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慢性肾脏病相关代谢性酸中毒:更新。

Metabolic Acidosis of CKD: An Update.

机构信息

Medical and Research Services, VHAGLA Healthcare System, UCLA Membrane Biology Laboratory, Los Angeles, CA; Division of Nephrology, VHAGLA Healthcare System and David Geffen School of Medicine, Los Angeles, CA.

Department of Medicine, Division of Nephrology, St. Elizabeth's Medical Center, Boston, MA; Department of Medicine, Tufts University School of Medicine, Boston, MA.

出版信息

Am J Kidney Dis. 2016 Feb;67(2):307-17. doi: 10.1053/j.ajkd.2015.08.028. Epub 2015 Oct 23.

DOI:10.1053/j.ajkd.2015.08.028
PMID:26477665
Abstract

The kidney has the principal role in the maintenance of acid-base balance. Therefore, a decrease in renal ammonium excretion and a positive acid balance often leading to a reduction in serum bicarbonate concentration are observed in the course of chronic kidney disease (CKD). The decrease in serum bicarbonate concentration is usually absent until glomerular filtration rate decreases to <20 to 25mL/min/1.73 m(2), although it can develop with lesser degrees of decreased kidney function. Non-anion gap acidosis, high-anion gap acidosis, or both can be found at all stages of CKD. The acidosis can be associated with muscle wasting, bone disease, hypoalbuminemia, inflammation, progression of CKD, and increased mortality. Administration of base may decrease muscle wasting, improve bone disease, and slow the progression of CKD. Base is suggested when serum bicarbonate concentration is <22 mEq/L, but the target serum bicarbonate concentration is unclear. Evidence that increments in serum bicarbonate concentration > 24 mEq/L might be associated with worsening of cardiovascular disease adds complexity to treatment decisions. Further study of the mechanisms through which metabolic acidosis contributes to the progression of CKD, as well as the pathways involved in mediating the benefits and complications of base therapy, is warranted.

摘要

肾脏在维持酸碱平衡方面起着主要作用。因此,在慢性肾脏病(CKD)的过程中,通常会观察到肾氨排泄减少和正酸平衡,这通常会导致血清碳酸氢盐浓度降低。尽管在肾功能下降较小的情况下也可能发生,但通常在肾小球滤过率下降至<20 至 25mL/min/1.73 m(2) 之前,血清碳酸氢盐浓度不会降低。在 CKD 的所有阶段都可以发现无阴离子间隙酸中毒、高阴离子间隙酸中毒或两者兼有。酸中毒可能与肌肉消耗、骨骼疾病、低白蛋白血症、炎症、CKD 进展和死亡率增加有关。碱的给予可以减少肌肉消耗、改善骨骼疾病并减缓 CKD 的进展。当血清碳酸氢盐浓度<22 mEq/L 时建议使用碱,但目标血清碳酸氢盐浓度尚不清楚。有证据表明,血清碳酸氢盐浓度增加>24 mEq/L 可能与心血管疾病恶化有关,这使得治疗决策更加复杂。进一步研究代谢性酸中毒导致 CKD 进展的机制,以及参与介导碱治疗的益处和并发症的途径,是必要的。

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