Chi-Yuan Hsu1,2, Raymond K Hsu3, Kathleen D Liu3, Jingrong Yang2, Amanda Anderson4, Jing Chen5, Vernon M Chinchilli6, Harold I Feldman7, Amit X Garg8, Lee Hamm5, Jonathan Himmelfarb9, James S Kaufman10,11, John W Kusek7, Chirag R Parikh12, Ana C Ricardo13, Sylvia E Rosas14, Georges Saab15, Daohang Sha16, Edward D Siew17, James Sondheimer18, Jonathan J Taliercio19, Wei Yang7, Alan S Go3,2. 1. Department of Medicine, University of California, San Francisco, San Francisco, California; hsuchi@medicine.ucsf.edu. 2. Division of Research, Kaiser Permanente Northern California, Oakland, California. 3. Department of Medicine, University of California, San Francisco, San Francisco, California. 4. Departments of Epidemiology and. 5. Medicine, Tulane University, New Orleans, Louisiana. 6. Department of Public Health Sciences, Penn State College of Medicine, Hershey, Pennsylvania. 7. Department of Biostatistics and Epidemiology, and. 8. Department of Medicine, Western University, London, Ontario, Canada. 9. Department of Medicine, University of Washington, Seattle, Washington. 10. Veterans Affairs New York Harbor Healthcare System, New York, New York. 11. Department of Medicine, New York University School of Medicine, New York, New York. 12. Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland. 13. Department of Medicine, University of Illinois, Chicago, Illinois. 14. Kidney and Hypertension Unit, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts. 15. Case Western Reserve University and Metrohealth Medical Center, Cleveland, Ohio. 16. Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania. 17. Vanderbilt University Medical Center and Nashville Veterans Affairs Hospital, Nashville, Tennessee. 18. Department of Medicine, Wayne State University School of Medicine, Detroit, Michigan; and. 19. Cleveland Clinic, Cleveland, Ohio.
Abstract
BACKGROUND: Prior studies of adverse renal consequences of AKI have almost exclusively focused on eGFR changes. Less is known about potential effects of AKI on proteinuria, although proteinuria is perhaps the strongest risk factor for future loss of renal function. METHODS: We studied enrollees from the Assessment, Serial Evaluation, and Subsequent Sequelae of AKI (ASSESS-AKI) study and the subset of the Chronic Renal Insufficiency Cohort (CRIC) study enrollees recruited from Kaiser Permanente Northern California. Both prospective cohort studies included annual ascertainment of urine protein-to-creatinine ratio, eGFR, BP, and medication use. For hospitalized participants, we used inpatient serum creatinine measurements obtained as part of clinical care to define an episode of AKI (i.e., peak/nadir inpatient serum creatinine ≥1.5). We performed mixed effects regression to examine change in log-transformed urine protein-to-creatinine ratio after AKI, controlling for time-updated covariates. RESULTS: At cohort entry, median eGFR was 62.9 ml/min per 1.73 m2 (interquartile range [IQR], 46.9-84.6) among 2048 eligible participants, and median urine protein-to-creatinine ratio was 0.12 g/g (IQR, 0.07-0.25). After enrollment, 324 participants experienced at least one episode of hospitalized AKI during 9271 person-years of follow-up; 50.3% of first AKI episodes were Kidney Disease Improving Global Outcomes stage 1 in severity, 23.8% were stage 2, and 25.9% were stage 3. In multivariable analysis, an episode of hospitalized AKI was independently associated with a 9% increase in the urine protein-to-creatinine ratio. CONCLUSIONS: Our analysis of data from two prospective cohort studies found that hospitalization for an AKI episode was independently associated with subsequent worsening of proteinuria.
BACKGROUND: Prior studies of adverse renal consequences of AKI have almost exclusively focused on eGFR changes. Less is known about potential effects of AKI on proteinuria, although proteinuria is perhaps the strongest risk factor for future loss of renal function. METHODS: We studied enrollees from the Assessment, Serial Evaluation, and Subsequent Sequelae of AKI (ASSESS-AKI) study and the subset of the Chronic Renal Insufficiency Cohort (CRIC) study enrollees recruited from Kaiser Permanente Northern California. Both prospective cohort studies included annual ascertainment of urine protein-to-creatinine ratio, eGFR, BP, and medication use. For hospitalized participants, we used inpatient serum creatinine measurements obtained as part of clinical care to define an episode of AKI (i.e., peak/nadir inpatient serum creatinine ≥1.5). We performed mixed effects regression to examine change in log-transformed urine protein-to-creatinine ratio after AKI, controlling for time-updated covariates. RESULTS: At cohort entry, median eGFR was 62.9 ml/min per 1.73 m2 (interquartile range [IQR], 46.9-84.6) among 2048 eligible participants, and median urine protein-to-creatinine ratio was 0.12 g/g (IQR, 0.07-0.25). After enrollment, 324 participants experienced at least one episode of hospitalized AKI during 9271 person-years of follow-up; 50.3% of first AKI episodes were Kidney Disease Improving Global Outcomes stage 1 in severity, 23.8% were stage 2, and 25.9% were stage 3. In multivariable analysis, an episode of hospitalized AKI was independently associated with a 9% increase in the urine protein-to-creatinine ratio. CONCLUSIONS: Our analysis of data from two prospective cohort studies found that hospitalization for an AKI episode was independently associated with subsequent worsening of proteinuria.
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