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 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.

Background: Glycemic variability (GV) may play an important role in metabolic outcomes after kidney transplantation (KT). This study aimed to evaluate the association between early post-transplant GV, assessed by continuous glucose monitoring (CGM), and the subsequent development of post-transplant dysglycemia. Methods: This prospective exploratory pilot study included adult recipients of primary deceased-donor KT at Martin University Hospital, Slovakia. The Dexcom G6 CGM system was applied immediately before KT and continuously measured interstitial glucose for seven days after KT. Demographic, clinical, and biochemical data were collected on day 0, and 7, and at months 3, 12. Results: Twenty patients completed the 12-month follow-up. PTDM/prediabetes developed in 10 (50%) and had higher HbA1c on day 7 (p = 0.038) and lower postprandial insulin (p = 0.042). At 3 and 12 months, HbA1c (p = 0.006), fasting insulin (p = 0.0219), and HOMA-IR (p = 0.006) were significantly elevated in this group. CGM demonstrated higher mean glucose (p = 0.021), SD (p = 0.001), and estimated HbA1c (p = 0.017), with longer time above range (p = 0.042) and shorter time in range (p = 0.037). In exploratory regression analyses, CV ≥ 36% (aOR 7.31, p = 0.049) and TAR (aOR 1.35, p = 0.045) were associated with subsequent PTDM/prediabetes. Conclusions: In this prospective exploratory pilot study, higher early postoperative GV was associated with subsequent post-transplant dysglycemia. These findings suggest that CGM-derived metrics may help identify patients at higher metabolic risk after KT; however, given the small sample size and exploratory design, the results should be interpreted as hypothesis-generating.

Background: Early post-transplant albuminuria is associated with adverse graft and cardiovascular outcomes and may reflect ischemia–reperfusion injury-induced damage to the glomerular filtration barrier. However, evidence for safe adjunctive interventions targeting these early pathophysiological processes remains limited. Methods: In this single-center prospective cohort study with historical controls, adult kidney transplant recipients transplanted between January 2020 and September 2022 served as controls, while consecutive recipients transplanted from October 2022 onward received adjunctive silymarin (900 mg/day for 30 days) in addition to standard immunosuppression. The principal renal outcome was UACR assessed during the first 3 months post-transplant. A ≥25% reduction in UACR between Months 1 and 3 was additionally evaluated as an exploratory responder outcome. Secondary outcomes included estimated glomerular filtration rate (eGFR), lipid profile parameters, tacrolimus exposure, and safety. Results: A total of 136 patients (78 silymarin-treated and 58 controls) were included. UACR was consistently lower in the silymarin group at months 1–3. In multivariable analysis, silymarin treatment was independently associated with lower UACR at month 3. In an exploratory responder analysis, a ≥25% reduction in UACR between Months 1 and 3 occurred more frequently in silymarin-treated patients (OR 3.28, 95% CI 1.38–7.79; p = 0.007). eGFR trajectories were similar between groups. No consistent independent effects on lipid parameters were observed after adjustment. Tacrolimus exposure and adverse event rates were comparable between groups. Conclusions: Short-term silymarin exposure initiated early after kidney transplantation was associated with lower UACR during the first three post-transplant months. These findings support a potential targeted effect on early glomerular injury and suggest that silymarin may represent a safe adjunctive strategy to modulate early post-transplant risk.