Tangri Navdeep, Mathur Vandana, Reaven Nancy L, Funk Susan E, Whitlock Reid H, Wesson Donald E, Bushinsky David A
Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba; Winnipeg, Manitoba, Canada.
MathurConsulting LLC, Woodside, CA, USA.
Clin Kidney J. 2023 Mar 14;16(7):1113-1121. doi: 10.1093/ckj/sfad034. eCollection 2023 Jul.
Epidemiological studies demonstrate an association between kidney stones and risk of chronic kidney disease (CKD) and CKD progression. Metabolic acidosis, as a consequence of CKD, results in a reduced urine pH which promotes the formation of some types of kidney stones and inhibits the formation of others. While metabolic acidosis is a risk factor for CKD progression, the association of serum bicarbonate with risk of incident kidney stones is not well understood.
We used an Integrated Claims-Clinical dataset of US patients to generate a cohort of patients with non-dialysis-dependent CKD with two serum bicarbonate values of 12 to <22 mmol/L (metabolic acidosis) or 22 to <30 mmol/L (normal serum bicarbonate). Primary exposure variables were baseline serum bicarbonate and change in serum bicarbonate over time. Cox proportional hazards models evaluated time to first occurrence of kidney stones during a median 3.2-year follow-up.
A total of 142 884 patients qualified for the study cohort. Patients with metabolic acidosis experienced post-index date kidney stones at greater frequency than patients with normal serum bicarbonate at the index date (12.0% vs 9.5%, < .0001). Both lower baseline serum bicarbonate [hazard ratio (HR) 1.047; 95% confidence interval (CI) 1.036-1.057] and decreasing serum bicarbonate over time (HR 1.034; 95% CI 1.026-1.043) were associated with increased risk of kidney stone development.
Metabolic acidosis was associated with a higher incidence of kidney stones and shorter time to incident stone formation in patients with CKD. Future studies may investigate the role of correcting metabolic acidosis to prevent stone formation.
流行病学研究表明肾结石与慢性肾脏病(CKD)及其进展风险之间存在关联。CKD导致的代谢性酸中毒会使尿液pH值降低,这会促进某些类型肾结石的形成,同时抑制其他类型肾结石的形成。虽然代谢性酸中毒是CKD进展的一个危险因素,但血清碳酸氢盐与新发肾结石风险之间的关联尚不清楚。
我们使用美国患者的综合索赔 - 临床数据集,生成了一组非透析依赖型CKD患者队列,其血清碳酸氢盐值分别为12至<22 mmol/L(代谢性酸中毒)或22至<30 mmol/L(正常血清碳酸氢盐)。主要暴露变量为基线血清碳酸氢盐和随时间变化的血清碳酸氢盐。Cox比例风险模型评估了在中位3.2年随访期间首次发生肾结石的时间。
共有142884名患者符合研究队列标准。代谢性酸中毒患者在索引日期后发生肾结石的频率高于索引日期时血清碳酸氢盐正常的患者(12.0%对9.5%,<0.0001)。较低的基线血清碳酸氢盐[风险比(HR)1.047;95%置信区间(CI)1.036 - 1.057]和随时间下降的血清碳酸氢盐(HR 1.034;95% CI 1.026 - 1.043)均与肾结石发生风险增加相关。
代谢性酸中毒与CKD患者肾结石发病率较高及结石形成时间较短有关。未来的研究可探讨纠正代谢性酸中毒在预防结石形成中的作用。