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. Author manuscript; available in PMC: 2021 Mar 1.
Published in final edited form as: Kidney Int. 2020 Jul 25;99(3):725–736. doi: 10.1016/j.kint.2020.07.007

New Table 3.

Predictive logistic models for ESKD according to baseline variables considered. Models were developed using 196 individuals selected for Macro-Albuminuria Study.

Model #1 Model #2 Model #3 Model #4*
OR 95% CI P Value OR 95% CI P Value OR 95% CI P Value OR 95% CI P Value
eGFR 0.98 (0.96–0.99) 0.0007 0.98 (0.97–1.00) 0.0545 0.98 (0.97–1.00) 0.0203 0.99 (0.97–1.01) 0.1696
HbA1c 1.57 (1.26–1.96) <.0001 1.60 (1.28–2.00) <.0001 1.60 (1.28–2.00) <.0001 1.50 (1.19–1.89) 0.0006
ACR 1.70 (1.26–2.30) 0.0005 1.62 (1.20–2.20) 0.0018 1.63 (1.20–2.21) 0.0016 1.66 (1.20–2.30) 0.0024
TNF-R1A 1.49 (1.04–2.13) 0.0279 1.24 (0.69–2.22) 0.4706
TNF-R1B 1.43 (1.02–2.00) 0.0373 0.73 (0.40–1.36) 0.3246
TNF-R6B 1.49 (1.03–2.17) 0.0357
TNF-R11A 1.73 (1.08–2.76) 0.0227
C statistics 0.774 0.788 0.784 0.815
*

Model #4: This model was developed by including 5 markers (eGFR, ACR, HbA1c, TNF-R1A and –R1B) and adding the TNF receptors that were selected from remaining 11 TNF receptors using backward elimination (p-for-stay = 0.1).

The effects of eGFR and HbA1c on development of ESKD were estimated as 1 ml/min/1.73m2 increase and as 1% increase, respectively. The effects of ACR, TNF-R1A, TNF-R1B, TNF-R6B, and TNF-R11A on development of ESKD were estimated as one quartile increase. ESKD, end-stage kidney disease. OR, odds ratio