학술논문

Risk for Chronic Kidney Disease Progression After Acute Kidney Injury: Findings From the Chronic Renal Insufficiency Cohort Study.
Document Type
Article
Source
Annals of Internal Medicine. Jul2023, Vol. 176 Issue 7, p961-968. 9p. 1 Diagram, 3 Charts.
Subject
*CHRONIC kidney failure
*ACUTE kidney failure
*DISEASE risk factors
*DISEASE progression
*COHORT analysis
Language
ISSN
0003-4819
Abstract
The effect of acute kidney injury in patients with chronic kidney disease is a subject of debate. This multicenter cohort study examined 3150 patients with chronic kidney disease to determine subsequent kidney function and trajectory after hospitalizations with acute kidney injury. Visual Abstract. Risk for Chronic Kidney Disease Progression After Acute Kidney Injury: Findings From the Chronic Renal Insufficiency Cohort Study The effect of acute kidney injury in patients with chronic kidney disease is a subject of debate. This multicenter cohort study examined 3150 patients with chronic kidney disease to determine subsequent kidney function and trajectory after hospitalizations with acute kidney injury. 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 (n  = 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 2) and eGFRcys (−3.61 [CI, −6.39 to −0.82] mL/min/1.73 m 2) 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 2 for eGFRcr and −0.15 (CI, −2.16 to 1.86) mL/min/1.73 m 2 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 2 per year) or cystatin C level (−0.56 [CI, −1.28 to 0.17] mL/min/1.73 m 2 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. [ABSTRACT FROM AUTHOR]