Background and Objectives: Post-transplant diabetes mellitus (PTDM) is a significant risk factor for the survival of graft recipients and occurs in 10–30% of patients after kidney transplant (KT). PTDM is associated with premature cardiovascular morbidity and mortality. Weight gain, obesity, and dyslipidemia are strong predictors of PTDM, and by modifying them with an active lifestyle it is possible to reduce the incidence of PTDM and affect the long-term survival of patients and grafts. The aim of our study was to determine the effect of regular physical activity on the development of PTDM and its risk factors in patients after KT. Materials and Methods: Participants in the study had to achieve at least 150 min of moderate-intensity physical exertion per week. The study group (n = 22) performed aerobic or combined (aerobic + strength) types of sports activities. Monitoring was provided by the sports tracker (Xiaomi Mi Band 4 compatible with the Mi Fit mobile application). The control group consisted of 22 stable patients after KT. Each patient underwent an oral glucose tolerance test (oGTT) at the end of the follow-up. The patients in both groups have the same immunosuppressive protocol. The total duration of the study was 6 months. Results: The patients in the study group had significantly more normal oGTT results at 6 months compared to the control group (p < 0.0001). In the control group, there were significantly more patients diagnosed with PTDM (p = 0.0212) and with pre-diabetic conditions (impaired plasma glucose and impaired glucose tolerance) at 6 months (p = 0.0078). Conclusions: Regular physical activity after KT provides significant prevention against the development of pre-diabetic conditions and PTDM.

Background: Protein–energy wasting (PEW) is a major predictor of morbidity and mortality in patients with chronic kidney disease (CKD), even before the initiation of dialysis. Its multifactorial pathogenesis includes reduced dietary intake, chronic inflammation, metabolic acidosis, hormonal disturbances, and dysbiosis of the gut microbiota. Early recognition and targeted management are crucial for preventing muscle loss, functional decline, and adverse outcomes. Methods: This narrative review summarises and integrates current evidence from the literature on nutritional and metabolic interventions to prevent and treat protein–energy wasting in patients with nondialysis chronic kidney disease. Relevant clinical trials, meta-analyses, and experimental studies published up to date were evaluated, focusing on dietary strategies, metabolic modulation, physical exercise, and gut microbiome-targeted therapies. Results: Adequate energy and protein intake remain the cornerstone of PEW management, based on available clinical and observational evidence. Individualised diets emphasising high-quality and plant-based proteins, oral nutritional supplements, and ketoanalogues can attenuate muscle wasting. Correction of metabolic acidosis and inflammation enhances protein anabolism and nitrogen balance. Physical exercise acts synergistically with dietary interventions to preserve muscle mass and function. Novel approaches—such as modulating the gut–kidney axis with pre-, pro-, and postbiotics or supplementing with short-chain fatty acids—show promise in improving metabolic and inflammatory profiles. Conclusions: The management of PEW in nondialysis CKD requires a personalised approach that integrates nutrition, physical activity, metabolic correction and microbiome modulation. Early, coordinated intervention may help to slow the progression of CKD and improve patient survival and quality of life.

Background: Keto analogues in combination with a (very) low-protein diet significantly reduces the progression to end-stage kidney disease. The question of their benefit and safety for kidney transplant recipients remains. This study aimed to show the renoprotective effect and safety of the use of this method in patients with chronic kidney disease and a kidney transplantation. Materials: This was a retrospective monocentric study conducted by the transplant nephrology department in Martin, in which patients with chronic kidney disease, with or without kidney transplant therapy, who received a low-protein diet and supplementation with keto analogues were included (n = 59). The changes in their glomerular filtration rate, proteinemia, calcaemia, weight, and glycaemia and the side effects associated with a low-protein diet and keto analogue use were studied in the patients with chronic kidney disease with or without kidney transplantation. Results: The kidney transplant recipients had a significantly more advanced stage of chronic kidney disease (p = 0.0001) than the non-transplanted patients at the time of the prescription of the keto analogues (p = 0.0001). Furthermore, the kidney transplant recipients had a significantly longer follow-up period (p = 0.0001), with a difference of 27 months within subgroups. During the observed period, we recorded a decrease in glomerular filtration, but without statistical significance. In our group, we did not confirm a significant occurrence of adverse effects associated with a low-protein diet and keto analogues. Conclusion: Keto analogues reduce the progression of chronic kidney disease and stabilise glomerular filtration in patients with chronic kidney disease. Based on our analysis, treatment with keto analogues is effective and safe for kidney transplant recipients after kidney transplantation.

