In recent years, the increase of the post-transplantation diabetes mellitus (PTDM) after renal transplantation encourages people to do a lot of research on the disease. This paper conducted a bibliometric study on PTDM related literature to explore the risk factors of diabetes after kidney transplantation, as well as the current status, hotspots and development trends of PTDM research, so as to provide reference for researchers in related fields.

We searched the Web of Science Core Collection (WoSCC) database for PTDM literature from January 1, 1990, to August 20, 2023, and used VOSviewer, CiteSpace, and the R package 'bibliometrix' to do bibliometric analysis.

Obesity, 3 months after transplantation tacrolimus concentration >10 ng/mL, temporary hyperglycemia, delayed graft function, acute rejection is specific risk factors related to PTDM in renal transplant recipients. In addition, 74 countries led by China and the United States published 1546 papers, and the number of PTDM-related publications is increasing every year. Primary institutions included the University of California, Los Angeles, Mayo Clinic, University of Oslo, and University of Toronto. The Journal of Transplantation is the most widely read journal in the subject. The authors with the most published literature are Trond Jenssen and Adnan Sharif, and the most cited author is Kasiske BL. Expectations for continued growth in global PTDM research are increasingly high. Future studies will mainly focus on exploring the risk factors of PTDM and identifying new therapeutic approaches and targets.

Organ transplantation is the treatment of choice for individuals with kidney failure requiring kidney replacement therapy, as well as for those with end-stage liver disease. Despite the significant reduction in long-term morbidity and mortality with transplantation, kidney and liver allograft recipients remain at high risk for cardiovascular disease (CVD) and premature death from cardiovascular causes. This heightened risk is represented across all phenotypes of CVD, including coronary heart disease, heart failure, arrhythmias, valvulopathies and pulmonary hypertension. Pre-existing vascular risk factors for CVD, coupled with superimposed cardiovascular-kidney-metabolic derangements after transplantation, driven at least in part by post-transplant weight gain, immunosuppressive therapies and de novo risk factors such as dyslipidaemia and diabetes, coalesce to increase total CVD risk. In this review, we summarise pathophysiological considerations for both the short- and long-term increase in CVD risk following kidney/liver transplantation. We review the different phenotypes of CVD, with unique considerations for post-transplant care in this patient population. Finally, we highlight the need for awareness about long-term CVD risk and a multidisciplinary approach to managing organ-specific CVD risk in kidney and liver transplant patients.

This study developed a predictive model for Post-Transplant Diabetes Mellitus (PTDM) by integrating clinical and radiological data to identify at-risk kidney transplant recipients. In a retrospective analysis across three Mayo Clinic sites, clinical metrics were combined with deep learning analysis of pre-transplant CT images, focusing on body composition parameters like adipose tissue and muscle mass instead of BMI or other biomarkers. Among 2,005 nondiabetic kidney recipients, 335 (16.7%) developed PTDM within the first year. PTDM patients were older, had higher BMIs, elevated triglycerides, and were more likely to be male and non-White. They exhibited lower skeletal muscle area, greater visceral adipose tissue (VAT), more intermuscular fat, and higher subcutaneous fat (all p < 0.001). Multivariable analysis identified age (OR: 1.05, 95% CI: 1.03-1.08, p < 0.0001), family diabetes history (OR: 1.55, CI: 1.14-2.09, p = 0.0061), White race (OR: 0.43, CI: 0.28-0.66, p < 0.0001), and VAT area (OR: 1.37, CI: 1.14-1.64, p = 0.0009) as predictors. The combined model achieved C-statistic of 0.724 (CI: 0.692-0.757), outperforming the clinical-only model (C-statistic 0.68). Patients with PTDM in the first year had higher mortality than those without PTDM. This model improves predictive precision, enabling accurate identification and intervention for at risk patients.

Tacrolimus (TAC) is an immunosuppressant widely utilized in organ transplantation. One of its primary adverse effects is glucose metabolism disorder, which significantly increases the risk of diabetes. Investigating the molecular mechanisms underlying TAC-induced diabetes is essential for developing effective prevention and treatment strategies for these adverse effects. In addition, TAC can induce cost-effective, non-obese animal models of diabetes, where the metabolic parameter changes closely resemble those observed during the onset and progression of type 2 diabetes (T2DM), post-transplantation diabetes mellitus (PTDM), and associated complications. This review, based on articles indexed in PubMed up to August 19, 2024, identified 48 studies focusing on TAC-induced diabetic rodent models and 22 studies exploring the effects of TAC on diabetic or obese rodent models. These studies were systematically summarized based on TAC dosage, route of administration, duration of administration, and glucose metabolism indices used for evaluation. Additionally, the impact of TAC dose reduction or discontinuation on glucose metabolism was assessed, along with pharmacological agents that modulate TAC-induced diabetes, including anti-diabetic medications, anti-inflammatory and antioxidant compounds, biologics, and antibiotics. Key signaling pathways implicated in TAC-induced diabetes include CaN/NFAT, PI3K/AKT/mTOR, and TGF-β/Smad, all of which impair islet β-cell function, thereby contributing to diabetes development. This review provides a concise summary of the characteristics of relevant murine models, offering valuable guidance for selecting appropriate and economical animal models for future research.

Kidney transplantation remains the best treatment for chronic kidney failure, offering better outcomes and quality of life compared with dialysis. Cardiovascular disease (CVD) is a major cause of morbidity and mortality in kidney transplant recipients and is associated with decreased patient survival and worse graft outcomes. Post-transplant CVD results from a complex interaction between traditional cardiovascular risk factors, such as hypertension and diabetes, and risk factors specific to kidney transplant recipients including chronic kidney disease, immunosuppressive drugs, or vascular access. An accurate assessment of cardiovascular risk is now needed to optimize the management of cardiovascular comorbidities through the detection of risk factors and the screening of hidden pretransplant coronary artery disease. Promising new strategies are emerging, such as GLP-1 receptor agonists and SGLT2 inhibitors, with a high potential to mitigate cardiovascular complications, although further research is needed to determine their role in kidney transplant recipients. Despite this progress, a significant gap remains in understanding the optimal management of post-transplant CVD, especially coronary artery disease, stroke, and peripheral artery disease. Addressing these challenges is essential to improve the short- and long-term outcomes in kidney transplant recipients. This narrative review aims to provide a comprehensive overview of cardiovascular risk assessment and post-transplant CVD management.

