Abstract: FR-PO097

Impact of AKI on Urine Protein Excretion

Session Information

Category: Acute Kidney Injury

  • 003 AKI: Clinical and Translational

Authors

  • Hsu, Chi-yuan, University of California San Francisco, San Francisco, California, United States
  • Kaufman, James S., VA New York Harbor Healthcare System, New York, New York, United States
  • Kimmel, Paul L., National Institute of Diabetes and Digestive Kidney Diseases (NIDDK), Bethesda, Maryland, United States
  • Kusek, John W., NIDDK, Bethesda, Maryland, United States
  • Parikh, Chirag R., Yale University and VAMC, New Haven, Connecticut, United States
  • Ricardo, Ana C., University of Illinois at Chicago, Chicago, Illinois, United States
  • Rosas, Sylvia E., Joslin Diabetes Center, Boston, Massachusetts, United States
  • Saab, Georges, MetroHealth Medical Center, Rocky River, Ohio, United States
  • Sha, Daohang, Uiversity of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Sondheimer, James H., Wayne State University School of Medicine, Detroit, Michigan, United States
  • Taliercio, Jonathan J., Glickman Urological and Kidney Institute, Cleveland, Ohio, United States
  • Hsu, Raymond K., University of California, San Francisco, San Francisco, California, United States
  • Yang, Wei, University of Pennsylvania , Philadelphia, Pennsylvania, United States
  • Go, Alan S., Kaiser Permanente Northern California, Oakland, California, United States
  • Liu, Kathleen D., University of California at San Francisco School of Medicine, San Francisco, California, United States
  • Anderson, Amanda Hyre, University of Pennsylvania , Philadelphia, Pennsylvania, United States
  • Chen, Jing, Tulane School of Medicine, New Orleans, Louisiana, United States
  • Chinchilli, Vernon M., Penn State College of Medicine, Hershey, Pennsylvania, United States
  • Feldman, Harold I., University of Pennsylvania , Philadelphia, Pennsylvania, United States
  • Garg, Amit X., London Health Sciences Centre, London, Ontario, Canada
  • Hamm, L. Lee, Tulane University School of Medicine, New Orleans, Louisiana, United States
Background

Little is known about the impact of AKI on proteinuria as existing studies of the adverse long-term renal consequences of AKI have almost exclusively focused on estimated glomerular filtration rate (eGFR). Some recent interventional studies suggest that mild-moderate severity AKI actually only lead to small loss of eGFR. However, examining changes in eGFR alone may underestimate the renal sequelae of AKI.

Methods

To increase sample size and generalizability, we combined data from participants of two prospective NIH cohort studies: all enrollees from ASsessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury (ASSESS-AKI)(2003-16)(N=1599) and the subset of Chronic Renal Insufficiency Cohort (CRIC) study enrollees recruited from Kaiser Permanente Northern California (KPNC), a large integrated healthcare delivery system (2003-15)(N=455). Urine protein-creatinine ratio (PCR) was measured centrally once a year per ASSESS-AKI and CRIC research protocols. For study participants who were hospitalized, inpatient serum creatinine (SCr) measurements obtained as part of clinical care were abstracted from medical records and AKI defined as peak/nadir inpatient SCr>1.5. Mixed effects regression was used to examine the impact of AKI on PCR, adjusting for demographics, co-morbidities and time-updated estimated GFR, sysotlic blood pressure (BP), number of BP medications and use of renin-angiotensin-system (RAS) blockers.

Results

Baseline eGFR was 66 (±25) ml/min/1.73m2 and median PCR 0.12 [IQR 0.07-0.25] (g/g), There were 275 episodes of AKI during follow-up, of which 58% were KDIGO stage 1 in severity, 23% stage 2 and 18% stage 3 (including 22 cases requiring dialyais). We found that an episode of AKI was independently associated with an increase in PCR of 0.17 g/g (P<0.0001). This increase in proteinuria is independent of changes in eGFR and does not appear to explained by higher BP or withdraw of BP medications (including RAS blockers) after AKI.

Conclusion

AKI is an independent risk factor for worsening of proteinuria among CKD patients.

Funding

  • NIDDK Support