We read with interest the study by Lovshin et al. (1) investigating the natriuretic effect of the dipeptidyl peptidase 4 (DPP-4) inhibitor sitagliptin in patients with type 2 diabetes (T2D). The authors report that 1 month of sitagliptin therapy increases creatinine-based fractional sodium excretion (FENa) compared with placebo, which is in line with our previous observation (2). As lithium clearance and (intra)renal hemodynamics were not affected, the authors suggest that sitagliptin inhibits tubular sodium reabsorption at a level that is likely downstream of the macula densa. In parallel with enhanced FENa, DPP-4 inhibition increased intact stromal cell–derived factor (SDF)-1α1–67 levels, suggesting a relevant natriuretic role for this DPP-4 substrate. We agree with the authors that their mechanistic findings are of potential clinical relevance, particularly when hypothesizing about the added natriuretic effect of combined pharmacological DPP-4/sodium–glucose cotransporter …

中文翻译：

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评论Lovshin等。二肽基肽酶4抑制作用可刺激2型糖尿病患者远端肾小管利尿和循环SDF- ^1α1-67的升高。2017年糖尿病护理； 40：1073–1081

我们感兴趣地阅读了Lovshin等人的研究。（1）研究二肽基肽酶4（DPP-4）抑制剂西他列汀在2型糖尿病（T2D）患者中的利钠作用。作者报告说，与安慰剂相比，西他列汀治疗1个月可增加基于肌酐的分数钠排泄（FENa），这与我们先前的观察一致（2）。由于锂清除率和（肾内）血流动力学不受影响，因此作者建议西他列汀以可能在黄斑densa下游的水平抑制肾小管钠的重吸收。在增强FENa的同时，DPP-4抑制作用增加了完整的基质细胞衍生因子（SDF）-1α1-67水平，表明该DPP-4底物具有利钠作用。我们同意作者的观点，他们的机制发现可能具有潜在的临床意义，