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首页> 外文期刊>Journal of Clinical Medicine Research >Increased Hematocrit During Sodium-Glucose Cotransporter 2 Inhibitor Therapy Indicates Recovery of Tubulointerstitial Function in Diabetic Kidneys
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Increased Hematocrit During Sodium-Glucose Cotransporter 2 Inhibitor Therapy Indicates Recovery of Tubulointerstitial Function in Diabetic Kidneys

机译:钠葡萄糖共转运蛋白2抑制剂治疗期间血细胞比容增加表明糖尿病肾的肾小管间质功能恢复。

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Sodium-glucose cotransporter 2 (SGLT2) inhibitors have been attracting attention for cardiovascular as well as antidiabetic effects since the results of the Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients (EMPA-REG OUTCOME Trial) were reported. The hematocrit increases during treatment with SGLT2 inhibitors, which have a diuretic effect but do not cause sufficient hemoconcentration to increase the risk of cerebral infarction. Elevation of the hematocrit during SGLT2 inhibitor therapy is presumed to involve enhancement of erythropoiesis in addition to hemoconcentration. In patients with diabetes, the erythropoietin level increases after initiation of treatment with the SGLT2 inhibitor dapagliflozin and reaches a plateau in 2 - 4 weeks. The reticulocyte count increases simultaneously, followed by elevation of hemoglobin and hematocrit. In patients with diabetes, the proximal tubules are overtaxed by excessive glucose reabsorption and the increased oxygen requirement causes tubulointerstitial hypoxia. Consequently, erythropoietin production is impaired because “neural crest-derived” fibroblasts surrounding the damaged renal tubules undergo transformation into dysfunctional fibroblasts. SGLT2 inhibitors reduce the workload of the proximal tubules and improve tubulointerstitial hypoxia, allowing fibroblasts to resume normal erythropoietin production. These drugs represent a new class of diuretics that have a renoprotective effect by improving tubulointerstitial hypoxia, which is the final common pathway to end-stage renal disease. In patients with diabetes, elevation of hematocrit may be a surrogate marker for recovery from reversible tubulointerstitial injury.J Clin Med Res. 2016;8(12):844-847doi: http://dx.doi.org/10.14740/jocmr2760w
机译:自从报道2型糖尿病患者依帕列净治疗心血管事件后的结果(EMPA-REG结果试验)以来,钠葡萄糖共转运蛋白2(SGLT2)抑制剂已引起心血管和抗糖尿病作用的关注。在使用SGLT2抑制剂治疗期间,血细胞比容增加,虽然具有利尿作用,但未引起足够的血液浓缩以增加脑梗塞的风险。据推测,SGLT2抑制剂治疗期间血细胞比容的升高除血液浓缩外,还包括促红细胞生成的增强。在糖尿病患者中,用SGLT2抑制剂达格列净治疗开始后,促红细胞生成素水平升高,并在2-4周内达到稳定水平。网织红细胞计数同时增加,随后血红蛋白和血细胞比容升高。在糖尿病患者中,近端肾小管因过多的葡萄糖重吸收而过度劳累,氧气需求增加导致肾小管间质性缺氧。因此,促红细胞生成素的生产受到损害,因为受损肾小管周围的“神经c衍生”成纤维细胞会转化为功能异常的成纤维细胞。 SGLT2抑制剂减少了近端小管的工作量并改善了小管间质性缺氧,使成纤维细胞恢复正常的促红细胞生成素的产生。这些药物代表了一类新型的利尿剂,通过改善肾小管间质性缺氧而成为具有肾脏保护作用的利尿剂,后者是终末期肾脏疾病的最终常见途径。在糖尿病患者中,血细胞比容升高可能是可逆性肾小管间质损伤恢复的替代指标。 2016; 8(12):844-847doi:http://dx.doi.org/10.14740/jocmr2760w

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