Background The criteria for kidney suitability in uncontrolled donors after circulatory death (uDCD) procured after regional normothermic perfusion are based on macroscopic appearance and renal haemodynamic values with final renal resistance (FRR). However, these criteria have not been analysed to predict the future graft function. This study presents a model to predict the outcome in uDCD kidneys and define the predictive FRR value. Methods All uDCD kidney transplants performed in our hospital from 2004 to 2016 were included. Donors and recipients and pre-transplantation data are described. The endpoint was glomerular filtration rate (GFR) 30mL/min at 6months after transplantation. Results A total of 194 recipients were included. FRR in donors 60years old was (meanSD) 0.27 +/- 0.11 versus 0.22 +/- 0.09mmHg/mL/min in donors <60years (P=0.042). Kidney survival was 88.2% versus 84% at 12months and 60.7% versus 30.8% at 120months (P=0.067). For the group of recipients from donors 60years, the FRR was 0.37 +/- 0.08mmHg/mL/min in the GFR<30mL/min group versus 0.18 +/- 0.06mmHg/mL/min in the GFR 30mL/min group (P<0.001). The value FRR 0.3mmHg/mL/min predicts 59-79% of GFR <30mL/min [odds ratio = 2.16, 95% confidence interval (CI) 1.80-6.40; P<0.001]. The predictive accuracy of FRR for GFR by ROC curve was 0.968 (95% CI). The best cut-off for FRR was 0.3mmHg/mL/min to predict GFR at 6months with a sensitivity of 67%, specificity of 100%, positive predictive value of 83% and negative predictive value of 92%. Conclusions Our results suggest that in uDCD donors the combination of donor age 60years together with FRR 0.3mmHg/mL/min could predict poor outcome at 6months after transplantation in low immunological risk recipients.

Diabetes mellitus (DM) in kidney transplant recipients (KTR) is a risk factor for mortality, increases the risk of infections and, in the long term, can lead to graft loss due to diabetic kidney disease. A preventive approach applied to those on the waiting list could decrease the incidence of post-transplant DM (PTDM) by detecting those patients at risk, thus allowing strategies to minimize the probability of developing a New Onset Diabetes After Transplant (NODAT). On the other hand, modifications of immunosuppressive therapy may improve glucose control in patients with KTR. In recent years, two new classes of antidiabetic drugs and non-steroidal mineralocorticoid receptor antagonists have demonstrated cardiovascular and renal benefits in randomized clinical trials where the transplant population has not been represented. Because of the potential benefit expected in this population, the clinical use of glucagon-like peptide-1 receptor agonists (GLP-1RA), sodium-glucose cotransporter 2 inhibitors (SGLT2i) and finerenone is increasing in the kidney transplant setting. This review focuses on comprehensive pharmacological interventions in KTR with glucose metabolism disorders. In-depth knowledge in this area will allow prevention and identification of potential adverse effects or drug interactions in the clinical course of KTR with DM.

Kidney transplantation (KT) represents a pivotal intervention for patients with chronic kidney disease (CKD), significantly improving survival and quality of life. However, KT recipients face an array of non-immunological complications, collectively amplifying cardiovascular (CV) and metabolic risks. This review explores the intersection of cardio-metabolic syndrome and KT, emphasizing the recently introduced cardiovascular–kidney–metabolic (CKM) syndrome. CKM syndrome integrates metabolic risk factors, CKD, and CV disease, with KT recipients uniquely predisposed due to immunosuppressive therapies and pre-existing CKD-related risks. Key issues include post-transplant hypertension, obesity, dyslipidemia, post-transplant diabetes mellitus (PTDM), and anemia. Immunosuppressive agents such as corticosteroids, calcineurin inhibitors, and mTOR inhibitors contribute significantly to these complications, exacerbating metabolic dysfunction, insulin resistance, and lipid abnormalities. For instance, corticosteroids and calcineurin inhibitors heighten the risk of PTDM, while mTOR inhibitors are strongly associated with dyslipidemia. These pharmacologic effects underscore the need for tailored immunosuppressive strategies. The management of these conditions requires a multifaceted approach, including lifestyle interventions, pharmacological therapies like SGLT2 inhibitors and GLP-1 receptor agonists, and close monitoring. Additionally, emerging therapies hold promise in addressing metabolic complications in KT recipients. Proactive risk stratification and early intervention are essential to mitigating CKM syndrome and improving outcomes. This comprehensive review highlights the importance of integrating cardio-metabolic considerations into KT management, offering insights into optimizing long-term recipient health and graft survival.

In 2011, the first Direct Acting Antiviral (DAA) agent was approved for HCV treatment, with high rates of sustained viral response (SVR). Absence of RNA‐HCV viral load 12 weeks after end of treatment is considered as permanent viral eradication. However anti‐HCV could remain positive despite successful antiviral therapy2.Moreover,HCV can infect extrahepatic tissues, including kidney. The infected extrahepatic tissues might play a role in both HCV persistence and reactivation of infection.

Osteoporosis and fragility fractures are among the most prevalent and clinically significant complications in patients with chronic kidney disease (CKD), particularly in stages G4–G5 and in those undergoing dialysis (G5D). These skeletal disorders are associated with markedly increased morbidity and mortality, including a 2- to 9-fold higher risk of hip fractures compared to the general population, prolonged hospitalization, functional decline, and excess postoperative mortality. Despite this substantial burden, CKD-associated osteoporosis remains underrecognized and undertreated. Limited inclusion of CKD patients in pivotal osteoporosis trials and the absence of high-evidence guidance in clinical guidelines have contributed to a persistent therapeutic gap. PTH analog agents such as teriparatide and abaloparatide have demonstrated robust efficacy in increasing bone mass and reducing fracture risk in the general population. However, their use in CKD remains limited. PTH analog are poorly prescribed in patients with CKD stage G3 and remain off-label for stages G4–G5D, despite the high prevalence of adynamic bone disease across all stages of CKD. Abaloparatide, a selective PTH1 receptor agonist, exerts potent anabolic effects with a lower incidence of hypercalcemia than teriparatide and may offer a favourable safety profile in carefully selected patients. Preliminary data suggest preservation of bone microarchitecture and potential benefits in low-turnover bone disease, although evidence in CKD is still limited. This narrative review examines current evidence on abaloparatide’s potential role in CKD, emphasizing its mechanism of action, efficacy, safety, and relevance for patients with low bone turnover and high fracture risk.