Diabetic kidney disease (DKD) is a serious consequence of diabetes mellitus (DM). If not managed effectively, DKD often develops into end-stage renal disease (ESRD). The most successful treatment for ESRD is kidney transplantation, offering improved quality of life and survival rates. For insulin-dependent diabetic patients with ESRD, simultaneous pancreas-kidney transplantation (SPKT) offers a treatment alternative that treats both kidney failure and the underlying diabetes. However, SPKT involves more complicated surgery, prolonged operative time, and a higher risk of complications. This review aims to highlight the impact of DM on kidney transplant recipients (KTRs) regarding post-transplant complications, graft survival, mortality rates, and the role of glucose-lowering medications and immunosuppressants. The incidence of urinary tract infections, cardiovascular complications, and diabetic foot disease was higher among KTRs. A decrease in graft survival rate at five years was observed among diabetics compared to non-diabetics, with similar graft survival rates among type 1 and type 2 DM. The mortality rate was notably higher among diabetic patients, with cardiovascular complications being the leading cause. The emergence of new-onset diabetes mellitus post-transplantation (NODAT) is a significant cause of concern. Certain risk factors, including a family history of DM, age >45 years, obesity, male gender, and immunosuppressive medications, have been linked to this phenomenon. Immunosuppression is a substantial challenge among diabetics as certain medications such as tacrolimus have shown to be considerably diabetogenic compared to cyclosporine and belatacept, and it is also postulated that corticosteroids can lead to hyperglycemia. Some studies proved that glucose-lowering medications, including insulin degludec, glucagon-like peptide-1 receptor agonists, thiazolidinediones, and sodium-glucose cotransporter 2 inhibitors, are safe and effective among KTRs. However, these studies are debatable and of low confidence. Hence, it is imperative to conduct large clinical trials and establish definitive guidelines to manage pre-existing diabetes and NODAT among KTRs with multidisciplinary care to help clinicians improve patient outcomes.

Post-transplant diabetes mellitus (PTDM) is a common, dynamic complication after kidney transplantation (KT) that may resolve over time. To better understand and prevent PTDM, we analyzed its prevalence, evolution, and influencing factors.

Data from the French national ASTRE database at different post-transplantation periods (P) were analyzed. PTDM was defined by fasting blood glucose (FBG) ≥1.26 g/L, HbA1c ≥ 6.5%, or the use of hypoglycemic medications in kidney transplant recipients without diabetes. Patient trajectories were identified using group-based trajectory models (GBTM), and associated factors were examined.

Among 2898 patients, PTDM prevalence was 27.3% at P1 (>M2, ≤M6), 21.3% at P2 (>M6, ≤M18), 19.8% at P3 (>M18, ≤M30), and 19.9% at P4 (>M30, ≤M42). Analysis of 1825 patients identified four trajectories: no PTDM (67%), late-onset PTDM (6%), remission after P1 (10%), and early, persistent PTDM (17%). Late-onset PTDM was linked to history of cardiovascular disease, higher BMI at transplantation, HCV positive status, and weight gain. Early, persistent PTDM was associated with older age, higher BMI, HVC positive status, history of cardiovascular disease, and tacrolimus use. PTDM remission was linked to lower BMI. Corticosteroids contributed to both late-onset and persistent PTDM, while switching between tacrolimus and cyclosporine did not significantly affect progression.

This study confirmed the high prevalence and dynamic nature of PTDM after transplantation, emphasizing the critical role of pretransplant cardiovascular disease, BMI, and early post-transplant weight gain in the onset or remission of PTDM.

To evaluate the impact of a proactive action of a specialized diabetes team (SDT) on different health outcomes in patients hospitalized in high complexity surgery units, including solid organ transplant surgical units, of a tertiary hospital.

Nested case control study matched (1:1) by age and gender. The control group consisted of patients (n = 120) who were under the standard of care diabetes management admitted three months' prior the cases. The cases were admitted in the same surgical units (n = 120) and were treated in the setting of the so called "Smart Diabetes Hospital" (SDH) consisting in a SDT that prioritized their actions through a digital map showing blood glucose levels obtained during the previous 24 h.

SDH implementation resulted in a significant reduction in both blood glucose levels (mean 162.1 ± SD 44.4 vs. mean 145.5 ± SD 48.0; p = 0.008) and hypoglycaemic episodes (19.7% vs. 8.4%: p = 0.002). Furthermore, a reduction of 3 days in the length of stay (LOS) was observed (15.6 ± 10.3 vs. 12.4 ± 6.0), which represents a significant cost-saving. Moreover, more new cases of diabetes were detected during the SDT period (2.5% vs. 6.7%, p = 0.04).

SDH is effective in diabetes management and reduce LOS in complex surgical units.

Posttransplantation diabetes mellitus (PTDM) is a form of diabetes developed after solid organ or stem cell transplantation. This condition shares physiopathological traits with type 2 diabetes, including insulin resistance and β-cells dysfunction and its prevalence varies significantly based on the diagnostic criteria used. Immunosuppressive drugs directly contribute to PTDM risk through intricate impacts on glucose regulation, insulin secretion, and inflammation. In addition, modifiable and non-modifiable environmental risk factors are associated with the onset of this condition. This review aims to provide a comprehensive overview of the multifactorial nature of PTDM in order to highlight candidate genes and variants for pharmacogenetic research. An extensive literature search was conducted to identify studies on pharmacological and genetic factors influencing PTDM development. This review stresses the importance of understanding these interactions for improving PTDM management and underscores the need for further research to refine preventive approaches, ultimately enhancing patient outcomes post-transplantation.

Post-transplant diabetes mellitus (PTDM) is a complex condition arising from various factors including immunosuppressive medications, insulin resistance, impaired insulin secretion and inflammatory processes. Its impact on patient and graft survival is a significant concern in kidney transplant recipients. PTDM's impact on kidney transplant recipients, including patient and graft survival and cardiovascular mortality, is a significant concern, given conflicting findings in previous studies. This meta-analysis was imperative not only to incorporate emerging evidence but also to delve into cause-specific mortality considerations. We aimed to comprehensively evaluate the association between PTDM and clinical outcomes, including all-cause and cardiovascular mortality, sepsis-related mortality, malignancy-related mortality and graft loss, in kidney transplant recipients.

PubMed, Ovid/Medline, Web of Science, Scopus and Cochrane Library databases were screened and studies evaluating the effect of PTDM on all-cause mortality, cardiovascular mortality, sepsis-related mortality, malignancy-related mortality and overall graft loss in adult kidney transplant recipients were included.

