María Molina

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.

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.

Background.: Uncontrolled donation after circulatory death (uDCD) increases organ availability for kidney transplantation (KT) at the expense of a higher risk of primary graft nonfunction (PNF). At least half of the cases of PNF are secondary to graft venous thrombosis. The potential benefit from prophylactic anticoagulation in this scenario remains unclear. Methods.: In this single-center retrospective study we compared 2 consecutive cohorts of KT from uDCD with increased (≥0.8) renal resistive index (RRI) in the Doppler ultrasound examination performed within the first 24–72 h after transplantation: 36 patients did not receive anticoagulation (“nonanticoagulation group”) and 71 patients underwent prophylactic anticoagulation until normalization of RRI in follow-up Doppler examinations (“anticoagulation group”). Results.: Anticoagulation was initiated at a median of 2 d (interquartile range, 2–3) after transplantation and maintained for a median of 12 d (interquartile range, 7–18). In 4 patients (5.6%), anticoagulation had to be prematurely stopped because of the development of a hemorrhagic complication. In comparison with the nonanticoagulation group, recipients in the anticoagulation group had a lower 2-wk cumulative incidence of graft venous thrombosis (19.4% versus 0.0%; P < 0.001) and PNF (19.4% versus 2.8%; P = 0.006). The competing risk analysis with nonthrombotic causes of PNF as the competitive event confirmed the higher risk of graft thrombosis in the nonanticoagulation group (P = 0.0001). The anticoagulation group had a higher incidence of macroscopic hematuria (21.1% versus 5.6%; P = 0.049) and blood transfusion requirements (39.4% versus 19.4%; P = 0.050) compared with the nonanticoagulation group. No graft losses or deaths were attributable to complications potentially associated with anticoagulation. Conclusions.: Early initiation of prophylactic anticoagulation in selected KT recipients from uDCD with an early Doppler ultrasound RRI of ≥0.8 within the first 24–72 h may reduce the incidence of graft venous thrombosis as a cause of PNF.

While patient care, kidney replacement therapy, and transplantation techniques for chronic kidney disease (CKD) have continued to progress, the incidence of malnutrition disorders in CKD appears to have remained unchanged over time. However, there is now a better understanding of the underlying pathophysiology according to the disease background, disease stage, and the treatment received. In CKD patients, the increased production of proinflammatory cytokines and oxidative stress lead to a proinflammatory milieu that is at least partially responsible for the increased morbidity and mortality in this patient population. New insights into the pathogenic role of innate immunity and the proinflammatory cytokine profile, characterized, for instance, by higher levels of IL-6 and TNF-α, explain some of the clinical and laboratory abnormalities observed in these patients. In this article, we will explore currently available nutritional–inflammatory biomarkers in distinct CKD populations (hemodialysis, peritoneal dialysis, transplantation) with a view to evaluating their efficacy as predictors of malnutrition and their involvement in the common proinflammatory process. Although there is a direct relationship between inflammatory-nutritional status, signs and symptoms [e.g., protein-energy wasting (PEW), anorexia], and comorbidities (e.g., atheromatosis, atherosclerosis), we are in need of clearly standardized markers for nutritional-inflammatory assessment to improve their performance and design appropriate bidirectional interventions.