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Multicenter Study
. 2023 Jul;176(7):961-968.
doi: 10.7326/M22-3617. Epub 2023 Jul 11.

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

Anthony N Muiru  1 , Jesse Y Hsu  2 , Xiaoming Zhang  2 , Lawrence J Appel  3 , Jing Chen  4 , Debbie L Cohen  5 , Paul E Drawz  6 , Barry I Freedman  7 , Alan S Go  8 , Jiang He  9 , Edward J Horwitz  10 , Raymond K Hsu  1 , James P Lash  11 , Kathleen D Liu  1 , Ian E McCoy  1 , Anna Porter  11 , Panduranga Rao  12 , Ana C Ricardo  11 , Hernan Rincon-Choles  13 , James Sondheimer  14 , Jonathan Taliercio  13 , Mark Unruh  15 , Chi-Yuan Hsu  16 ; CRIC Study Investigators
Collaborators, Affiliations
Multicenter Study

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

Anthony N Muiru et al. Ann Intern Med. 2023 Jul.

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 (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 m2) and eGFRcys (-3.61 [CI, -6.39 to -0.82] mL/min/1.73 m2) after AKI. However, in fully adjusted models, the decreases were attenuated to -0.38 (CI, -1.35 to 0.59) mL/min/1.73 m2 for eGFRcr and -0.15 (CI, -2.16 to 1.86) mL/min/1.73 m2 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 m2 per year) or cystatin C level (-0.56 [CI, -1.28 to 0.17] mL/min/1.73 m2 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.

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Conflict of interest statement

Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M22-3617.

Figures

Figure 1:
Figure 1:
Participant flow diagram - CRIC: Chronic Renal Insufficiency Cohort study; eGFR estimated glomerular filtration rate; ESRD: End Stage Renal Disease
See this image and copyright information in PMC

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