Key result
Higher baseline KIM-1 is linked to ~6% lower urine sodium concentration per two-fold increase.
Why the study?
Greater sodium avidity in AHF is associated with worse outcomes, but whether kidney tubule injury is associated with sodium avidity and impaired diuretic responsiveness remains underexplored.
Does kidney tubular injury, as assessed by urine KIM-1 and NAG, reduce urinary sodium excretion and diuretic responsiveness in patients hospitalized with acute heart failure?
Cross-Sectional (n=339)
Yes
Does kidney tubular injury, as assessed by urine KIM-1 and NAG, reduce urinary sodium excretion and diuretic responsiveness in patients hospitalized with acute heart failure?
Kidney tubular injury, indicated by elevated urine KIM-1 and NAG levels, is associated with greater sodium avidity and impaired diuretic responsiveness in patients with acute heart failure.
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May identify acute HF patients with greater sodium avidity; hypothesis-generating for tubular injury in diuretic resistance.
Aims Greater sodium avidity in acute heart failure (AHF) is associated with worse outcomes, but whether kidney tubule injury is associated with sodium avidity and impaired diuretic responsiveness remains underexplored. Methods We evaluated 339 participants from the ROSE-AHF trial, which enrolled patients hospitalized for AHF with kidney dysfunction and randomized them to the dopamine, nesiritide or placebo group. Urinary kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and neutrophil gelatinase-associated lipocalin (NGAL) were measured at enrollment. Associations between these biomarkers and urinary sodium (uNa) concentration at baseline, fractional excretion of sodium (FeNa), as well as total uNa output and urine output over 72-hours were assessed using multivariable regression models. Results Higher KIM-1 and NAG values at baseline were associated with lower uNa concentration at baseline (-6.1% [-8.5%, -3.7%], p < 0.001 and -5.9% [-9.2%, -2.6%], p = 0.001, respectively, per two-fold increase in each biomarker). Higher baseline KIM-1 and NAG were also associated with lower FeNa (-6.1% [-8.5%, -3.6%], p < 0.001 and -5.2% [-8.6%, -3.6%], p = 0.001, respectively, per two-fold increase in each biomarker). Higher baseline KIM-1 was associated with lower total uNa excretion over 72-hours (-3.6% [-6.8%, -0.2%], p = 0.037 per two-fold increase). None of the biomarkers were associated with urine output over 72-hours. Conclusion Kidney tubular injury, as assessed by urine KIM-1 and NAG, is associated with greater sodium avidity and higher KIM-1 is associated with impaired diuretic responsiveness in AHF.
Horiuchi et al. (2026) conducted a cross-sectional in Acute heart failure with kidney dysfunction (n=339). Higher baseline urinary kidney tubule injury biomarkers (KIM-1 and NAG) vs. Lower baseline biomarker levels was evaluated on Urine sodium (uNa) concentration at baseline (enrollment) (-6.1% change per two-fold increase in KIM-1, 95% CI -8.5%, -3.7%, p=<0.001). Higher baseline levels of kidney tubule injury biomarkers (KIM-1 and NAG) were significantly associated with lower baseline urine sodium concentration (reduced by 6.1% per two-fold increase in KIM-1), indicating greater sodium avidity.
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