In this study, we investigate the association between selected inflammatory-related biomarkers and post-transplant hyperglycemia in kidney transplant recipients. This retrospective analysis comprises 852 patients receiving a kidney transplant at the Norwegian national transplant center between 2007 and 2012, all having a normal oral glucose tolerance test (OGTT) before transplantation. A diagnostic OGTT was performed 10 weeks post-transplant to examine the association between inflammation-related biomarkers and two-hour plasma glucose (2HPG) by multivariable linear regression models adjusting for BMI, age, graft function, fasting insulin levels, dosage of prednisolone, and concentration of calcineurin inhibitors. Six of 20 biomarkers were significantly associated with 2HPG in multivariate analyses showing strong associations with soluble tumor necrosis factor type 1 (P = 0.027), Pentraxin 3 (P = 0.019), macrophage migration inhibitory factor (P = 0.024), and endothelial protein C receptor (P = 0.001). These associated markers reflect several distinct but also overlapping pathways including activation of tumor necrosis factor, macrophages, and endothelial cells. The multinomial logistic regression model showed a clear association between the inflammatory biomarkers and post-transplant diabetes mellitus (PTDM). The association between a range of inflammation markers and PTDM suggests that these markers may be target for future studies on pathogenesis and perhaps also treatment of PTDM.

In the general population, low‐grade inflammation has been established as a risk factor for all‐cause mortality. We hypothesized that an inflammatory milieu beyond the time of recovery from the surgical trauma could be associated with increased long‐term mortality in kidney transplant recipients (KTRs). This cohort study included 1044 KTRs. Median follow‐up time post‐engraftment was 10.3 years. Inflammation was assessed 10 weeks after transplantation by different composite inflammation scores based on 21 biomarkers. We constructed an overall inflammation score and five pathway‐specific inflammation scores (fibrogenesis, vascular inflammation, metabolic inflammation, growth/angiogenesis, leukocyte activation). Mortality was assessed with Cox regression models adjusted for traditional risk factors. A total of 312 (29.9%) patients died during the follow‐up period. The hazard ratio (HR) for death was 4.71 (95% CI: 2.85–7.81, p < .001) for patients in the highest quartile of the overall inflammation score and HRs 2.35–2.54 (95% CI: 1.40–3.96, 1.52–4.22, p = .001) for patients in the intermediate groups. The results were persistent when the score was analyzed as a continuous variable (HR 1.046, 95% CI: 1.033–1.056, p < .001). All pathway‐specific analyses showed the same pattern with HRs ranging from 1.19 to 2.70. In conclusion, we found a strong and consistent association between low‐grade systemic inflammation 10 weeks after kidney transplantation and long‐term mortality.