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2016 ; 33
(1
): 15-20
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The Biology of Hemodialysis Vascular Access Failure
#MMPMID27011423
Brahmbhatt A
; Misra S
Semin Intervent Radiol
2016[Mar]; 33
(1
): 15-20
PMID27011423
show ga
Arteriovenous fistulas (AVFs) are essential for patients and clinicians faced
with end-stage renal disease (ESRD). While this method of vascular access for
hemodialysis is preferred to others due to its reduced rate of infection and
complications, they are plagued by intimal hyperplasia. The pathogenesis of
intimal hyperplasia and subsequent thrombosis is brought on by uremia, hypoxia,
and shear stress. These forces upregulate inflammatory and proliferative
cytokines acting on leukocytes, fibroblasts, smooth muscle cells, and platelets.
This activation begins initially with the progression of uremia, which induces
platelet dysfunction and primes the body for an inflammatory response. The
vasculature subsequently undergoes changes in oxygenation and shear stress during
AVF creation. This propagates a strong inflammatory response in the vessel
leading to cellular proliferation. This combined response is then further
subjected to the stressors of cannulation and dialysis, eventually leading to
stenosis and thrombosis. This review aims to help interventional radiologists
understand the biological changes and pathogenesis of access failure.
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