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急性肾损伤后慢性肾脏病进展的风险:来自慢性肾功能不全队列研究的结果。

Risk for Chronic Kidney Disease Progression After Acute Kidney Injury: Findings From the Chronic Renal Insufficiency Cohort Study.

机构信息

Division of Nephrology, University of California, San Francisco School of Medicine, San Francisco, California (A.N.M., R.K.H., K.D.L., I.E.M.).

Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania (J.Y.H., X.Z.).

出版信息

Ann Intern Med. 2023 Jul;176(7):961-968. doi: 10.7326/M22-3617. Epub 2023 Jul 11.

Abstract

BACKGROUND

Prior studies associating acute kidney injury (AKI) with more rapid subsequent loss of kidney function had methodological limitations, including inadequate control for differences between patients who had AKI and those who did not.

OBJECTIVE

To determine whether AKI is independently associated with subsequent kidney function trajectory among patients with chronic kidney disease (CKD).

DESIGN

Multicenter prospective cohort study.

SETTING

United States.

PARTICIPANTS

Patients with CKD ( = 3150).

MEASUREMENTS

Hospitalized AKI was defined by a 50% or greater increase in inpatient serum creatinine (SCr) level from nadir to peak. Kidney function trajectory was assessed using estimated glomerular filtration rate (eGFR) based on SCr level (eGFRcr) or cystatin C level (eGFRcys) measured at annual study visits.

RESULTS

During a median follow-up of 3.9 years, 433 participants had at least 1 AKI episode. Most episodes (92%) had stage 1 or 2 severity. There were decreases in eGFRcr (-2.30 [95% CI, -3.70 to -0.86] mL/min/1.73 m) and eGFRcys (-3.61 [CI, -6.39 to -0.82] mL/min/1.73 m) after AKI. However, in fully adjusted models, the decreases were attenuated to -0.38 (CI, -1.35 to 0.59) mL/min/1.73 m for eGFRcr and -0.15 (CI, -2.16 to 1.86) mL/min/1.73 m for eGFRcys, and the CI bounds included the possibility of no effect. Estimates of changes in eGFR slope after AKI determined by either SCr level (0.04 [CI, -0.30 to 0.38] mL/min/1.73 m per year) or cystatin C level (-0.56 [CI, -1.28 to 0.17] mL/min/1.73 m per year) also had CI bounds that included the possibility of no effect.

LIMITATIONS

Few cases of severe AKI, no adjudication of AKI cause, and lack of information about nephrotoxic exposures after hospital discharge.

CONCLUSION

After pre-AKI eGFR, proteinuria, and other covariables were accounted for, the association between mild to moderate AKI and worsening subsequent kidney function in patients with CKD was small.

PRIMARY FUNDING SOURCE

National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health.

摘要

背景

先前将急性肾损伤(AKI)与肾功能更快丧失相关联的研究存在方法学限制,包括对 AKI 患者和未发生 AKI 患者之间的差异进行充分控制。

目的

确定 AKI 是否与慢性肾脏病(CKD)患者的后续肾功能轨迹独立相关。

设计

多中心前瞻性队列研究。

设置

美国。

参与者

CKD 患者(n=3150)。

测量

住院 AKI 定义为住院期间血清肌酐(SCr)水平从最低点到峰值增加 50%或以上。通过在年度研究就诊时测量的 SCr 水平(eGFRcr)或胱抑素 C 水平(eGFRcys)评估肾功能轨迹。

结果

在中位随访 3.9 年期间,433 名参与者至少发生了 1 次 AKI 发作。大多数发作(92%)为 1 级或 2 级严重程度。AKI 后 eGFRcr(-2.30[95%CI,-3.70 至-0.86]mL/min/1.73m)和 eGFRcys(-3.61[CI,-6.39 至-0.82]mL/min/1.73m)下降。然而,在完全调整的模型中,eGFRcr 的下降幅度减弱至-0.38(CI,-1.35 至 0.59)mL/min/1.73m,eGFRcys 的下降幅度减弱至-0.15(CI,-2.16 至 1.86)mL/min/1.73m,CI 边界包括无影响的可能性。通过 SCr 水平(0.04[CI,-0.30 至 0.38]mL/min/1.73m/年)或胱抑素 C 水平(-0.56[CI,-1.28 至 0.17]mL/min/1.73m/年)确定的 AKI 后 eGFR 斜率变化的估计值,其 CI 边界也包括无影响的可能性。

局限性

严重 AKI 的病例较少,未对 AKI 原因进行裁决,以及出院后缺乏关于肾毒性暴露的信息。

结论

在考虑 AKI 前的 eGFR、蛋白尿和其他协变量后,轻度至中度 AKI 与 CKD 患者后续肾功能恶化之间的关联较小。

主要资金来源

美国国立卫生研究院国家糖尿病、消化和肾脏疾病研究所。

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