Kidney transplantation is currently the treatment of choice for patients with end-stage kidney diseases. Although significant advancements in kidney transplantation have been achieved over the past decades, the host’s immune response remains the primary challenge, often leading to potential graft rejection. Effective management of the immune response is essential to ensure the long-term success of kidney transplantation. To address this issue, immunosuppressives have been developed and are now fully integrated into the clinical management of transplant recipients. However, the considerable inter- and intra-patient variability in pharmacokinetics (PK) and pharmacodynamics (PD) of these drugs represents the primary cause of graft rejection. This variability is primarily attributed to the polymorphic nature (genetic heterogeneity) of genes encoding xenobiotic-metabolizing enzymes, transport proteins, and, in some cases, drug targets. These genetic differences can influence drug metabolism and distribution, leading to either toxicity or reduced efficacy. The main objective of the present review is to report an historical overview of the pharmacogenetics of immunosuppressants, shedding light on the most recent findings and also suggesting how relevant is the research and investment in developing validated NGS-based commercial panels for pharmacogenetic profiling in kidney transplant recipients. These advancements will enable the implementation of precision medicine, optimizing immunosuppressive therapies to improve graft survival and kidney transplanted patient outcomes.

Background/Objectives: Risk stratification of patients presenting to the emergency department (ED) with suspected infection is essential. Soluble urokinase plasminogen activator receptor (suPAR) has emerged as a promising biomarker of immune activation and outcome prediction, but its role in febrile ED patients remains to be fully defined. The aim of this study was to evaluate the prognostic value of suPAR and its potential clinical application in the ED. Methods: A single-center retrospective study including 125 patients was performed. Plasma suPAR levels were measured together with C-reactive protein (CRP) and procalcitonin (PCT), and their association with 28-day mortality using Cox regression and ROC curve analyses was assessed. Results: SuPAR was independently associated with the risk of 28-day mortality, showing a very high negative predictive value. Higher suPAR levels were associated with an increased risk of death. Conclusions: SuPAR may represent a valuable tool to support early patient assessment and risk stratification in the ED, potentially improving resource utilization and patient prioritization.