Table 2.

Association of circulating CML and CEL with cardiovascular and all-cause mortality in 555 kidney transplant recipients

Models	CML Concentration,			CEL Concentration,
	per 1‒SD Increment			per 1‒SD Increment
	aHR	95% CI	P Value	bHR	95% CI	P Value
Cardiovascular mortality
Unadjusted	1.50	1.23 to 1.82	<0.001	1.37	1.13 to 1.66	0.001
Model 1	1.55	1.24 to 1.95	<0.001	1.53	1.18 to 1.98	0.002
Model 2	1.55	1.23 to 1.96	<0.001	1.55	1.18 to 2.04	0.002
Model 3	1.53	1.21 to 1.93	<0.001	1.54	1.18 to 2.00	0.001
Model 4	1.56	1.23 to 1.97	<0.001	1.46	1.12 to 1.91	0.005
All-cause mortality
Unadjusted	1.31	1.12 to 1.55	0.001	1.31	1.13 to 1.52	<0.001
Model 1	1.24	1.02 to 1.50	0.03	1.32	1.08 to 1.61	0.006
Model 2	1.23	1.01 to 1.50	0.04	1.34	1.09 to 1.64	0.006
Model 3	1.22	1.01 to 1.48	0.04	1.33	1.09 to 1.62	0.005
Model 4	1.24	1.02 to 1.50	0.03	1.31	1.07 to 1.60	0.01

Cox proportional-hazards regression analyses were performed to assess the association of circulating CML and CEL with cardiovascular (n=63) and all-cause (n=122) mortality. Multivariable-adjusted model 1 included adjustment for age, body mass index, history of diabetes, smoking status, high-sensitivity C-reactive protein, eGFR, and proteinuria. CML, N^ε-(Carboxymethyl)lysine; CEL, N^ε-(Carboxyethyl)lysine; HR, hazard ratio; 95% CI, 95% confidence interval.

^aAdditional adjustment was performed for cardiovascular history and diastolic BP (model 2), alcohol use (model 3), and use of proliferation inhibitor (model 4).

^bAdditional adjustment was performed for cardiovascular history and use of angiotensin-converting enzyme or angiotensin II receptor blocker (model 2), homeostasis model assessment of insulin resistance (model 3), and dialysis vintage, use of proliferation inhibitor and cumulative prednisolone dose (model 4).