Fifty-three studies, encompassing a total of 138 917 patients, evaluating the association between PTDM and clinical outcomes were included. Our analysis revealed a significant increase in all-cause mortality [risk ratio (RR) 1.70, 95% confidence interval (CI) 1.53 to 1.89, P < .001] and cardiovascular mortality (RR 1.86, 95% CI 1.36 to 2.54, P < .001) among individuals with PTDM. Moreover, PTDM was associated with a higher risk of sepsis-related mortality (RR 1.96, 95% CI 1.51 to 2.54, P < .001) but showed no significant association with malignancy-related mortality (RR 1.20, 95% CI 0.76 to 1.88). Additionally, PTDM was linked to an increased risk of overall graft failure (RR 1.33, 95% CI 1.16 to 1.54, P < .001).

These findings underscore the importance of comprehensive management strategies and the need for research targeting PTDM to improve outcomes in kidney transplant recipients.

Cardiovascular disease is a leading cause of post-transplant mortality in kidney transplant recipients (KTRs), especially those with diabetes. Although glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have demonstrated cardiovascular and kidney benefits in the general population with type 2 diabetes mellitus (T2DM), evidence regarding their effects in diabetic KTRs is limited.

This retrospective cohort study utilized data from the Global Collaborative Network in TriNetX, spanning January 1, 2006, to June 1, 2023. Propensity score matching (PSM) with 1:1 ratio was employed to create balanced cohorts. Adult KTRs with T2DM who received GLP-1 RAs within 3 months post-transplant were compared to a matched cohort of KTRs who did not. The primary outcome was all-cause mortality, with secondary outcomes including major adverse cardiovascular events (MACEs) and major adverse kidney events (MAKEs).

A total of 35,488 adult KTRs with T2DM (mean [SD] age, 57.7 [12.2] years; 57.7% men) were identified and 9.8% patients used GLP-1 RAs among 3 months post-transplant. Following PSM, 3564 GLP-1 RAs users were matched with an equal number of nonusers. After a median follow-up of 2.5 years, GLP-1 RAs users had lower risks of mortality (adjusted hazard ratio (aHR), 0.39; 95% CI 0.31-0.50), MACEs (aHR 0.66; 95% CI 0.56-0.79), and MAKEs (aHR 0.66; 95% CI 0.58-0.75). Adverse effects included higher risks of nausea, vomiting and diarrhea, while risks of suicide, hypoglycemia, retinopathy, and pancreatitis were not increased.

In KTRs with T2DM, GLP-1 RAs use was associated with substantial reductions in all-cause mortality, MAKEs, and MACEs compared to nonuse without increasing complications. However, the underutilization of GLP-1 RAs represents a significant opportunity to improve post-transplant outcomes in this high-risk population.

To compare risk factors for new-onset diabetes after transplantation (NODAT) among renal transplant recipients (RTRs) from 1989 to 2018 in the City Clinical Hospital №52, with a systematic analysis of published studies on this topic.

In a 30-year (1989-2018) retrospective study, we found statistically significant differences in age, gender, polycystic kidney disease, cadaveric kidney, cyclosporine, i-mTOR, and steroids between two groups of recipients with and without NODAT. Patients with NODAT were older, more male, more likely to have polycystic kidney disease and deceased donor kidneys, and more likely to be treated with cyclosporine, i-mTOR, and steroids (p<0.05). We conducted a meta-analysis to evaluate the impact of these indicators on the development of NODAT. MEDLINE, Scopus, and the Cochrane Central Register of Controlled Trials were searched for eligible case-control studies of risk factors for NODAT in RTRs published between 1990 and 2019. Meta-analysis of proportions was performed using the Freeman-Tukey transformation to calculate weighted summary proportions from a fixed and random effects model.

A total of 13 case-control studies were included in the meta-analysis. Of the total 849 studies found, 13 were included in the systematic review and meta-analysis, including ours, with a total of n=6797 RTRs, of which n=1305 patients with NODAT and n=5492 without NODAT. A wide range of data was recorded for the analysis of the incidence of NODAT (6.5-50.7%), with an average of 17.9% (fixed model) or 24.3% (random model). The proportion of NODAT recorded in the Russian registry of the City Clinical Hospital №52 was lower (11.5%), however, the data in the analyzed studies were highly heterogeneous: I2=98.14%, 95% CI: from 97.61 to 98.55, p<0.0001, Begg's test (p=0.05) and Egger's test (p=0.01) do not exclude the presence of publication bias in this case. Data on NODAT risk factors were less heterogeneous. This meta-analysis showed that age, polycystic kidney disease, i-mTOR and steroid therapy were associated with NODAT, whereas gender, calcineurin inhibitor use, and cadaveric kidney were not. There was no evidence of selection bias in any of the cases.

Risk factors for NODAT in kidney transplant recipients include older age, polycystic kidney disease, i-mTOR and steroid therapy, which initiate a state of insulin resistance. To reduce the risk of NODAT, the possibility of modifying immunosuppression regimens and the use of drugs that reduce insulin resistance and have a nephroprotective effect in RTRs should be considered. Therefore, randomized studies are needed to evaluate SGLT2 inhibitor in RTRs.

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.

To determine the rate of prediabetes among and the pre-transplant plasma high-sensitivity C-reactive protein (hs-CRP) value predictive of prediabetes in patients during their first year post-living donor kidney transplant.

A total of 538 patients underwent living donor kidney transplantation between January 2018 and December 2020, 413 of whom met the inclusion criteria for this study. All patients underwent oral glucose tolerance tests (OGTTs) with 75 g glucose/200 mL solution, starting 3 months post-transplant and repeating the test every 3 months for the first year. Clinical and paraclinical indicators and plasma hs-CRP concentrations were quantified the day prior to the transplant. Prediabetes was diagnosed according to the American Diabetes Association 2018 criteria as a 2-h OGTT result between 140 mg/dL (7.8 mmol/L) and 199 mg/dL (11.0 mmol/L).

The rate of prediabetes among the study subjects was 38.3 % (158/413). Body mass index (BMI) and pre-transplant plasma triglycerides, high-density lipoprotein cholesterol (HDLC), and hs-CRP levels were related factors predictive of prediabetes in patients within the first year post-kidney transplant based on multivariate logistic regression and receiver operative characteristic curve models. Hs-CRP was the factor with the best predictive value (area under the curve = 0.89; p < 0.001).

Pre-transplant plasma hs-CRP levels were a good predictor of prediabetes in the first year post-living donor kidney transplant.

