BackgroundRejection and graft failure remain common in kidney transplant recipients. Non-adherence to immunosuppressive medications is considered a major contributary factor to reduced long-term graft survival, particularly in younger people. Improvements in clinical practice based on adherence studies has been minimal. MethodsJoanna Briggs' Institute Methodology was used. MedlineALL, Embase, Web of Science Core Collection and Scopus databases were searched from January 2000 through to December 2023. Abstract and full text reviews were undertaken independently by two reviewers. Data was collated using a pre-designed extraction tool. Results359 articles met the inclusion criteria. Non-adherence was commonly defined using self-reported questionnaires or pharmacy re-fill rates. Prevalence of non-adherence varied widely. There was little correlation between method of measurement and reported rates of non-adherence. Despite younger age being identified as a risk factor for non-adherence, pooled reported prevalence did not differ significantly in studies reporting prevalence in children, adolescents, or young adults vs. older adults (36.0 % vs. 34.0 %). Interventional studies to detect or improve adherence are highly heterogenous, often report small effects and are limited by the lack of gold-standard methods to measure adherence. DiscussionThis scoping review outlines the complexities of non-adherence to immunosuppressive medications among kidney transplant recipients, highlighting significant variability in adherence definitions, measurements, and intervention efficacy. Reported non-adherence rates vary widely (2–89 %), underscoring the need for standardisation of the definition of non-adherence in research. Findings suggest that non-adherence to immunosuppressive medication is driven by a mix of demographic, psychosocial, and transplant-specific factors. Future research should prioritise standardised definitions of adherence, validated tools to measure adherence, and focus on clinically significant outcomes in non-adherent populations to develop meaningful, impactful interventions for long-term patient benefit.

Lung transplant (LTx) physicians are responsible for highly complex post-LTx care, including monitoring of kidney function and responding to kidney function loss. Better survival of the LTx population and changing patient characteristics, including older age and increased comorbidity, result in growing numbers of LTx patients with chronic kidney disease (CKD). CKD after LTx is correlated with worse survival, decreased quality of life and high costs. Challenges lie in different aspects of post-LTx renal care. First, serum creatinine form the basis for estimating renal function, under the assumption that patients have stable muscle mass. Low or changes in muscle mass is frequent in the LTx population and may lead to misclassification of CKD. Second, standardizing post-LTx monitoring of kidney function and renal care might contribute to slow down CKD progression. Third, new treatment options for CKD risk factors, such as diabetes mellitus, proteinuria and heart failure, have entered clinical practice. These new treatments have not been studied in LTx yet but are of interest for future use. In this review we will address the difficult aspects of post-LTx renal care and evaluate new and promising future approaches to slow down CKD progression.

Chronic lung allograft dysfunction (CLAD) is the major long-term cause of morbidity and mortality after lung transplantation. Both bronchiolitis obliterans syndrome and restrictive lung allograft syndrome, two main types of CLAD, lead to fibrosis in either the small airways or alveoli and pleura. Pathological pathways in CLAD and other types of fibrosis, for example idiopathic pulmonary fibrosis, are assumed to overlap and therefore fibrosis biomarkers could aid in the early detection of CLAD. These biomarkers could help to differentiate between different phenotypes of CLAD and could, in comparison to biomarkers of inflammation, possibly distinguish an infectious event from CLAD when a decline in lung function is present. This review gives an overview of known CLAD specific biomarkers, describes new promising fibrosis biomarkers currently investigated in other types of fibrosis, and discusses the possible use of these fibrosis biomarkers for CLAD.