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Abstract: PO2251

Plasma Oxalate and Risk of Adverse Outcomes in CKD

Session Information

Category: CKD (Non-Dialysis)

  • 2101 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Tio, Maria Clarissa, Division of Renal Medicine, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Srivastava, Anand, Division of Nephrology and Hypertension, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States
  • Curhan, Gary C., Division of Renal Medicine, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Feldman, Harold I., Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Rhee, Eugene P., Division of Nephrology, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Ramachandran, Vasan S., Section of Preventive Medicine and Epidemiology and Cardiovascular Medicine, Departments of Medicine and Epidemiology, Boston University Schools of Medicine and Public Health, Boston, Massachusetts, United States
  • Kimmel, Paul L., Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, United States
  • Waikar, Sushrut S., Section of Nephrology, Department of Medicine, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts, United States

Group or Team Name

  • CRIC Investigators, CKD Biomarkers Consortium
Background

Oxalate is a novel risk factor for CKD but data on plasma oxalate (POx) and outcomes are limited to primary hyperoxaluria. We studied the associations of POx with CKD progression and death in common forms of CKD using the Chronic Renal Insufficiency Cohort (CRIC).

Methods

We measured POx in 1,800 randomly selected CRIC participants at the year 1 visit using the Broad’s high-throughput liquid chromatography-mass spectrometry untargeted metabolomics panel. Multivariable Cox proportional hazards regression tested the associations of POx with CKD progression (50% eGFR decline/ESKD) and death. We also tested whether eGFR modified these associations.

Results

Mean eGFR decreased with higher POx quartiles. eGFR modified the associations of POx with CKD progression (P=0.01) and death (P=0.02). In participants with eGFR>45, higher POx quartiles were associated with CKD progression after adjusting for demographic factors, comorbidities, medications, lab values (including hemoglobin, serum albumin, urine protein-to-creatinine ratio), and eGFR (Q3 vs Q1: HR 2.07, 95% CI 1.12-3.82; Q4 vs. Q1: HR 2.23, 95% CI 1.24-3.99). Higher POx was associated with death in participants with eGFR>45 after multivariable adjustment (Q4 vs. Q1, HR 1.94, 95% CI 1.10-3.44). POx doubling was associated with a 34% increased risk of CKD progression and 28% increased risk of death (Table 1A). In those with eGFR<45, higher POx was associated with CKD progression after adjusting for demographic factors, comorbidities, medications, and lab values. Adjusting for eGFR attenuated these associations, with higher POx trending towards being protective of CKD progression. Associations of POx and death were not significant after adjusting for covariates and trended towards being protective after adjusting for eGFR (Table 1B). Sensitivity analyses adjusting for 24-hour urinary oxalate did not change these associations.

Conclusion

Higher plasma oxalate may be an independent risk factor for CKD progression/ESKD and death in persons with eGFR>45.

Funding

  • NIDDK Support