Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern, Dallas, Texas.
Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Clin J Am Soc Nephrol. 2021 Mar 8;16(3):348-355. doi: 10.2215/CJN.06960520.
Sickle cell trait and sickle cell disease are associated with faster GFR decline compared with normal hemoglobin phenotypes. We sought to compare the AKI risk in sickle cell trait/disease to normal hemoglobin phenotypes and investigate the association between AKI and GFR decline in sickle cell trait/disease.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This multicenter observational study used registry data (January 2005-June 2018) of adult Black patients with sickle cell trait/disease (exposures) and normal hemoglobin phenotype (reference) ascertained by hemoglobin electrophoresis. Outcomes of interest (incident AKI [1.5 times baseline serum creatinine or higher], incident severe AKI [doubling of baseline serum creatinine or higher], and incident sustained AKI [AKI persisting for ≥72 hours]) were adjudicated by chart review and evaluated by Cox regression. The association between AKI and GFR decline (linear mixed models) was also investigated.
We identified 8968 reference patients, 1279 patients with sickle cell trait, and 254 patients with sickle cell disease with a median follow-up of 7.6 years and mean baseline serum creatinine of 0.8 mg/dl. We observed 796 AKI events, 452 sustained AKI events, and 466 severe AKI events. Compared with people with a normal hemoglobin phenotype, sickle cell trait was associated with higher risk for sustained AKI (adjusted hazard ratio, 1.64; 95% confidence interval, 1.27 to 2.11), but not AKI (adjusted hazard ratio, 1.11; 95% confidence interval, 0.91 to 1.36) or severe AKI (adjusted hazard ratio, 1.26; 95% confidence interval, 0.96 to 1.64). Sickle cell disease was associated with AKI (adjusted hazard ratio, 2.85; 95% confidence interval, 2.13 to 3.81), severe AKI (adjusted hazard ratio, 2.38; 95% confidence interval, 1.65 to 3.42), and sustained AKI (adjusted hazard ratio, 2.50; 95% confidence interval, 1.68 to 3.71). Post-AKI GFR decline was significantly faster in sickle cell trait (0.37 ml/min per 1.73 m per year faster, <0.01) and disease (1.69 ml/min per 1.73 m per year faster, <0.01) compared with the reference.
Sickle cell trait and disease are associated with higher risk of AKI, which is associated with accelerated decline in eGFR.
镰状细胞特征和镰状细胞病与正常血红蛋白表型相比,肾小球滤过率(GFR)下降更快。我们旨在比较镰状细胞特征/疾病与正常血红蛋白表型的急性肾损伤(AKI)风险,并探讨镰状细胞特征/疾病中 AKI 与 GFR 下降之间的关系。
这是一项多中心观察性研究,使用登记数据(2005 年 1 月至 2018 年 6 月),通过血红蛋白电泳确定镰状细胞特征/疾病(暴露)的成年黑人患者和正常血红蛋白表型(参考)。感兴趣的结局(新发 AKI[基线血清肌酐升高 1.5 倍或更高]、新发严重 AKI[基线血清肌酐升高 2 倍或更高]和新发持续 AKI[AKI 持续≥72 小时])通过病历审查进行裁决,并通过 Cox 回归进行评估。还研究了 AKI 与 GFR 下降(线性混合模型)之间的关系。
我们确定了 8968 名参考患者、1279 名镰状细胞特征患者和 254 名镰状细胞病患者,中位随访时间为 7.6 年,基线血清肌酐均值为 0.8mg/dl。我们观察到 796 例 AKI 事件、452 例持续 AKI 事件和 466 例严重 AKI 事件。与血红蛋白表型正常的患者相比,镰状细胞特征与持续 AKI 的风险增加相关(调整后的危险比,1.64;95%置信区间,1.27 至 2.11),但与 AKI(调整后的危险比,1.11;95%置信区间,0.91 至 1.36)或严重 AKI(调整后的危险比,1.26;95%置信区间,0.96 至 1.64)无关。镰状细胞病与 AKI(调整后的危险比,2.85;95%置信区间,2.13 至 3.81)、严重 AKI(调整后的危险比,2.38;95%置信区间,1.65 至 3.42)和持续 AKI(调整后的危险比,2.50;95%置信区间,1.68 至 3.71)相关。与参考组相比,镰状细胞特征(肾小球滤过率每年下降 0.37ml/min/1.73m,<0.01)和疾病(肾小球滤过率每年下降 1.69ml/min/1.73m,<0.01)后 GFR 下降速度明显更快。
镰状细胞特征和疾病与 AKI 风险增加相关,AKI 与 eGFR 下降加速有关。