Wu Yun, Wang Ying, Huang Weijun, Guo Xi, Hou Baoluo, Tang Jingyi, Wu Yuqi, Zheng Huijuan, Pan Yanling, Liu Wei Jing
Renal Research Institution of Beijing University of Chinese Medicine, and Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.
Department of Chinese Medicine, the Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Front Pharmacol. 2024 Aug 26;15:1411933. doi: 10.3389/fphar.2024.1411933. eCollection 2024.
We investigated the efficacy and safety of oral sodium bicarbonate in kidney-transplant recipients and non-transplant patients with chronic kidney disease (CKD), which are currently unclear.
PubMed, Cochrane Library, Embase, and Web of Science were searched for randomized controlled trials investigating the efficacy and safety of sodium bicarbonate placebo or standard treatment in kidney-transplant and non-transplant patients with CKD.
Sixteen studies of kidney-transplant recipients (two studies, 280 patients) and non-transplant patients with CKD (14 studies, 1,380 patients) were included. With non-transplant patients, sodium bicarbonate slowed kidney-function declines (standardized mean difference [SMD]: 0.49, 95% confidence interval [CI]: 0.14-0.85, = 0.006) within ≥12 months (SMD: 0.75 [95% CI: 0.12-1.38], = 0.02), baseline-serum bicarbonate <22 mmol/L (SMD: 0.41 [95% CI: 0.19-0.64], = 0.0004) and increased serum-bicarbonate levels (mean difference [MD]: 2.35 [95% CI: 1.40-3.30], < 0.00001). In kidney-transplant recipients, sodium bicarbonate did not preserve graft function (SMD: -0.07 [95% CI: -0.30-0.16], = 0.56) but increased blood pH levels (MD: 0.02 [95% CI: 0.00-0.04], = 0.02). No significant adverse events occurred in the kidney-transplant or non-transplant patients (risk ratio [RR]: 0.89, [95% CI: 0.47-1.67], = 0.72; and RR 1.30 [95% CI: 0.84-2.00], = 0.24, respectively). However, oral sodium bicarbonate correlated with increased diastolic pressure and worsened hypertension and edema (MD: 2.21 [95% CI: 0.67-3.75], = 0.005; RR: 1.44 [95% CI: 1.11-1.88], = 0.007; and RR: 1.28 [95% CI: 1.00-1.63], = 0.05, respectively).
Oral sodium bicarbonate may slow kidney-function decline in non-transplant patients with CKD taking sodium bicarbonate supplementation for ≥12 months or a baseline serum bicarbonate level of <22 mmol/L, without preserving graft function in kidney-transplant recipients. Sodium bicarbonate may increase diastolic pressure, and elevate a higher incidence of worsening hypertension and edema.
https://www.crd.york.ac.uk/prospero/, identifier CRD42023413929.
我们研究了口服碳酸氢钠对肾移植受者和非移植慢性肾脏病（CKD）患者的疗效和安全性，目前这些尚不清楚。
检索了PubMed、Cochrane图书馆、Embase和科学网，以查找关于碳酸氢钠、安慰剂或标准治疗对肾移植和非移植CKD患者疗效和安全性的随机对照试验。
纳入了16项关于肾移植受者（2项研究，280例患者）和非移植CKD患者（14项研究，1380例患者）的研究。对于非移植患者，碳酸氢钠在≥12个月内减缓了肾功能下降（标准化均数差[SMD]：0.49，95%置信区间[CI]：0.14 - 0.85，P = 0.006）（SMD：0.75[95%CI：0.12 - 1.38]，P = 0.02），基线血清碳酸氢盐<22 mmol/L（SMD：0.41[95%CI：0.19 - 0.64]，P = 0.0004）且血清碳酸氢盐水平升高（均数差[MD]：2.35[95%CI：1.40 - 3.30]，P < 0.00001）。在肾移植受者中，碳酸氢钠未保留移植肾功能（SMD： - 0.07[95%CI： - 0.30 - 0.16]，P = 0.56）但提高了血液pH值（MD：0.02[95%CI：0.00 - 0.04]，P = 0.02）。肾移植或非移植患者均未发生显著不良事件（风险比[RR]：0.89，[95%CI：0.47 - 1.67]，P = 0.72；以及RR 1.30[95%CI：0.84 - 2.00]，P = 0.24）。然而，口服碳酸氢钠与舒张压升高以及高血压和水肿加重相关（MD：2.21[95%CI：0.67 - 3.75]，P = 0.005；RR：1.44[95%CI：1.11 - 1.88]，P = 0.007；以及RR：1.28[95%CI：1.00 - 1.63]，P = 0.05）。
口服碳酸氢钠可能会减缓接受碳酸氢钠补充≥12个月或基线血清碳酸氢盐水平<22 mmol/L的非移植CKD患者的肾功能下降，但对肾移植受者的移植肾功能无保留作用。碳酸氢钠可能会升高舒张压，并增加高血压和水肿加重的发生率。
