Veterans Affairs Salt Lake City Health Care System and Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah, Salt Lake City, Utah
J Am Soc Nephrol. 2018 Feb;29(2):376-382. doi: 10.1681/ASN.2017040422. Epub 2017 Oct 13.
Metabolic acidosis is not uncommon in CKD and is linked with bone demineralization, muscle catabolism, and higher risks of CKD progression and mortality. Clinical practice guidelines recommend maintaining serum total CO at ≥22 mEq/L to help prevent these complications. Although a definitive trial testing whether correcting metabolic acidosis improves clinical outcomes has not been conducted, results from small, single-center studies support this notion. Furthermore, biologic plausibility supports the notion that a subset of patients with CKD have acid-mediated organ injury despite having a normal serum total CO and might benefit from oral alkali before overt acidosis develops. Identifying these individuals with subclinical metabolic acidosis is challenging, but recent results suggest that urinary acid excretion measurements may be helpful. The dose of alkali to provide in this setting is unknown as well. The review discusses these topics and the prevalence and risk factors of metabolic acidosis, mechanisms of acid-mediated organ injury, results from interventional studies, and potential harms of alkali therapy in CKD.
代谢性酸中毒在 CKD 中并不少见，与骨矿物质化、肌肉分解代谢以及 CKD 进展和死亡风险增加有关。临床实践指南建议维持血清总 CO2≥22mEq/L，以帮助预防这些并发症。虽然尚未进行测试纠正代谢性酸中毒是否改善临床结局的明确试验，但来自小型单中心研究的结果支持这一观点。此外，生物学合理性支持这样一种观点，即尽管血清总 CO2 正常，但 CKD 的一部分患者存在酸介导的器官损伤，并且可能受益于在明显酸中毒发生之前口服碱剂。确定这些具有亚临床代谢性酸中毒的个体具有挑战性，但最近的结果表明，尿酸排泄测量可能有帮助。在此情况下提供的碱剂量也是未知的。本文讨论了这些主题以及代谢性酸中毒的患病率和危险因素、酸介导的器官损伤机制、干预研究的结果以及 CKD 中碱治疗的潜在危害。
