Key result
Higher urinary NAG linked to ~17% higher risk of death or HF rehospitalization per SD.
Why the study?
Mitral regurgitation aggravates hypoperfusion and hypoxia in heart failure, and renal tubular damage is common, but the correlation between tubular dysfunction and mitral regurgitation has not been studied.
Does higher urinary N-acetyl-β-d-glucosaminidase (uNAG) predict the composite of all-cause mortality or HF rehospitalization in adult patients with heart failure and mitral regurgitation?
Cohort (n=390)
No
Does higher urinary N-acetyl-β-d-glucosaminidase (uNAG) predict the composite of all-cause mortality or HF rehospitalization in adult patients with heart failure and mitral regurgitation?
Effect estimate: HR 1.17 (95% CI 1.02-1.33)
p-value: p=0.022
Elevated urinary NAG levels at admission independently predict a higher risk of all-cause mortality or heart failure rehospitalization in patients with heart failure and mitral regurgitation.
May aid risk stratification in HF with mitral regurgitation; hypothesis-generating and requires prospective validation.
Background: Mitral regurgitation (MR) has a high prevalence and aggravates hypoperfusion and hypoxia in heart failure (HF). Renal tubular epithelial cells are sensitive to hypoxia, and therefore tubulointerstitial damage is quite common in HF. However, the correlation between tubular dysfunction and MR has not been studied. The aim of this work was to evaluate the prognostic significance of urinary N-acetyl-β-d-glucosaminidase (uNAG), a biomarker of renal tubular damage, in patients with HF and MR. Methods: This was a prospective cohort study of 390 patients (mean age 64 years; 65.6% male) with uNAG measurement on admission (expressed as urinary NAG/urinary creatinine) and at least 1 year of follow-up data. The pre-defined primary endpoint was the composite of all-cause mortality or rehospitalization for HF after discharge. Cox regression analysis, restricted cubic splines, and subgroup analysis were used to investigate the prognostic value of uNAG modeled as a categorical (quartiles) or continuous (per SD increase) variable. Results: A total of 153 (39.23%) patients reached the composite endpoint over a median follow-up time of 1.2 years. The uNAG level correlated with the severity of HF and with the incidence of adverse events. In a multivariable Cox regression model, each SD (13.80 U/g⋅Cr) of increased uNAG was associated with a 17% higher risk of death or HF rehospitalization (95% confidence interval, 2–33%, p = 0.022), and a 19% higher risk of HF rehospitalization (p = 0.027). Subgroup analysis revealed the associations between uNAG and poor prognosis were only significant in younger patients (≤65 years) and in patients without obvious cardiovascular comorbidities. Conclusions: uNAG levels at admission were associated with the risk of adverse outcomes in patients with HF and MR. Additional studies are needed to further investigate the heart-kidney interaction.
No takes yet. Share an insight, caveat, or question.
Zhao et al. (2023) conducted a cohort in Heart Failure and Mitral Regurgitation (n=390). Urinary N-acetyl-β-d-glucosaminidase (uNAG) was evaluated on Composite of all-cause mortality or heart failure rehospitalization (HR 1.17, 95% CI 1.02-1.33, p=0.022). Each standard deviation increase in urinary N-acetyl-β-d-glucosaminidase levels was associated with a 17% higher risk of all-cause mortality or heart failure rehospitalization (HR 1.17).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: