Department of Internal Medicine, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Seven Oaks General Hospital, Manitoba, R2V 3M3, Winnipeg, Canada.
Strategic Health Resources, La Cañada, California, USA.
BMC Nephrol. 2021 May 19;22(1):185. doi: 10.1186/s12882-021-02385-z.
Management of chronic kidney disease (CKD) requires the management of risk factors, such as hypertension and albuminuria, that affect CKD progression. Identification of additional modifiable risk factors is necessary to develop new treatment strategies for CKD. We sought to quantify the association of metabolic acidosis with CKD progression and mortality in a large U.S. community-based cohort.
In this longitudinal, retrospective cohort study we identified non-dialysis-dependent patients with stage 3‒5 CKD from Optum's de-identified integrated electronic health records. We selected cohorts of patients with confirmed metabolic acidosis or normal serum bicarbonate levels based on 2 consecutive serum bicarbonate values: 12 to < 22 mEq/L or 22-29 mEq/L, respectively, 28‒365 days apart. The primary composite outcome was ≥ 40 % decline in estimated glomerular filtration rate (eGFR), renal replacement therapy (chronic dialysis or kidney transplant), or all-cause mortality (DD40). Secondary outcomes included each component of the composite outcome. Cox proportional hazards models were used for the DD40 outcome and secondary outcomes, while logistic regression models were used for the DD40 outcome at 2 years.
A total of 51,558 patients qualified for the study. The unadjusted 2-year incidence of adverse renal and fatal outcomes was significantly worse among patients in the metabolic acidosis group vs. those who had normal serum bicarbonate levels: 48 % vs. 17 % for DD40, 10 % vs. 4 % for ≥ 40 % decline in eGFR, 20 % vs. 6 % for renal replacement therapy, and 31 % vs. 10 % for all-cause mortality (all P < 0.001). Over a ≤ 10-year period, for each 1-mEq/L increase in serum bicarbonate, the adjusted hazard ratio for DD40 was 0.926 (95 % confidence interval [CI], 0.922-0.930; P < 0.001); over a ≤ 2-year period, the adjusted odds ratio for DD40 was 0.873 (95 % CI, 0.866-0.879; P < 0.001).
In this large community cohort of patients with stage 3‒5 CKD, the presence of metabolic acidosis was a significant, independent risk factor for the composite adverse outcome of CKD progression, renal replacement therapy, and all-cause mortality (DD40).
慢性肾脏病（CKD）的管理需要管理影响 CKD 进展的风险因素，如高血压和白蛋白尿。确定其他可改变的风险因素对于制定 CKD 的新治疗策略是必要的。我们试图在一个大型美国社区为基础的队列中量化代谢性酸中毒与 CKD 进展和死亡率的关系。
在这项纵向、回顾性队列研究中，我们从 Optum 的去识别的综合电子健康记录中确定了 3 至 5 期 CKD 的非透析依赖性患者。我们根据连续两次血清碳酸氢盐值选择了代谢性酸中毒或正常血清碳酸氢盐水平的患者队列：分别为 12 至<22 mEq/L 或 22-29 mEq/L，间隔 28-365 天。主要复合结局是估算肾小球滤过率（eGFR）下降≥40%，肾替代治疗（慢性透析或肾移植）或全因死亡率（DD40）。次要结局包括复合结局的每个组成部分。Cox 比例风险模型用于 DD40 结局和次要结局，而逻辑回归模型用于 DD40 结局的 2 年。
共有 51558 名患者符合研究条件。与血清碳酸氢盐水平正常的患者相比，代谢性酸中毒组的未调整 2 年不良肾脏和致命结局的发生率显著更高：DD40 为 48%，eGFR 下降≥40%为 10%，肾替代治疗为 20%，全因死亡率为 31%（均 P<0.001）。在长达 10 年的时间内，血清碳酸氢盐每增加 1 mEq/L，DD40 的调整后危险比为 0.926（95%置信区间[CI]，0.922-0.930；P<0.001）；在 2 年的时间内，DD40 的调整后优势比为 0.873（95%CI，0.866-0.879；P<0.001）。
在这个患有 3-5 期 CKD 的大型社区队列中，代谢性酸中毒的存在是 CKD 进展、肾替代治疗和全因死亡率（DD40）复合不良结局的一个显著、独立的危险因素。
