Abstract: FR-PO412

Soluble ST-2 and Galectin-3 and Risk of CKD Progression

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 301 CKD: Risk Factors for Incidence and Progression

Authors

  • Alam, Mariam L., University of Washington, Seattle, Washington, United States
  • Himmelfarb, Jonathan, Kidney Research Institute, Seattle, Washington, United States
  • Kestenbaum, Bryan R., Kidney Research Institute, Seattle, Washington, United States
  • Kretzler, Matthias, U.Michigan, Ann Arbor, Michigan, United States
  • Steigerwalt, Susan P., University of Michigan, Ann Arbor, Michigan, United States
  • Bansal, Nisha, Kidney Research Institute, Seattle, Washington, United States
  • Katz, Ronit, Kidney Research Institute, Seattle, Washington, United States
  • Bellovich, Keith A., St. John Hospital Medical Center, Detroit, Michigan, United States
  • Bhat, Zeenat Yousuf, Wayne State University, Detroit, Michigan, United States
  • Brosius, Frank C., University of Arizona, Tucson, Arizona, United States
  • de Boer, Ian H., Kidney Research Institute, Seattle, Washington, United States
  • Gadegbeku, Crystal A., Temple University, Philadelphia, Pennsylvania, United States
  • Gipson, Debbie S., University of Michigan, Ann Arbor, Michigan, United States
  • Hawkins, Jennifer Joyce, University of Michigan, Ann Arbor, Michigan, United States
Background

Cardiac biomarkers soluble ST-2 (sST-2) and galectin-3 may reflect inflammation and fibrosis. sST-2 and galectin-3 have been shown to be associated with cardiovascular events, but less is known about their associations with kidney disease. We examined associations of sST-2 and galectin-3 with kidney function decline in two chronic kidney disease (CKD) cohort studies.

Methods

The Clinical Phenotyping Phenotyping and Resource Biobank (CPROBE) and Seattle Kidney Study (SKS) are prospective studies of CKD patients. We measured serum concentrations of sST-2 and galectin-3 at baseline. Outcomes were 1) progression to end-stage renal disease (ESRD) (need for dialysis/transplant or eGFR <15 ml/min/1.73m2) and 2) annualized relative change in eGFR. We used Cox regression and generalized estimating equation models to study the association of biomarker levels with kidney outcomes, adjusting for eGFR, urine ACR (UACR), demographics, cardiovascular disease, diabetes, body mass index, blood pressure and anti-hypertensive use.

Results

Among the 561 participants in CPROBE, the mean age was 55 ± 16 years, 42% were male and 35% had diabetes. Baseline eGFR was 55 ± 31 ml/min/1.73m2 and median UACR was 217 (interquartile range [IQR] 16, 885) mg/g. Among the 280 SKS participants, the mean age was 62 ± 13 years, 82% were male and 56% had diabetes. Baseline eGFR was 42 ± 16 ml/min/1.73m2 and median UACR was 118 (IQR 15, 626) mg/g. Incidence rates of ESRD were 5.41 (110 events) and 3.73 (30 events) per 100 person-years in CPROBE and SKS, respectively. Higher sST-2 was associated with a greater annual decline in eGFR in both CPROBE and SKS, but was not associated with progression to ESRD. Higher galectin-3 was associated with an increased risk of ESRD in CPROBE only (Table).

Conclusion

Higher levels of sST-2 and galectin-3 are associated with progression of CKD, highlighting possible shared cardiac and renal mechanisms that contribute to these diseases.

Funding

  • NIDDK Support