Chronic kidney disease (CKD) impacts millions of people in the world, and those diagnosed with cardiovascular disease (CVD) are at a higher risk of mortality. Accumulated uremic toxins increases the risks of CVD in CKD patients and symptoms of CVD include endothelial injury, inflammatory reaction, vessel calcification and occlusion, and blood clot. Calciphylaxis is a complication of CKD that is life-threatening; it is a uremic vascular disease in which calcified micro-vessels cause painful skin lesions, and there is currently no effective diagnosis nor treatment. CKD patients with calciphylaxis require hemodialysis to survive and the most effective approach is through arteriovenous fistula (AVF). AVF connects an artery and vein to increase the blood flow needed for hemodialysis treatment. However, complications, such as stenosis of AVF portends a bad prognosis for patients. This study focuses on the microarchitecture of AVF to observe the abnormal changes in structure of vessels. By identifying the specific changes in the AVF, possible therapeutics can be made to target mechanisms of calciphylaxis and AVF to provide patients with successful rates of hemodialysis and recovery. In this study, it is observed that smooth muscle cell proliferation, necrosis of muscle tissue, accumulation of proteoglycan in the intima, and scarring of collagen contribute to abnormalities observed in AVF. / 2023-11-22T00:00:00Z
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/43444 |
| Date | 22 November 2021 |
| Creators | Le, John |
| Contributors | Chitalia, Vipul, Yin, Wenqing |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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