INTRODUCTION: Adipose tissue is involved in the synthesis of hormones that have an impact on food intake regulation, control of insulin sensitivity or regulation of infl ammatory processes. The aim of this study was to determine the importance of adipocytokines and interleukins levels for the development of post-transplant diabetes mellitus (PTDM) after kidney transplantation (KT). MATERIAL AND METHODS: In the prospective analysis, the studied sample (n = 104) was divided into the control group, prediabetes group and PTDM group. Prior to transplantation, and subsequently, at 3, 6 and 12 months after KT, we recorded the basic characteristics of the donor and recipient, including parameters refl ecting graft function, metabolic and anthropometric parameters. At the same time, we monitored the levels of adiponectin, leptin and interleukins during the monitored period. RESULTS: Using multivariate logistic regression, we identifi ed hyperleptinemia 12 months after KT as an independent risk factor for PTDM development 1 year after KT [OR 1.0320; 95% Cl 0.9785-1.0884 (p=0.0038)]. At the same time, we confi rmed that age at the time of KT is also an independent risk factor for PTDM [OR 1.0903; 95% Cl 1.0149-1.1714 (p = 0.0180)]. CONCLUSION: We confi rmed that elevated leptin level 12 months after KT is associated with the development of PTDM (Tab.

OBJECTIVES: The aim of the study was to stratify the immunological risk based on the presence of risk factors using different induction immunosuppressive protocols. BACKGROUND: The path to successful kidney transplantation refl ects the accuracy of immunological risk assessment and choice of correct induction and maintenance of immunosuppression to avoid acute kidney rejection. METHODS: We performed a multicentre prospective analysis consisting of patients after kidney transplantation with a 12-month follow-up. RESULTS: In total, 152 kidney transplant recipients were included, of whom 100 were males (66.4 %). We divided patients according to the induction immunosuppression as follows: no induction (n = 19), induction with basiliximab (n = 60), and induction with ATG at cumulative doses of 3.5 mg/kg (n = 42) and 6 mg/kg (n = 31). In our study, we demonstrated a shorter survival of patients without induction immunosuppression. In the basiliximab group, the duration of dialysis ≥ 3 years (p = 0.0191), cold ischaemia time ≥ 1,020 minutes or expected delayed graft function (p < 0.0001) are independent risk factors for graft loss (p = 0.0097). CONCLUSIONS: Risk of no induction immunosuppression signifi cantly exceeds the risks associated with its administration and is desirable even in patients at low immunological risk. Induction immunosuppression should be tailored individually and thus differ from patient to patient (Tab. 6, Fig. 1, Ref. 15).