Effect of Advanced Glycation End-Products (AGE) Lowering Drug ALT-711 on Biochemical, Vascular, and Bone Parameters in a Rat Model of CKD-MBD.

摘要: Chronic kidney disease-mineral bone disorder (CKD-MBD) is a systemic that affects blood measures of and mineral homeostasis, vascular calcification, bone. We hypothesized the accumulation advanced glycation end-products (AGEs) in CKD may be responsible for pathologies via alteration collagen. treated naturally occurring model CKD-MBD, Cy/+ rat, with normal high dose AGE crosslink breaker alagebrium (ALT-711), or calcium drinking water to mimic phosphate binders 10 weeks. These animals were compared (NL) untreated animals. The results showed animals, had elevated urea nitrogen (BUN), PTH, FGF23 phosphorus. Treatment ALT-711 no effect on function but 3 mg/kg lowered whereas PTH. Vascular calcification aorta assessed biochemically was increased NL, decreased by normal, not ALT-711, parallel decreases left ventricular hypertrophy. (3 mg/kg) did alter content, reduced expression receptor end products (RAGE) NADPH oxidase 2 (NOX2), suggesting effects related oxidative stress at cellular level. total both cortical porosity treatment, only improved properties. In summary, treatment CKD-MBD an FGF23, without improvement mechanics. suggest little collagen, potential effects. data also highlights need better measure specific types proteins tissue level order fully elucidate impact AGEs CKD-MBD. © 2019 American Society Bone Mineral Research.