<b>Introduction:</b> Chronic kidney disease (CKD) is a global public health problem, occurring more frequently in developed countries. In Poland, it affects approximately 4 million people, which constitutes 10.8% of the population. End-stage renal disease (ESRD) requires renal replacement therapy - dialysis therapy or kidney transplantation. Kidney transplantation, supported by immunosuppressive therapy, is the preferred method of treating ESRD, improving the quality and length of life of patients.<b>Aim and Methods:</b> The aim of the study was to determine the long-term effects of kidney transplantation, including proper graft function, the frequency of adverse effects of immunosuppressive therapy, the degree of patient compliance with therapeutic recommendations, and the incidence of malignancies. A survey was conducted in a group of 137 patients who underwent kidney transplantation between 2006 and 2015. Hospitalization data were also analyzed, including age, body weight and blood type of the recipient.<b>Results:</b> Of the 137 patients studied, 61 were women and 76 were men. The mean age of the patients was 45.1 years. The most common etiology of CKD was glomerulonephritis. After kidney transplantation, 86.86% of patients declared normal graft function. Post-transplant weight gain was noted in 75.18% of patients. 11.68% of recipients developed malignancies, with an average time from transplantation to diagnosis of 5.1 years. Of the patients with cancer, 93.75% maintained normal graft function.<b>Conclusions:</b> Long-term effects of kidney transplantation are satisfactory, with a high percentage of patients maintaining normal graft function. Complications associated with immunosuppressive therapy are comparable to literature data. It is necessary to increase patient awareness of modifiable risk factors to improve treatment outcomes. The incidence of malignancy after transplantation is lower than in the literature, but the methodological limitations of the study must be taken into account. Cancer treatment had no significant effect on graft function in most cases.

Kidney transplantation is the preferred treatment for patients with end-stage renal disease, significantly preserving kidney function and patient quality of life. However, post-transplant diabetes mellitus (PTDM) is a common complication, occurring in approximately one-third of renal transplant recipients. This study aims to evaluate the role of pulse wave parameters in predicting PTDM and to identify other pre-transplant risk factors.

This prospective cohort study included 105 patients on the kidney transplant waiting list from 2017 to 2022. Exclusion criteria included any pre-existing diabetes mellitus. Patients underwent physical examinations, laboratory analyses, and pulse wave analysis before transplantation and one year post-transplant. PTDM diagnosis followed International Consensus Guidelines. Data were analyzed using Wilcox test, Bonferroni correction, May-Whitney U-test, and Fisher's exact test, with p < 0.05 considered statistically significant.

Post-transplant, 21% of patients were diagnosed with PTDM, increasing to 35% 3months post-transplant and 43% at one year post-transplant. Significant findings included: Pre-transplat risk factors for developing PTDM: Proteinuria (p = 0.037, OR = 3.942) and perioperative hyperglycemia (p = 0.003, OR = 4.219 at 3 months; p = 0.001, OR = 4.571 at 1 year). Pulse wave parameters for developing PTDM: Pre-transplant Aortic PP > 45 mmHg (AUC = 0.757) and PWV > 8.5 m/s (AUC = 0.730) were strong predictors of the development of PTDM after 3 months (p < 0.0001). Moreover, we found significant improvements in aortic pulse pressure (Aortic PP) and pulse wave velocity (PWV) post-transplant (p < 0.0001).

Our study confirms that pulse wave parameters, such as Aortic PP and PWV, are significant predictors of PTDM in kidney transplant recipients (KTR). These findings support incorporating pulse wave analysis into routine pre-transplant evaluations to identify high-risk patients. Additionally, monitoring these parameters post-transplant may aid in early intervention and prevention of PTDM, ultimately improving patient outcomes.

Ethical approval was obtained from the Ethics Committee of Medical faculty and University Hospital Olomouc (approval no. 94/15).

Limited data are available on the adverse effects of new-onset diabetes after transplantation (NODAT) in solid organ transplantation (TPL) other than kidney. This study aimed to identify the risk of complications associated with NODAT in recipients of kidney, liver, or heart TPL.

Using the Korean National Health Insurance Service database, recipients of kidney, liver, or heart TPL between 2009 and 2015 were identified. The incidence of coronary artery disease (CAD), cerebrovascular accident (CVA), and malignancy was compared across groups with NODAT, pretransplant diabetes mellitus (DM), and without DM using Cox regression analysis.

A total of 9,632 kidney, liver, or heart TPL recipients were included. During the median follow-up of 5.9 years, NODAT independently increased the incidence of CAD (hazard ratio [HR], 2.46; 95% confidence interval [CI], 1.39 to 4.30) and overall mortality (HR, 1.48; 95% CI, 1.14 to 1.95) compared to the reference group even after adjustment for confounders; this was more prominent in kidney TPL than in liver TPL. The risk of CVA was significantly increased by pretransplant DM but not by NODAT in both kidney and liver TPL (HR, 2.47; 95% CI, 1.68 to 3.65; and HR, 3.18; 95% CI, 1.07 to 9.48, respectively). NODAT increased the risk of malignancy in the crude model, which lost its statistical significance after confounder adjustment.

NODAT independently increases the risk of CAD and mortality after TPL, which is more evident in kidney recipients. There was no additional increased risk of CVA or malignancy with NODAT in solid organ TPL.

Tacrolimus and mycophenolate are important immunosuppressive agents used to prevent organ rejection in post-transplant patients. While highly effective, their use is associated with significant toxicity, requiring careful management. Tacrolimus, a calcineurin inhibitor, is linked to nephrotoxicity, neurotoxicity, metabolic disturbances such as diabetes mellitus and dyslipidemia, and cardiovascular complications such as hypertension and arrhythmias. Mycophenolate, a reversible inhibitor of inosine monophosphate dehydrogenase, frequently causes gastrointestinal disturbances, including diarrhea and colitis, as well as hematologic side effects like anemia and leukopenia, which increase infection risk. Therapeutic drug monitoring (TDM) and pharmacogenomics have emerged as essential strategies for mitigating these toxicities. TDM ensures tacrolimus trough levels are maintained within a therapeutic range, minimizing the risks of nephrotoxicity and rejection. Pharmacogenomic insights, such as CYP3A5 polymorphisms, allow for personalized tacrolimus dosing based on individual metabolic profiles. For mycophenolate, monitoring inosine monophosphate dehydrogenase activity provides a pharmacodynamic approach to dose optimization, reducing gastrointestinal and hematologic toxicities. Emerging tools, including dried blood spot sampling and pharmacokinetic modeling, offer innovative methods to simplify monitoring and enhance precision in outpatient settings. Despite their utility, the toxicity profiles of these drugs, including those of early immunosuppressants such as cyclosporine and azathioprine, necessitate further consideration of alternative immunosuppressants like sirolimus, everolimus, and belatacept. Although promising, these newer agents require careful patient selection and further research. Future directions in immunosuppressive therapy include integrating individual pharmacogenetic data to refine dosing, minimize side effects, and improve long-term graft outcomes. This narrative review underscores the importance of personalized medicine and advanced monitoring in optimizing post-transplant care.