Background/Objectives: Potent immunosuppression lowers the incidence of acute graft rejection but increases the risk of infections. In order to decrease either infectious complications or acute rejection, it is necessary to identify risk groups of patients profiting from personalized induction immunosuppressive treatment. The aim of our analysis was to find whether there were higher incidences of infectious complications after kidney transplantation (KT) in groups with different induction immunosuppressive treatment and also to find independent risk factors for recurrent infections. Materials: We retrospectively evaluated all patients with induction treatment with basiliximab after kidney transplantation from 2014 to 2019 at our center relative to age- and sex-matched controls of patients with thymoglobulin induction immunosuppression. Results: Our study consisted of two groups: basiliximab (39) and thymoglobulin (39). In the thymoglobulin group we observed an increased incidence of recurrent infection in every observed interval; however, acute rejection was seen more often in the basiliximab group. A history of respiratory diseases and thrombocytopenia were identified as independent risk factors for recurrent bacterial infections from the first to sixth month after KT. Decreased eGFR from the first month, infections caused by multi-drug-resistant bacteria, and severe infections (reflected by the need for hospitalization) were identified as independent risk factors for recurrent bacterial infections from the first to the twelfth month after KT. Conclusions: We found that in the group of patients with thymoglobulin induction immunosuppressive treatment, infectious complications occurred significantly more often during the entire monitored period with decreased incidence of acute humoral and cellular rejection occurred more often.

Background: The diagnosis of graft rejection relies on the identification of donor-specific antibodies along with histological findings. Borderline changes are particularly challenging, representing non-rejection findings in up to 70% of cases. The analysis aimed to compare the results of histopathological conclusions with the findings from examination using a molecular microscope, which assesses gene expression (whole-genome microarray chip technology). Methods: Molecular microscope examination (MMDx) was applied to twelve patients (six men and six women) who underwent either indication or protocol graft biopsy. Results: The average age of patients was 46.6 years ± 4.2 (average follow-up from kidney transplantation was 6.1 months ± 1.2). MMDx examination was performed during indication biopsy in 11 patients and protocol biopsy in 1 patient. A total of 33% of the findings matched and 50% did not. Finally, we present a case of a patient with acute cellular rejection findings without clinical and laboratory correlation, where the use of MMDx significantly altered the treatment strategy. Conclusions: MMDx examination is suitable for complementing patients with ambiguous histological findings and a clinical picture not corresponding to biopsy results. The limitations of MMDx include cost and its inability to evaluate the potential recurrence of the underlying kidney disease in the graft.

BACKGROUND The recurrence of IgA nephropathy (IgAN) after kidney transplantation (KT) varies between 9% and 51%. Our analysis aimed to identify risk and protective HLA alleles for the development of IgAN and its recurrence after KT. MATERIAL AND METHODS This retrospective single-center analysis included all patients after KT. Patients underwent HLA typing prior to being listed on the waiting list for KT. Comparisons were performed with a cohort of 10 000 healthy donors from the Eurotransplant registry. RESULTS A total of 470 patients were included. Biopsy-proven IgAN, as the underlying cause of renal failure, was found in 7.2% (n=48), of whom 77% were male (n=37). The DRB1*11 allele was present in 47.92% and was identified as a significant risk factor for IgAN (OR 2.09, P=0.0048). The DRB1*03 allele was detected in 4.17%, and we identified it as potentially protective (OR 0.2, P=0.5472). Recurrence of IgAN was detected in 20.8%, 100% of whom were male. The mean time to confirm recurrence was 56.1 months. We identified the DRB1*11 risk allele in 77.8% of patients with confirmed recurrence but did not identify it as an independent risk factor (HR 2.3967; P=0.3956). We found a significant correlation of IgAN recurrence with the development of DSA after KT (r 0.3980, P=0.0218). CONCLUSIONS Our study identified a 20.8% incidence of IgAN recurrence after KT; 77.8% of these patients had the HLA-DRB1*11 allele, which we also identified as a risk allele for the development of IgAN in native kidneys. De novo DSA after KT was correlated with IgAN recurrence.