Pre-existing arterial pathologic changes affecting arteriovenous fistula patency and cardiovascular mortality in hemodialysis patients.

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diabetes mellitus 1 endocrinologydiseases
hyperphosphatemia 1 endocrinologydiseases
vascular calcification 3 endocrinologydiseases

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diabetes mellitus 1936 creation, the primary failure rate did not decrease [[8]]. This suggests that in addition to old age, diabetes mellitus (DM), and a small-diameter vessel, pre-existing arteriosclerotic changes at AVF anastomosis sites may
hyperphosphatemia 12486 patientsSeveral factors play a role in arterial micro-calcification (AMiC) in ESRD patients. Hypercalcemia, hyperphosphatemia , dyslipidemia, hypertension, DM, and uremic toxin induce vascular calcification [[41],[42]]. This leads
vascular calcification 12561 patients. Hypercalcemia, hyperphosphatemia, dyslipidemia, hypertension, DM, and uremic toxin induce vascular calcification [[41],[42]]. This leads to osteoblastic conversion of vascular smooth muscle cells [[43]]. The process
vascular calcification 12739 vascular smooth muscle cells [[43]]. The process is facilitated by decreased levels of inhibitors of vascular calcification such as fetuin A, matrix Gla protein, osteopontin, osteoprotegerin, and pyrophosphate. Along with uremic
vascular calcification 12968 toxin, oxidative stress and inflammation, which are commonly found in ESRD patients, are involved in vascular calcification [[41],[42]]. Shroff et al. [[44]] demonstrated that dialysis accelerates AMiC by triggering smooth muscle

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