Post-transplantation diabetes mellitus and carbohydrate intolerance (PTDM/iCHO) are complications following solid organ transplantation, which significantly increases the risk of graft loss and mortality. However, data concerning long-term outcomes in paediatric kidney transplant recipients with PTDM/iCHO are scarce. This study aimed to evaluate the risk of graft loss in paediatric kidney transplant recipients with PTDM or iCHO compared with non-PTDM/iCHO.

The study cohort included patients aged <18 who underwent a kidney transplant in a transplant centre from 2005 to 2022. The primary outcome was graft survival loss; secondary outcomes were acute rejection, renal function and mortality. Cumulative incidence of graft loss and acute rejection was estimated, considering death a competing risk. Fine and Gray's proportional subdistribution hazard model was used to analyse the effect of PTDM/iCHO status on the event.

Seventy-six paediatric kidney transplant recipients were included. The incidence of PTDM and iCHO was 6.6% and 9.2%, respectively. Patients with PTDM/iCHO had a significantly higher cumulative graft loss incidence than those without (34.4% vs 13.9% at 36 months, p<0.008). Multivariable analysis revealed a threefold increased risk of graft loss in patients with PTDM/iCHO (HRadjusted 3.33, 95% CI 1.19 to 9.30, p=0.022). PTDM/iCHO was associated with a higher incidence of acute rejection (33.3% vs 14.5% at 1 year, p=0.025). Patients with PTDM/iCHO also exhibited significantly worse eGFR at all time points compared with patients without PTDM/iCHO (p=0.036) CONCLUSION: Patients with PTDM and iCHO had a higher risk of graft loss and lower renal function in paediatric kidney transplant recipients. This justifies close monitoring of metabolic complications in these patients.

Diabetes is the most common cause of kidney disease in individuals that receive a kidney transplant, and those without pre-existing diabetes are at greater risk of developing diabetes following kidney transplant. A class of diabetes treatment medications called glucagon-like peptide-1 receptor agonists (GLP-1RA) has seen recent widespread use for people with diabetes or obesity, with efficacy for improved glycemic control, weight loss, and reduced risk of cardiovascular events. Given these benefits, and indications for use that often co-occur in kidney transplant recipients, use of GLP-1RAs warrants consideration in this population. Therefore, we sought to review the current literature to better understand the mechanisms of action, clinical application, and person-centred considerations of GLP-1RAs in kidney transplant recipients.

Original articles were identified between December 2023 and July 2024 from electronic databases including the Ovid MEDLINE database, PubMed, and Google Scholar using terms "kidney transplant," "GLP-1," "glucagon-like peptide-1 receptor agonist," and "diabetes."

A comprehensive review of the literature was conducted to explore the relationship between GLP-1RAs and kidney transplant recipients. We reviewed the current state of evidence across the research disciplines of basic or fundamental science, clinical and health services research, and person-centred equity science, and highlighted important knowledge gaps that offer opportunities for future research.

Numerous clinical studies have demonstrated the benefit of GLP-1RAs in people with and without diabetic kidney disease, including decreased risk of cardiovascular events. However, there is a paucity of high-quality randomized controlled trials and observational studies analyzing use of GLP-1RAs in kidney transplant recipients. Evidence of benefit in this population is therefore limited to small studies or inferred from research conducted in nontransplant populations. Growing evidence from preclinical and clinical studies may elucidate renoprotective mechanisms of GLP-1RAs and remove barriers to application of these drugs in the transplant recipient population. Individuals who are female, non-white, have lower socioeconomic status, and live in rural communities are at greater risk of diabetes and have lower uptake of GLP-1RAs. There is a need for clinical trials across diverse kidney transplant populations to estimate the efficacy of GLP-1RAs on important health outcomes.

The search strategy for this narrative review may not have been sensitive to identify all relevant articles. Our search was limited to English language articles.

With the increasing global incidence of diabetes mellitus, physicians may encounter more patients with acute and chronic complications of medication-induced hyperglycemia and diabetes. Moreover, medication-induced diabetes may be an important contributing factor to the high rates of diabetes, and recognizing its impact and risk is a critical step in curtailing its effect on the global population. It has long been recognized that multiple classes of medications are associated with hyperglycemia through various mechanisms, and the ability to foresee this and implement adequate management strategies are important. Moreover, different antihyperglycemic medications are better suited to combat the hyperglycemia encountered with different classes of medications, so it is critical that physicians can recognize which agents should be used, and which medications to avoid in certain types of medication-induced hyperglycemia. In this review, we will discuss the evidence behind the main classes of medications that cause hyperglycemia, their mechanism of action, specific agents that are associated with worsened glycemic control, and, most importantly, management strategies that are tailored to each specific class.

Posttransplantation complications pose a major challenge to the long-term survival and quality of life of organ transplant recipients. These complications encompass immune-mediated complications, infectious complications, metabolic complications, and malignancies, with each type influenced by various risk factors and pathological mechanisms. The molecular mechanisms underlying posttransplantation complications involve a complex interplay of immunological, metabolic, and oncogenic processes, including innate and adaptive immune activation, immunosuppressant side effects, and viral reactivation. Here, we provide a comprehensive overview of the clinical features, risk factors, and molecular mechanisms of major posttransplantation complications. We systematically summarize the current understanding of the immunological basis of allograft rejection and graft-versus-host disease, the metabolic dysregulation associated with immunosuppressive agents, and the role of oncogenic viruses in posttransplantation malignancies. Furthermore, we discuss potential prevention and intervention strategies based on these mechanistic insights, highlighting the importance of optimizing immunosuppressive regimens, enhancing infection prophylaxis, and implementing targeted therapies. We also emphasize the need for future research to develop individualized complication control strategies under the guidance of precision medicine, ultimately improving the prognosis and quality of life of transplant recipients.

Kidney transplantation (KT) improves the cardiovascular outcomes of patients with end-stage kidney disease. However, cardiovascular disease remains the leading cause of premature death and graft loss in KT recipients (KTRs) with diabetes. We evaluated the cardioprotective effects of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in KTRs with diabetes.

A total of 750 KTRs with diabetes were enrolled from 6 tertiary hospitals. Among them, 129 patients (17.2%) were prescribed SGLT2i. The primary outcome was the incidence of major adverse cardiovascular events (MACE), which comprised myocardial infarction (MI), death from cardiovascular causes, hospitalization for heart failure, and stroke. Multivariable Cox regression analysis and propensity score matching were used to investigate the effect of SGLT2i on clinical outcomes.

