Shah Samir N, Abramowitz Matthew, Hostetter Thomas H, Melamed Michal L
Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY, USA.
Am J Kidney Dis. 2009 Aug;54(2):270-7. doi: 10.1053/j.ajkd.2009.02.014. Epub 2009 Apr 25.
Animal models of kidney disease have linked metabolic acidosis with renal damage. The role of low serum bicarbonate levels in kidney disease progression in humans has not been studied.
Retrospective cohort study.
SETTING & PARTICIPANTS: Adults visiting a medical clinic in the Bronx, NY, from January 1, 2001, to December 31, 2003, were included in the study (n = 5,422) and followed up until June 30, 2007.
Serum bicarbonate level.
Kidney disease progression was defined as either a decrease in estimated glomerular filtration rate (eGFR) by 50% or reaching an eGFR less than 15 mL/min/1.73 m(2) (n = 337).
Patients' baseline demographics, comorbid conditions, laboratory data, and socioeconomic status were recorded. Serial outpatient serum creatinine levels were collected (median, 5 measurements/person).
Mean age was 52 years, 69% were women, 45% were African American, 31% were Hispanic, 21% had diabetes mellitus, 41% had hypertension, and 9% had a baseline eGFR less than 60 mL/min/1.73 m(2). Kidney disease progressed as defined in 337 patients (6.2%). Compared with the reference group (bicarbonate level, 25 to 26 mEq/L), hazard ratios for progression after adjustment for potential confounders were 1.54 (95% confidence interval [CI], 1.13 to 2.09) for bicarbonate levels of 22 mEq/L or less, 0.97 (95% CI, 0.70 to 1.35) for 23 to 24 mEq/L, and 1.14 (95% CI, 0.84 to 1.55) for 27 mEq/L or greater (global P for inclusion of serum bicarbonate level in the model = 0.01). These results were similar using different definitions of the outcome (eGFR decrease of 30%, 1,288 outcomes [24%]; or doubling of serum creatinine level, 268 outcomes [4.9%]).
Data used in the study were collected for clinical, not research, purposes.
Low serum bicarbonate level is associated with progression of kidney disease independent of baseline eGFR and other clinical, demographic, and socioeconomic factors. Prospective studies are needed to confirm this relationship and evaluate the efficacy of alkali supplements for slowing progression.
肾脏疾病的动物模型已将代谢性酸中毒与肾损伤联系起来。血清碳酸氢盐水平低在人类肾脏疾病进展中的作用尚未得到研究。
回顾性队列研究。
2001年1月1日至2003年12月31日期间到纽约布朗克斯区一家诊所就诊的成年人被纳入研究(n = 5422),并随访至2007年6月30日。
血清碳酸氢盐水平。
肾脏疾病进展定义为估计肾小球滤过率(eGFR)下降50%或eGFR降至低于15 mL/min/1.73 m²(n = 337)。
记录患者的基线人口统计学特征、合并症、实验室数据和社会经济状况。收集系列门诊血清肌酐水平(中位数,每人5次测量)。
平均年龄为52岁,69%为女性,45%为非裔美国人,31%为西班牙裔,21%患有糖尿病,41%患有高血压,9%的基线eGFR低于60 mL/min/1.73 m²。337例患者(6.2%)出现了定义中的肾脏疾病进展。与参照组(碳酸氢盐水平为25至26 mEq/L)相比,在对潜在混杂因素进行调整后,碳酸氢盐水平为22 mEq/L或更低时进展的风险比为1.54(95%置信区间[CI],1.13至2.09),23至24 mEq/L时为0.97(95%CI,0.70至1.35),27 mEq/L或更高时为1.14(95%CI,0.84至1.55)(将血清碳酸氢盐水平纳入模型的总体P值 = 0.01)。使用不同的结果定义(eGFR下降30%,1288例结果[24%];或血清肌酐水平翻倍,268例结果[4.9%])时,这些结果相似。
研究中使用的数据是为临床而非研究目的收集的。
血清碳酸氢盐水平低与肾脏疾病进展相关,独立于基线eGFR以及其他临床、人口统计学和社会经济因素。需要进行前瞻性研究来证实这种关系并评估碱补充剂减缓进展的疗效。