Tenapanor--治疗终末期肾病高磷血症的新方法:临床研究综述

Leema Lobo, N. Kishore, Manjari Sharma
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摘要

几十年来,人们已经充分认识到磷酸盐调节在慢性肾脏病(CKD)中的极端重要性。但是,经常适用于常规医疗护理的新发现仍在不断发展。不良的健康状况、更高的发病率、更低的生活质量以及更高的心血管疾病死亡率都与慢性肾脏病--骨矿物质疾病的发展有关。在这种情况下,根据 CKD-骨矿物质疾病的建议,调节 CKD-骨矿物质疾病患者的血清磷酸盐水平至关重要。如果透析和饮食干预无法控制血磷水平,建议使用磷酸盐结合剂。虽然磷酸盐结合剂通过主动结合饮食中的磷酸盐来成功降低血磷水平,但某些人可能会因不良反应而限制其使用。Tenapanor是一种新型药物,它通过抑制钠/氢输出器同工酶3(NHE3)发挥作用,NHE3主要通过减少被动的细胞旁磷酸盐流来降低肠道对磷酸盐的吸收。Tenapanor 还能减少钠磷 2b 转运蛋白(NaPi2b)的表达,从而限制主动的跨细胞磷酸盐吸收补偿。这被认为是更有效的磷吸收调节剂,也是量身定制药物治疗的更好靶点。本临床研究汇总报告探讨了目前已发表的评估特纳帕诺治疗血液透析终末期肾病患者高磷血症的研究。关键词特纳帕诺 磷酸盐结合剂 高磷酸盐血症 慢性肾病 磷酸盐控制 磷酸盐结合剂 磷酸盐吸收 磷酸盐吸收抑制剂
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Tenapanor-A Novel Approach for Management of Hyperphosphatemia in End Stage Renal Disease: A Clinical Study Aggregate Review
The critical importance of phosphate regulation in chronic kidney disease (CKD) has been well understood for decades. But new findings, frequently applicable to routine medical care, continue to evolve. Poor health outcomes, greater morbidity, lowered quality of life, and a higher death rate from cardiovascular disease are all linked to the development of CKD-bone mineral ailment. Increased blood phosphate levels are linked to an increased risk of mortality in hemodialysis patients due to changes in phosphate breakdown and declining renal function as CKD advances.In this setting, according to  CKD-mineral bone disease recommendations, it is critical to regulate serum phosphate  levels in patients with CKD-mineral bone problem. If dialysis and dietary intervention fail to control blood phosphate levels, the use of phosphate binders is advised. Although phosphate binders are successful in lowering blood phosphate levels by actively binding to dietary phosphate, certain individuals have adverse effects that may restrict their use.These medications also have a significant pill load, which might result in poor treatment compliance. Tenapanor, a novel medication, works by inhibiting the sodium/hydrogen exporter isoform 3 (NHE3), which lowers intestinal phosphate absorption primarily by decreasing passive paracellular phosphate flow. Tenapanor also reduces the expression of the sodium phosphorus 2b transport protein (NaPi2b), which limits active transcellular phosphate absorption compensation. This is considered to be more effective phosphorous absorption regulator and a better target for tailored medication therapy. This clinical study aggregate report explores the currently published studies that have evaluated Tenapanor for the treatment of hyperphosphatemia in end stage renal disease patients on haemodialysis. Keywords: Tenapanor, phosphate binding agents, hyperphosphatemia, chronic kidney disease, phosphate control, phosphate binders, phosphate absorption, phosphate absorbtion inhibitor.
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