The kynurenine:tryptophan ratio as a predictor of incident type 2 diabetes mellitus in individuals with coronary artery disease

Figures

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  Fig. 1. Cox regression with penalised smoothing splines showing the associations of (a) plasma KTR and (b) urine KTR to incident type 2 diabetes (n = 2263). The solid lines denote HRs and the grey areas, 95% CIs on the (loge-transformed) y-axes. Density plots show the distributions of (loge transformed) plasma and urine KTR concentrations on the x-axes. The vertical red lines mark the 25th, 50th and 75th percentiles. Both models include adjustments for age, sex, BMI, eGFR, CRP, HbA1c, serum triacylglycerol, ApoA-1, urine albumin:creatinine ratio, and use of loop diuretics, ACE inhibitors or angiotensin II receptor blockers, statins and β-blockers. Ranges from the 2.5th to 97.5th percentiles of exposure variables are included

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  Fig. 2. Multivariate adjusted HRs of urine KTR for incident type 2 diabetes in subgroups. Dichotomous subgroups were generated for sex and significant CAD at coronary angiography (at least one stenosis with ≥50% luminal narrowing in a main coronary artery or its major side branches, identified by coronary angiography), or according to the median values of continuous variables. HRs are represented by squares and are reported per SD increment of loge transformed urine KTR levels. The horizontal lines indicate 95% CIs. HRs are adjusted for age, sex, BMI, eGFR, CRP, HbA1c, serum triacylglycerol, ApoA-1, urine albumin:creatinine (U-alb:creat) ratio, and use of loop diuretics, ACE inhibitors or angiotensin II receptor blockers, statins and β-blockers