Arteriovenous conduits for hemodialysis: how to better modulate the pathophysiological vascular response to optimize vascular access durability

Autor: Joris I. Rotmans, Timmy Lee, Yan-Ting Shiu, Wouter J. Geelhoed, Daniel B. Pike
Jazyk: angličtina
Rok vydání: 2019
Předmět:
congenital
hereditary
and neonatal diseases and abnormalities
medicine.medical_specialty
Intimal hyperplasia
Physiology
medicine.medical_treatment
030232 urology & nephrology
Vascular access
Lumen (anatomy)
Arteriovenous fistula
outward remodeling
Vascular Remodeling
030204 cardiovascular system & hematology
Anastomosis
Prosthesis Design
arteriovenous graft
Blood Vessel Prosthesis Implantation
03 medical and health sciences
Arteriovenous Shunt
Surgical
0302 clinical medicine
Renal Dialysis
Risk Factors
Internal medicine
Animals
Humans
Medicine
Treatment Failure
cardiovascular diseases
arteriovenous fistula
Vascular Patency
business.industry
Graft Occlusion
Vascular
medicine.disease
Pathophysiology
Blood Vessel Prosthesis
Prosthesis Failure
Clinical trial
inflammation
Cardiology
Stress
Mechanical
Hemodialysis
business
intimal hyperplasia
Perspectives
Zdroj: American Journal of Physiology-Renal Physiology, 316(5), F794-F806. AMER PHYSIOLOGICAL SOC
Am J Physiol Renal Physiol
Popis: Vascular access is the lifeline for patients on hemodialysis. Arteriovenous fistulas (AVFs) are the preferred vascular access, but AVF maturation failure remains a significant clinical problem. Currently, there are no effective therapies available to prevent or treat AVF maturation failure. AVF maturation failure frequently results from venous stenosis at the AVF anastomosis, which is secondary to poor outward vascular remodeling and excessive venous intimal hyperplasia that narrows the AVF lumen. Arteriovenous grafts (AVGs) are the next preferred vascular access when an AVF creation is not possible. AVG failure is primarily the result of venous stenosis at the vein-graft anastomosis, which originates from intimal hyperplasia development. Although there has been advancement in our knowledge of the pathophysiology of AVF maturation and AVG failure, this has not translated into effective therapies for these two important clinical problems. Further work will be required to dissect out the mechanisms of AVF maturation failure and AVG failure to develop more specific therapies. This review highlights the major recent advancements in AVF and AVG biology, reviews major clinical trials, and discusses new areas for future research.
Databáze: OpenAIRE
Externí odkaz: