尿液 pH 值-铵酸碱度评分与慢性肾功能衰竭进展。

IF 10.3 1区 医学 Q1 UROLOGY & NEPHROLOGY
Samuel Levi Svendsen, Amalie Quist Rousing, Rasmus Kirkeskov Carlsen, Dinah Khatir, Danny Jensen, Nikita Misella Hansen, Louise Salomo, Henrik Birn, Niels Henrik Buus, Jens Leipziger, Mads Vaarby Sorensen, Peder Berg
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引用次数: 0

摘要

导言:酸中毒与慢性肾脏病(CKD)肾功能丧失加剧有关。目前,酸碱状态是通过血浆测量来评估的,但对器官造成损害的隐性酸中毒(亚临床酸中毒)可能在血浆中反映出来之前就已经存在。尿液中 NH4+ 的低排泄量与慢性肾脏病患者肾脏的不良预后有关,并被认为是亚临床酸中毒的标志物。然而,NH4+排泄量低可能是排酸能力低或排酸需求低所致。我们假设,同时反映酸排泄需求和能力的尿酸/碱分数能更好地预测 CKD 的进展。方法:从三项 CKD 3 期和 4 期患者的临床研究中收集 24 小时尿液:开发队列(82 人)、变异队列(58 人)和验证队列(73 人)。根据尿液 pH 值和[NH4+]得出并计算尿酸/碱值。亚临床酸中毒的定义是酸/碱分数低于健康对照组 95% 预测区间的下限。主要结果为 18 个月后测量的 GFR 变化和长达 10 年的随访期间 CKD 进展(定义为 eGFR 下降≥50%、开始长期透析或肾移植):亚临床酸中毒在所有队列中都很普遍(n=54/82、48/73 和 40/58,∼67%)。亚临床酸中毒与 18 个月后测量的 GFR 下降 18% (95% CI: 2-32) 相关。在中位随访 6 年期间,亚临床酸中毒与 CKD 进展风险显著增高有关。在发展队列中,调整后的危险比为 9.88(95% CI 1.27-76.7),在验证队列中为 11.1(95% CI:2.88-42.5)。酸/碱分数对CKD进展的预测价值高于单独的NH4+排泄量:结论:以新的尿酸/碱分数定义的亚临床酸中毒与 CKD 3 期和 4 期患者较高的 CKD 进展风险相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Urine pH-Ammonium Acid/Base Score and CKD Progression.
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来源期刊
Journal of The American Society of Nephrology
Journal of The American Society of Nephrology 医学-泌尿学与肾脏学
CiteScore
22.40
自引率
2.90%
发文量
492
审稿时长
3-8 weeks
期刊介绍: The Journal of the American Society of Nephrology (JASN) stands as the preeminent kidney journal globally, offering an exceptional synthesis of cutting-edge basic research, clinical epidemiology, meta-analysis, and relevant editorial content. Representing a comprehensive resource, JASN encompasses clinical research, editorials distilling key findings, perspectives, and timely reviews. Editorials are skillfully crafted to elucidate the essential insights of the parent article, while JASN actively encourages the submission of Letters to the Editor discussing recently published articles. The reviews featured in JASN are consistently erudite and comprehensive, providing thorough coverage of respective fields. Since its inception in July 1990, JASN has been a monthly publication. JASN publishes original research reports and editorial content across a spectrum of basic and clinical science relevant to the broad discipline of nephrology. Topics covered include renal cell biology, developmental biology of the kidney, genetics of kidney disease, cell and transport physiology, hemodynamics and vascular regulation, mechanisms of blood pressure regulation, renal immunology, kidney pathology, pathophysiology of kidney diseases, nephrolithiasis, clinical nephrology (including dialysis and transplantation), and hypertension. Furthermore, articles addressing healthcare policy and care delivery issues relevant to nephrology are warmly welcomed.
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