In the matched cohort, MACE occurred in 5 patients (3.9%) in the SGLT2i group and 15 patients (11.8%) in the non-SGLT2i group, out of 127 patients in each group over 55.3 months. The incidence of MACE and MI was lower in the SGLT2i group than in the non-SGLT2i group (P = 0.036 and 0.008, respectively). In multivariate analysis, the SGLT2i group had a lower risk of MACE and MI than the non-SGLT2i group (adjusted hazard ratio [HR], 0.30 and 0.04; 95% confidence interval [CI], 0.10-0.88 and 0.004-0.40; P = 0.028 and 0.006, respectively). There was no difference in the incidence of urinary tract infection (UTI) between the 2 groups.

SGLT2i significantly decreased the risk of cardiovascular events in KTRs with diabetes, particularly lowering the incidence of MI and death from cardiovascular causes. SGLT2i can be used to reduce the burden of cardiovascular disease in KTRs with diabetes.

The comparative effects of specific blood pressure (BP) lowering treatments on patient-important outcomes following kidney transplantation are uncertain. Our 2009 Cochrane review found that calcium channel blockers (CCBs) improved graft function and prevented graft loss, while the evidence for other BP-lowering treatments was limited. This is an update of the 2009 Cochrane review.

To compare the benefits and harms of different classes and combinations of antihypertensive drugs in kidney transplant recipients.

We contacted the Information Specialist and searched the Cochrane Kidney and Transplant Register of Studies up to 3 July 2024 using search terms relevant to this review. Studies in the Register were identified through searches of CENTRAL, MEDLINE, EMBASE, conference proceedings, the International Clinical Trials Registry Platform (ICTRP) Search Portal, and ClinicalTrials.gov.

Randomised controlled trials (RCTs) and quasi-RCTs evaluating any BP-lowering agent in recipients of a functioning kidney transplant for at least two weeks were eligible.

Two authors independently assessed the risks of bias and extracted data. Treatment estimates were summarised using the random-effects model and expressed as relative risk (RR) or mean difference (MD) with 95% confidence intervals (CI). Evidence certainty was assessed using Grades of Recommendation, Assessment, Development and Evaluation (GRADE) processes. The primary outcomes included all-cause death, graft loss, and kidney function.

Ninety-seven studies (8706 participants) were included. One study evaluated treatment in children. The overall risk of bias was unclear to high across all domains. Compared to placebo or standard care alone, CCBs probably reduce all-cause death (23 studies, 3327 participants: RR 0.83, 95% CI 0.72 to 0.95; I2 = 0%; moderate certainty evidence) and graft loss (24 studies, 3577 participants: RR 0.84, 95% CI 0.75 to 0.95; I2 = 0%; moderate certainty evidence). CCBs may make little or no difference to estimated glomerular filtration rate (eGFR) (11 studies, 2250 participants: MD 1.89 mL/min/1.73 m2, 95% CI -0.70 to 4.48; I2 = 48%; low certainty evidence) and acute rejection (13 studies, 906 participants: RR 10.8, 95% CI 0.85 to 1.35; I2 = 0%; moderate certainty evidence). CCBs may reduce systolic BP (SBP) (3 studies, 329 participants: MD -5.83 mm Hg, 95% CI -10.24 to -1.42; I2 = 13%; low certainty evidence) and diastolic BP (DBP) (3 studies, 329 participants: MD -3.98 mm Hg, 95% CI -5.98 to -1.99; I2 = 0%; low certainty evidence). CCBs have uncertain effects on proteinuria. Compared to placebo or standard care alone, angiotensin-converting-enzyme inhibitors (ACEi) may make little or no difference to all-cause death (7 studies, 702 participants: RR 1.13, 95% CI 0.58 to 2.21; I2 = 0%; low certainty evidence), graft loss (6 studies, 718 participants: RR 0.75, 95% CI 0.49 to 1.13; I2 = 0%; low certainty evidence), eGFR (4 studies, 509 participants: MD -2.46 mL/min/1.73 m2, 95% CI -7.66 to 2.73; I2 = 64%; low certainty evidence) and acute rejection (4 studies, 388 participants: RR 1.75, 95% CI 0.76 to 4.04; I2 = 0%; low certainty evidence). ACEi may reduce proteinuria (5 studies, 441 participants: MD -0.33 g/24 hours, 95% CI -0.64 to -0.01; I2 = 67%; low certainty evidence) but had uncertain effects on SBP and DBP. Compared to placebo or standard care alone, angiotensin receptor blockers (ARB) may make little or no difference to all-cause death (6 studies, 1041 participants: RR 0.69, 95% CI 0.36 to 1.31; I2 = 0%; low certainty evidence), eGRF (5 studies, 300 participants: MD -1.91 mL/min/1.73 m2, 95% CI -6.20 to 2.38; I2 = 57%; low certainty evidence), and acute rejection (4 studies, 323 participants: RR 1.00, 95% CI 0.44 to 2.29; I2 = 0%; low certainty evidence). ARBs may reduce graft loss (6 studies, 892 participants: RR 0.35, 95% CI 0.15 to 0.84; I2 = 0%; low certainty evidence), SBP (10 studies, 1239 participants: MD -3.73 mm Hg, 95% CI -7.02 to -0.44; I2 = 63%; moderate certainty evidence) and DBP (9 studies, 1086 participants: MD -2.75 mm Hg, 95% CI -4.32 to -1.18; I2 = 47%; moderate certainty evidence), but has uncertain effects on proteinuria. The effects of CCBs, ACEi or ARB compared to placebo or standard care alone on cardiovascular outcomes (including fatal or nonfatal myocardial infarction, fatal or nonfatal stroke) or other adverse events were uncertain. The comparative effects of ACEi plus ARB dual therapy, alpha-blockers, and mineralocorticoid receptor antagonists compared to placebo or standard care alone were rarely evaluated. Head-to-head comparisons of ACEi, ARB or thiazide versus CCB, ACEi versus ARB, CCB or ACEi versus alpha- or beta-blockers, or ACEi plus CCB dual therapy versus ACEi or CCB monotherapy were scarce. No studies reported outcome data for cancer or life participation.

For kidney transplant recipients, the use of CCB therapy to reduce BP probably reduces death and graft loss compared to placebo or standard care alone, while ARB may reduce graft loss. The effects of ACEi and ARB compared to placebo or standard care on other patient-centred outcomes were uncertain. The effects of dual therapy, alpha-blockers, and mineralocorticoid receptor antagonists compared to placebo or standard care alone and the comparative effects of different treatments were uncertain.

