• Anthony N Muiru, Jesse Y Hsu, Xiaoming Zhang, Lawrence J Appel, Jing Chen, Debbie L Cohen, Paul E Drawz, Barry I Freedman, Alan S Go, Jiang He, Edward J Horwitz, Raymond K Hsu, James P Lash, Kathleen D Liu, Ian E McCoy, Anna Porter, Panduranga Rao, Ana C Ricardo, Hernan Rincon-Choles, James Sondheimer, Jonathan Taliercio, Mark Unruh, Chi-Yuan Hsu, and CRIC Study Investigators.
• 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.).
• Ann. Intern. Med. 2023 Jul 1; 176 (7): 961968961-968.

BackgroundPrior 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.ObjectiveTo determine whether AKI is independently associated with subsequent kidney function trajectory among patients with chronic kidney disease (CKD).DesignMulticenter prospective cohort study.SettingUnited States.ParticipantsPatients with CKD (n = 3150).MeasurementsHospitalized 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.ResultsDuring 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.LimitationsFew cases of severe AKI, no adjudication of AKI cause, and lack of information about nephrotoxic exposures after hospital discharge.ConclusionAfter 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 SourceNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health.

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