in hemodialysis patients. Markers of vascular calcification are associated with cardiovascular outcomes and mortality in this population, but their association with vascular access outcomes is unknown. In this study, we aimed to evaluate the association between selected vascular calcification makers and vascular access complications in a cohort of hemodialysis patients. Method: Fetuin-A, osteopontin (OPN), osteoprotegerin (OPG), and bone morphogenetic protein-7 (BMP-7) were measured in blood samples from 219 dialysis patients in the Choice for Healthy Outcomes in Caring for end-stage renal disease study; these patients were using a permanent vascular access. Participants were followed for up to 1 year or until the occurrence of a vascular access intervention or replacement. Associations with AV fistula (AVF) and AV graft (AVG) intervention-free survival were assessed in models adjusted for demographic characteristics, comorbidities, and inflammation. Results: A total of 24 out 103 participants with an AVF and 43 out of 116 participants with an AVG had an intervention during follow-up. Lower fetuin-A, higher OPN, and higher BMP-7 were associated with a higher risk of AVF intervention (adjusted hazard ratios [aHR] for highest versus lowest tertile = 0.30 [95% CI 0.10–0.94]) for fetuin-A, 3.84 (95% CI 1.16–12.74) for OPN, and 3.49 (95% CI 1.16–10.52) for BMP-7. OPG was not significantly associated with the risk of AVF intervention. The associations of OPN and BMP-7 with AVF intervention appeared stronger among participants without diabetes (aHR 8.06; 95% CI 1.11–58.57 for OPN and aHR 2.55; 95% CI 1.08–6.08 for BMP-7, respectively) than among their counterparts with diabetes (p interaction = 0.06). None of the markers studied were significantly associated with AVG interventions. Conclusion: Lower fetuin-A and higher OPN and BMP-7 are associated with complications in AVF but not in AVG, suggesting a role for calcification in the pathogenesis AVF failure.

Low Muscle Mass in Patients Receiving Hemodialysis: Correlations with Vascular Calcification and Vascular Access Failure

“…VC induces vascular access failure through several molecular mechanisms [37]. The risk of arteriovenous fistula interventions is associated with VC markers, such as fetuin-A, osteopontin, osteoprotegerin, and bone morphogenetic protein-7 [38]. However, to the best of our knowledge, no reports have shown an association between low muscle mass and recurrent vascular access failure.…”

Oxidative stress: An essential factor in the process of arteriovenous fistula failure

“…In clinical studies, elevated serum levels of CRP and sclerostin, an osteogenic protein with increased expression specifically in calcified VSMCs, were found to be independent predictors of AVF failure ( 95 ). Other vascular calcification markers such as fetuin-A, osteopontin, and bone morphogenetic protein-7 were also associated with the development of AVF complications in a cohort of dialysis patients ( 96 ). However, a prospective clinical study came to the opposite conclusion ( 97 ).…”

Terapia de reemplazo renal, una alternativa para la calidad de vida de los pacientes

“…35,43 Otro tipo de acceso vascular que también se ve afectado es la fistula arteriovenosa presentando trombosis, embolias, aneurismas o isquemia [44][45][46] , algunas de estas complicaciones se encuentran asociadas con marcadores de calcificación vascular. 47 Los accesos vasculares también pueden causar hemorragias, incluso hasta comprometer la vida como sucede en 0,4% de los pacientes o producir un sangrado posterior a la diálisis sin compromiso vital, que definido como de 4Ml, esta pérdida moderada aumenta la anemia y por lo tanto la mortalidad. 35 Hay comorbilidades que pueden incrementar las probabilidades de sufrir ciertas complicaciones como el síndrome antifosfolípido, microangiopatías, disminución de los anticoagulantes naturales como la proteína S y aumento de la síntesis de los factores promotores de la coagulación como los V y VIII que pueden predisponer a los pacientes que reciben TRR a sufrir de trombosis del acceso vascular, ya que estas enfermedades alteran la cascada de la coagulación, el endotelio y la función plaquetaria, 32 sumado a la hiperplasia de la íntima y al aumento del perfil inflamatorio que presentan las personas que se encuentran en hemodiálisis.…”