Diabetes mellitus (DM) significantly impacts renal and hepatic function, necessitating comprehensive understanding and management strategies. Renal involvement, namely diabetic kidney disease (DKD), presents a global challenge, with increasing prevalence paralleling DM rates. Lifestyle modifications and pharmacotherapy targeting hypertension and glycemic control have pivotal roles in DKD management. Concurrently, hepatic involvement in DM, characterized by metabolic dysfunction-associated steatotic liver disease (MASLD), presents a bidirectional relationship. DM exacerbates MASLD progression, while MASLD predisposes to DM development and worsens glycemic control. Screening for MASLD in DM patients is of high importance, utilizing non-invasive methods like ultrasound and fibrosis scores. Lifestyle modifications, such as weight loss and a Mediterranean diet, mitigate MASLD progression. Promising pharmacotherapies, like SGLT2 inhibitors and GLP-1 agonists, demonstrate efficacy in both DM and MASLD management. Special populations, such as diabetic individuals undergoing hemodialysis or kidney transplant recipients, demand special care due to unique clinical features. Similarly, DM exacerbates complications in MASLD patients, elevating the risks of hepatic decompensation and hepatocellular carcinoma. Recognizing the interconnectedness of DM, renal, and hepatic diseases underscores the need for multidisciplinary approaches for optimal patient outcomes. The present review aims to present the main characteristics and crucial points not to be overlooked regarding the renal and hepatic involvement in DM patients focusing on the inter-relationships between the renal and the hepatic involvements.

Cardiovascular disease, infection, malignancy, and thromboembolism are major causes of morbidity and mortality in kidney transplant recipients (KTR). Prospectively identifying monogenic conditions associated with post-transplant complications may enable personalized management. Therefore, we developed a transplant morbidity panel (355 genes) associated with major post-transplant complications including cardiometabolic disorders, immunodeficiency, malignancy, and thrombophilia. This gene panel was then evaluated using exome sequencing data from 1590 KTR. Additionally, genes associated with monogenic kidney and genitourinary disorders along with American College of Medical Genetics (ACMG) secondary findings v3.2 were annotated. Altogether, diagnostic variants in 37 genes associated with Mendelian kidney and genitourinary disorders were detected in 9.9% (158/1590) of KTR; 25.9% (41/158) had not been clinically diagnosed. Moreover, the transplant morbidity gene panel detected diagnostic variants for 56 monogenic disorders in 9.1% KTRs (144/1590). Cardiovascular disease, malignancy, immunodeficiency, and thrombophilia variants were detected in 5.1% (81), 2.1% (34), 1.8% (29) and 0.2% (3) among 1590 KTRs, respectively. Concordant phenotypes were present in half of these cases. Reviewing implications for transplant care, these genetic findings would have allowed physicians to set specific risk factor targets in 6.3% (9/144), arrange intensive surveillance in 97.2% (140/144), utilize preventive measures in 13.2% (19/144), guide disease-specific therapy in 63.9% (92/144), initiate specialty referral in 90.3% (130/144) and alter immunosuppression in 56.9% (82/144). Thus, beyond diagnostic testing for kidney disorders, sequence annotation identified monogenic disorders associated with common post-transplant complications in 9.1% of KTR, with important clinical implications. Incorporating genetic diagnostics for transplant morbidities would enable personalized management in pre- and post-transplant care.

Hepatitis C virus (HCV) can cause a range of kidney diseases. HCV is the primary cause of mixed cryoglobulinaemia, which leads to cryoglobulinaemic vasculitis and cryoglobulinaemic glomerulonephritis (GN). Patients with acute cryoglobulinaemic vasculitis often exhibit acute kidney disease due to HCV infection, which typically progresses to acute kidney injury (AKI). HCV also increases the risk of chronic kidney disease (CKD) and the likelihood of developing end-stage renal disease (ESRD). Currently, direct-acting antiviral agents (DAAs) can be used to treat kidney disease at different stages. This review focuses on key findings regarding HCV and kidney disease, discusses the impact of DAAs, and highlights the need for further research and treatment.

Post-transplant diabetes mellitus (PTDM) is a common complication of solid organ transplantation. PTDM prevalence varies due to different diabetes definitions. Consensus guidelines for the diagnosis of PTDM have been published based on random blood glucose levels, glycated hemoglobin (HbA1c), and oral glucose tolerance test (OGTT). The task of diagnosing PTDM continues to pose challenges, given the potential for diabetes to manifest at different time points after transplantation, thus demanding constant clinical vigilance and repeated testing. Interpreting HbA1c levels can be challenging after renal transplantation. Pre-transplant risk factors for PTDM include obesity, sedentary lifestyle, family history of diabetes, ethnicity (e.g., African-Caribbean or South Asian ancestry), and genetic risk factors. Risk factors for PTDM include immunosuppressive drugs, weight gain, hepatitis C, and cytomegalovirus infection. There is also emerging evidence that genetic and epigenetic variation in the organ transplant recipient may influence the risk of developing PTDM. This review outlines many known risk factors for PTDM and details some of the pathways, genetic variants, and epigenetic features associated with PTDM. Improved understanding of established and emerging risk factors may help identify people at risk of developing PTDM and may reduce the risk of developing PTDM or improve the management of this complication of organ transplantation.

New-Onset Diabetes Mellitus after Transplantation (NODAT) emerges as a prevalent complication post-kidney transplantation, with its incidence influenced by variations in NODAT definitions and follow-up periods. The condition's pathophysiology is marked by impaired insulin sensitivity and β-cell dysfunction. Significant risk factors encompass age, gender, obesity, and genetics, among others, with the use of post-transplant immunosuppressants intensifying the condition. NODAT's significant impact on patient survival and graft durability underscores the need for its prevention, early detection, and treatment. This review addresses the complexities of managing NODAT, including the challenges posed by various immunosuppressive regimens crucial for transplant success yet harmful to glucose metabolism. It discusses management strategies involving adjustments in immunosuppressive protocols, lifestyle modifications, and pharmacological interventions to minimize diabetes risk while maintaining transplant longevity. The importance of early detection and proactive, personalized intervention strategies to modify NODAT's trajectory is also emphasized, advocating for a shift towards more anticipatory post-transplant care.

