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Abstract: TH-PO0753

Changes in Glomerular Filtration and Tubular Health/Damage Markers in Patients with Acute Decompensated Heart Failure

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Haeger, Sarah, University of Washington, Seattle, Washington, United States
  • Prince, David K., University of Washington, Seattle, Washington, United States
  • O'Brien, Kevin D., University of Washington, Seattle, Washington, United States
  • Lum, Dawn Marie, University of Washington, Seattle, Washington, United States
  • Shlipak, Michael G., San Francisco VA Health Care System, San Francisco, California, United States
  • Estrella, Michelle M., University of California San Francisco, San Francisco, California, United States
  • Testani, Jeffrey M., Yale University, New Haven, Connecticut, United States
  • Bansal, Nisha, University of Washington, Seattle, Washington, United States
Background

Changes in kidney function, measured by markers of glomerular filtration, are common in patients with acute decompensated heart failure (ADHF). We sought to determine if changes in glomerular filtration correlate with changes in tubular health/damage and if there are clusters of patients with distinct changes in glomerular filtration and tubular health/damage markers that have disparate outcomes.

Methods

We performed a prospective observational study of 400 patients with ADHF. Markers of glomerular filtration/integrity (serum creatinine, serum cystatin C, and urine albumin) and tubular health/damage (urine cystatin C, β2-microglobulin, IL-18, KIM-1, NGAL, clusterin, osteopontin, EGF, and UMOD) were measured at admission and euvolemia, which was defined by the transition from intravenous to oral diuretics. Urine markers were indexed to urine creatinine. A K-means cluster analysis was performed to identify clusters of participants with distinct patterns of change in glomerular filtration and tubular health/damage markers.

Results

Changes in glomerular and tubular markers were common. For each marker, ≥60% of participants exhibited a >±10% change from admission to euvolemia. Changes in serum creatinine and cystatin C correlated modestly with each other (r 0.63); however, changes in creatinine and cystatin C only weakly correlated with changes in tubular markers (max |r| 0.19). A cluster analysis using changes in all markers showed two clusters. Cluster 1 contained participants with a decrease in tubular markers, while those in cluster 2 had an increase in tubular markers. Patients in both clusters, on average, had minimal change in glomerular markers. In adjusted analyses, cluster 2 participants, in comparison to cluster 1 participants, had a longer in-hospital length of stay (mean difference 5.54 days, 95% CI 0.36 to 10.72), time to euvolemia (mean difference 1.68 days, 95% CI 0.13 to 3.24), and a greater decrease in weight from admission to euvolemia (mean difference -3.31kg, 95% CI -5.05 to -1.57).

Conclusion

Glomerular filtration/integrity and tubular health/damage markers are dynamic in patients with ADHF. Changes in glomerular markers do not correlate with changes in tubular markers. Tubular markers appear to capture prognostic information distinct from glomerular markers and may distinguish ADHF subphenotypes that correlate with clinical outcomes.

Funding

  • NIDDK Support