Table 3.
Independent predictors of renal tubular damage and worsening renal function
| Multivariable model* | ||
|---|---|---|
| OR (95%CI) | P‐value | |
| Renal tubular damage (dependent variable)a | ||
| NT‐proBNP (per doubling) | 1.26 (1.07‐1.49) | P = .006 |
| eGFR (per 10 mL/min/1.73 m2 decrease) | 1.16 (1.03‐1.32) | P = .015 |
| WRF (dependent variable)b | ||
| Loop diuretics (per 40 mg furosemide equivalent. dose increase) | 1.30 (1.07‐1.59) | P = .010 |
| MRAs (per 25 mg spironolactone equivalent. dose decrease) | 1.85 (1.10‐3.09) | P = .019 |
| eGFR (per 10 mL/min/1.73 m2 decrease) | 0.73 (0.63‐0.85) | P < .001 |
Note: OR indicates odds ratio for having a more severe tubular damage or WRF; 95%CI indicates 95% confidence interval for the corresponding OR; eGFR indicates estimated glomerular filtration rate, MRAs indicates mineralocorticoid receptor antagonists.
Covariates that were found to be different across categories of tubular damage with P < .10 (see Table 1) were entered into a multivariable ordinal regression model and those were: age, NYHA class, diabetes, use of cardiac resynchronization therapy (CRT), diastolic blood pressure, NT‐proBNP, cTnT, and eGFR.
*Represents only covariates with P‐value <.05 were presented in the table.
Covariates that were found to be different between WRF patient and non‐WRF patients with P < .10 (see Table 2) were entered into a multivariable binary regression model and those were: diastolic blood pressure, NT‐proBNP, hs‐cTnT, eGFR, urinary NAG, prior myocardial infarction, loop diuretics and MRAs doses.