Navaneethan Sankar D, Shao Jun, Buysse Jerry, Bushinsky David A
Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas.
Tricida, Inc., South San Francisco, CA; and.
Clin J Am Soc Nephrol. 2019 Jul 5;14(7):1011-1020. doi: 10.2215/CJN.13091118. Epub 2019 Jun 13.
Metabolic acidosis is associated with progression of CKD and has significant adverse effects on muscle and bone. A systematic review and meta-analysis was conducted to evaluate the benefits and risks of metabolic acidosis treatment with oral alkali supplementation or a reduction of dietary acid intake in those with CKD.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: MEDLINE, Embase, and Cochrane CENTRAL were searched for relevant trials in patients with stage 3-5 CKD and metabolic acidosis (<22 mEq/L) or low-normal serum bicarbonate (22-24 mEq/L). Data were pooled in a meta-analysis with results expressed as weighted mean difference for continuous outcomes and relative risk for categorical outcomes with 95% confidence intervals (95% CIs), using a random effects model. Study quality and strength of evidence were assessed using Cochrane risk of bias and the Grading of Recommendations Assessment, Development and Evaluation criteria.
Fourteen clinical trials were included (=1394 participants). Treatment of metabolic acidosis with oral alkali supplementation or a reduction of dietary acid intake increased serum bicarbonate levels (14 studies, 1378 patients, mean difference 3.33 mEq/L, 95% CI, 2.37 to 4.29) and resulted in a slower decline in eGFR (13 studies, 1329 patients, mean difference -3.28 ml/min per 1.73 m, 95% CI, -4.42 to -2.14; moderate certainty) and a reduction in urinary albumin excretion (very-low certainty), along with a reduction in the risk of progression to ESKD (relative risk, 0.32; 95% CI, 0.18 to 0.56; low certainty). Oral alkali supplementation was associated with worsening hypertension or the requirement for increased antihypertensive therapy (very-low certainty).
Low-to-moderate certainty evidence suggest that oral alkali supplementation or a reduction in dietary acid intake may slow the rate of kidney function decline and potentially reduce the risk of ESKD in patients with CKD and metabolic acidosis.
代谢性酸中毒与慢性肾脏病（CKD）的进展相关，且对肌肉和骨骼有显著不良影响。本研究进行了一项系统评价和荟萃分析，以评估口服碱补充剂或减少饮食酸摄入量治疗CKD患者代谢性酸中毒的益处和风险。
设计、研究地点、参与者及测量指标：检索MEDLINE、Embase和Cochrane CENTRAL数据库，查找3-5期CKD且伴有代谢性酸中毒（<22 mEq/L）或血清碳酸氢盐水平略低于正常（22-24 mEq/L）患者的相关试验。采用随机效应模型将数据汇总进行荟萃分析，连续变量结果以加权均数差表示，分类变量结果以相对危险度表示，并给出95%置信区间（95%CI）。使用Cochrane偏倚风险评估和推荐分级评估、制定与评价标准来评估研究质量和证据强度。
纳入14项临床试验（n=1394名参与者）。口服碱补充剂或减少饮食酸摄入量治疗代谢性酸中毒可提高血清碳酸氢盐水平（14项研究，1378例患者，均数差3.33 mEq/L，95%CI：2.37至4.29），并减缓估算肾小球滤过率（eGFR）下降速度（13项研究，1329例患者，均数差-3.28 ml/min/1.73 m²，95%CI：-4.42至-2.14；中等确定性），减少尿白蛋白排泄（极低确定性），同时降低进展至终末期肾病（ESKD）的风险（相对危险度0.32；95%CI：0.18至0.56；低确定性）。口服碱补充剂与高血压恶化或降压治疗需求增加相关（极低确定性）。
低至中等确定性证据表明，口服碱补充剂或减少饮食酸摄入量可能减缓CKD合并代谢性酸中毒患者的肾功能下降速度，并可能降低ESKD风险。
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