Potassium-Alkali-Enriched Diet, Hypertension, and Proteinuria following Uninephrectomy.

IF 10.3 1区 医学 Q1 UROLOGY & NEPHROLOGY
Donna L Ralph, Darren Ha, Hillmin Lei, Taylor S Priver, Scotti D Smith, Brandon E McFarlin, Seth Schwindt, Drishti Pandya, Hermann Koepsell, Nuria M Pastor-Soler, Aurelie Edwards, Alicia A McDonough
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引用次数: 0
高钾高碱饮食、高血压和单肾切除术后的蛋白尿
背景:失去或捐献肾脏与罹患高血压和白蛋白尿的风险有关。很少有研究涉及其机制或干预措施。我们研究了富含 K+-碱性饮食的潜在益处以及蛋白尿的发生机制:方法:雄性 Sprague Dawley 大鼠在接受肾切除术前,先喂食 2% NaCl + 0.95% KCl 饮食(HNa-LK)或 0.74% NaCl + 3% K+-alkali 饮食(HK-alk)3 周,然后在各自的饮食中维持 12 周。对肾切除术前后的血压(通过尾袖带)、尿液、血液和肾脏蛋白进行分析:结果:肾切除术前,HK-alk 与 HNa-LK 喂养的大鼠表现出相似的血压和血浆[K+]、[Na+],但近端(NHE3、NBCe1、NaPi2)转运体丰度较低,远端(NCC、ENaC、pendrin)转运体丰度较高,这种模式有利于 K+ 和 HCO3- 的分泌。单肾切除术后,两种饮食的单肾肾小球 GFR 均增加 50%,Li+ 清除率增加一倍;HK-alk 与 HNa-LK 相比:血压升高较小,氨生成较低,近端肾小管转运体丰度仍然较低,ENaC-α 下降,NCCp 上升,这与 K+ 保护一致。肾切除术后,与饮食无关,白蛋白尿增加了 8 倍,内细胞受体丰度降低(megalin 降低 44%,dab2 降低 25-35%),KIM-1 增加:结论:富含 K-alkali-enriched diet(钾-碱饮食)通过抑制近端 Na+ 转运体和增加 K+ -碱分泌,缓解了肾切除术后的高血压并促进了酸的清除。此外,与未肾切除术相关的蛋白尿至少可部分归因于 SNGFR 的升高和 megalin 的下调,后者降低了蛋白质的部分内吞和 Vmax。
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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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