Irisin is a myokine with potential effects on glucose metabolism and the development of diabetes in humans. We analysed irisin serum levels (ISL) in 47 patients without diabetes before and 1, 2, 3, 4 and 5 weeks after kidney transplantation (KTx). All measurements of irisin before KTx levels were lower than 25 ng/mL (median 8.4 ng/mL). We found an outstanding increase in ISL measured after KTx, reaching more than 1000 times in 44% of patients (HIL-high irisin level group). The increase appeared at the first measurement (one week after KTx). Factors connected to the large growth of ISL were, i.e., BMI > 30 (p = 0.04) and subsequent KTx-second and third (p < 0.001). The global mean blood glucose level during the first two weeks after KTx was significantly lower in the HIL group (p = 0.002), the same as the day-by-day analysed mean fasting and postprandial serum glucose in the first days after KTx. In 12 months of observation, diabetes requiring insulin therapy occurred in the HIL group at a rate of 19%, while in the rest of the patients, the rate was 27%, p = 0.526. Irisin levels increase significantly in some patients after kidney transplantation, accompanied by lower blood glucose levels in the early post-transplant period. Whether an increase in irisin levels results in better glycaemic control remains questionable and requires further research, as well as the relationship between irisin levels and the occurrence of PTDM.

Multiple risk factors are involved in new-onset diabetes mellitus (DM) after organ transplantation; however, their ability to predict clinical prognosis remains unclear. Therefore, we investigated whether patient-specific induced pluripotent stem cells (iPSCs) could help predict DM development before performing kidney transplantation (KT).

We first performed whole transcriptome and functional enrichment analyses of KT patient-derived iPSCs. Our results revealed that insulin resistance, type 2 DM, and transforming growth factor beta signaling pathways are associated between the groups of DM and non-DM. We next determined whether the genetic background was associated with development of iPSCs into pancreatic progenitor (PP) cells.

The levels of differentiation-related key markers of PP cells were significantly lower in the DM group than in the non-DM group. Moreover, the results of tacrolimus toxicity screening showed a significant decrease in the number of PP cells of the DM group compared with the non-DM group, suggesting that these cells are more susceptible to tacrolimus toxicity.

Taken together, these results indicate that PP cells of the DM group showed low developmental potency accompanied by a significantly different genetic background compared with the non-DM group. Thus, genetic analysis can be used to predict the risk of DM before KT.

The success of solid organ transplantation (SOT) and the use of immunosuppressive agents offer hope to patients with end-stage diseases. However, the impact of posttransplant diabetes mellitus (PTDM) on SOT patients has become increasingly evident. In our study, we utilized the Scientific Registry of Transplant Recipients (SRTR) database to investigate the association between PTDM and patient survival in various types of organ transplantations, including liver, kidney, intestinal, heart, lung, and combined heart-lung transplantations (all P<0.001). Our findings revealed a negative effect of PTDM on the survival of these patients. Furthermore, we examined the effects of both generic and innovator immunosuppressive agents on the development of PTDM and the overall survival of different SOT populations. Interestingly, the results were inconsistent, indicating that the impact of these agents may vary depending on the specific type of transplantation and patient population. Overall, our study provides a comprehensive and systematic assessment of the effects of different immunosuppressive agents on prognosis, as well as the impact of PTDM on the survival of patients undergoing various types of SOT. These findings emphasize the need for further research and highlight the importance of optimizing immunosuppressive regimens and managing PTDM in SOT patients to improve their long-term outcomes.

Evidence supporting glucagon-like peptide-1 receptor agonists (GLP-1RAs) in kidney transplant recipients (KTRs) remains scarce. This systematic review and meta-analysis aims to evaluate the safety and efficacy of GLP-1RAs in this population.

A comprehensive literature search was conducted in the MEDLINE, Embase and Cochrane databases from inception through May 2023. Clinical trials and observational studies that reported on the safety or efficacy outcomes of GLP-1RAs in adult KTRs were included. Kidney graft function, glycaemic and metabolic parameters, weight, cardiovascular outcomes and adverse events were evaluated. Outcome measures used for analysis included pooled odds ratios (ORs) with 95% confidence intervals (CIs) for dichotomous outcomes and standardized mean difference (SMD) or mean difference (MD) with 95% CI for continuous outcomes. The protocol was registered in the International Prospective Register of Systematic Reviews (CRD 42023426190).

Nine cohort studies with a total of 338 KTRs were included. The median follow-up was 12 months (interquartile range 6-23). While treatment with GLP-1RAs did not yield a significant change in estimated glomerular filtration rate [SMD -0.07 ml/min/1.73 m2 (95% CI -0.64-0.50)] or creatinine [SMD -0.08 mg/dl (95% CI -0.44-0.28)], they were associated with a significant decrease in urine protein:creatinine ratio [SMD -0.47 (95% CI -0.77 to -0.18)] and haemoglobin A1c levels [MD -0.85% (95% CI -1.41 to -0.28)]. Total daily insulin dose, weight and body mass index also decreased significantly. Tacrolimus levels remained stable [MD -0.43 ng/ml (95% CI -0.99 to 0.13)]. Side effects were primarily nausea and vomiting (17.6%), diarrhoea (7.6%) and injection site pain (5.4%).

GLP-1RAs are effective in reducing proteinuria, improving glycaemic control and supporting weight loss in KTRs, without altering tacrolimus levels. Gastrointestinal symptoms are the main side effects.

Our goal was to evaluate the neutrophil:lymphocyte (NLR) and platelet:lymphocyte (PLR) ratios measured before transplantation and their correlation with new-onset diabetes after transplantation (NODAT) in renal transplant recipients.

We conducted our study in 324 adult patients consecutively admitted to Military Hospital 103, Ha Noi, Viet Nam, who received kidney allografts from living donors. These patients were followed-up during the first 2 years post-transplantation for NODAT. We examined the association between NLR and PLR measured prior to transplantation in patients with NODAT: NLR and PLR were calculated based on the results of the complete blood count. The criteria for diagnosis of a fully symptomatic NODAT case were based on the guidelines established by the American Diabetes Association and included fasting venous blood glucose and glycosylated hemoglobin A1c (HbA1c) levels, with or without an oral glucose tolerance test.

The overall rate of NODAT during the two years after kidney transplantation was 13.6%. We found mean values of age and body mass index (BMI), and median values of NLR, PLR, high sensitivity C-reactive protein (hs-CRP) levels, and the arteriosclerosis ratio in the NODAT group to be significantly higher than those of the non-NODAT group (all p < 0.05). Furthermore, an adjusted multivariate regression analysis showed that age (area under the curve [AUC] = 0.727, p < 0.001), BMI (AUC = 0.846, p < 0.001), serum hs-CRP levels (AUC = 0.884, p < 0.001), NLR (AUC = 0.888; p < 0.001), and PLR (AUC = 0.818; p < 0.001) had predictive value for NODAT.

NLR and PLR measured before transplantation were good predictors for NODAT in the first 2 years post-renal transplantation.