The impact of HLA mismatch and induction therapy in simultaneous pancreas-kidney transplantation on outcomes remains incompletely defined. We conducted a retrospective cohort study of 1705 SPK recipients transplanted in the UK between 2007 and 2019. Using national transplant registry data, we analysed the impact of locus-specific HLA mismatch and induction therapy (Alemtuzumab vs. Basiliximab) on pancreas graft survival primarily. Kidney graft and patient survival were also analysed as secondary outcomes. Multivariable Cox proportional hazards models were adjusted for donor, recipient, and transplant variables. Pancreas graft survival at 1- and 10-year post-transplant was estimated to be 88.6% and 72.7%, respectively. Kidney graft and patient survival at 10 years were 76.7% and 75.3%. In adjusted analyses, donor age, cold ischaemic time, and HLA-DQ mismatch were significantly associated with pancreas graft loss. No significant survival difference was seen between Alemtuzumab and Basiliximab induction therapy. Induction therapy and HLA-mismatch status were not associated with pancreas graft outcome in this large registry study.

In this article, we comment on the article by Sessa et al published in the recent issue of the World Journal of Transplantation, who revisit the three-decade single centre cohort of Muñoz-Serrano et al and conclude that chronic kidney disease (CKD) after liver transplantation (LT) is a modifiable determinant of long-term survival rather than an unavoidable consequence of calcineurin inhibitor exposure. We share their central position and welcome the weight they give to perioperative acute kidney injury (AKI), to calcineurin inhibitor minimisation through basiliximab induction and mycophenolate, and to the disciplined control of hypertension and metabolic disease. Our intention is to carry the argument one step further, because three problems lie beneath the literature they assemble and constrain what any inventory of risk factors can deliver. The first is metrological. Almost every reported association, including the signal attached to female sex, and the reported incidence itself, which varies according to the definition of CKD applied, the time point of ascertainment and whether creatinine-based or measured filtration is used, derive from creatinine-based estimates of glomerular filtration, a measure the same authors concede performs poorly in patients who are sarcopenic, oedematous and metabolically deranged. The second concerns timing, since the most powerful and most modifiable determinant of chronic injury is the passage from early AKI to fixed nephropathy, a transition that draws surveillance away from isolated tacrolimus trough concentrations, which did not predict one year disease in the index cohort, towards intrapatient variability and time within the therapeutic range. The third is therapeutic, because the prevailing synthesis omits the sodium glucose cotransporter 2 inhibitors, agents with established renal benefit in non-transplant CKD populations that deserve formal evaluation after LT. Measured accurately, protected early and evaluated pharmacologically, the kidney of the liver transplant recipient is more defensible than current practice assumes.

In this review summarizes studies presenting a propensity-matched comparative analysis evaluating alemtuzumab vs basiliximab induction in kidney transplant recipients with aligned immunological risk profiles and extended follow-up. Alemtuzumab, a potent lymphocyte-depleting agent, has therefore been widely adopted on the premise that deeper early immune suppression confers durable graft protection. Whether this assumption holds true beyond the early post-transplant period remains uncertain. A recent study demonstrates comparable rates of acute rejection between induction strategies, effectively neutralising rejection as the differentiating endpoint in contemporary practice. In contrast, clinically meaningful divergence emerges in longer-term outcomes. Alemtuzumab induction is associated with inferior graft function, higher rates of cytomegalovirus and BK viremia, increased post-transplant malignancy, and greater death-censored graft loss. These findings highlight a central paradox in transplant immunology: Strategies that achieve potent early immune suppression may incur delayed biological costs related to immune reconstitution, impaired immune surveillance, and cumulative graft injury. Collectively, the data argue for a shift away from rejection-centred metrics toward a more proportional and individualised approach to induction selection, in which long-term graft preservation and complication risk are weighed as carefully as early rejection prevention.

Pharmacokinetic monitoring is insufficient to estimate the intensity of immunosuppression after kidney transplantation (Tx). The randomized controlled IVIST trial demonstrated that additional steering of immunosuppressive therapy by virus-specific CD4[+] T cells (Tvis) is safe and reduces exposure to immunosuppressants. The adenovirus-specific CD4[+] T cells (ADV-Tvis) proved to be particularly suitable due to their stability and high prevalence. Another promising biomarker for post-Tx immunomonitoring is the Torque Teno virus (TTV) but pediatric data are very limited. This descriptive longitudinal analysis aimed to evaluate the post-Tx course of TTV load compared to Tvis levels after pediatric Tx. In the IVIST trial, 31 pediatric kidney recipients were randomized to the intervention group with Tvis-guided immunosuppression. The immunosuppressive therapy consisted of basiliximab, cyclosporine A (CsA), everolimus (Eve), and prednisolone. In 27 out of 31 intervention group patients, TTV-DNA was analysed retrospectively in frozen plasma samples from 20 visits [1-24 months (mo) after Tx]. Associations of TTV-DNA with ADV-Tvis and with immunosuppressants over the post-Tx period were evaluated using linear mixed models, adjusted for time since Tx and accounting for repeated measurements within patients. Mean TTV-DNA (n = 474) ± standard deviation was 4.4 ± 1.3 log10 copies/ml (1.4 to 9.4 log10). TTV-DNA was associated with post-Tx follow-up time. Under intensive immunosuppression immediately after Tx, TTV-DNA increased, peaking at 3 mo post-Tx (5.5 ± 1.4 log10); after reduction of immunosuppression, TTV load decreased (6 mo: 4.3 ± 1.1 log10; 16 mo: 3.9 ± 0.9 log10). Mean ADV-Tvis levels showed a minimum at 2 mo post-Tx and increased over time: from 1.5 ± 1.1 cells/µl (2 mo) to 2.0 ± 1.8 cells/µl (6 mo) and 2.4 ± 1.7 cells/µl (22 mo). TTV-DNA showed overall positive correlations with mean daily doses and trough levels of CsA and Eve. The longitudinal analysis of TTV load presented an opposite post-Tx course compared to ADV-Tvis. TTV-DNA was associated with post-Tx follow-up time and with immunosuppressants after pediatric Tx. In comparison to ADV-Tvis minimum, the mean TTV-DNA showed a late peak at 3 mo post-Tx suggesting delayed response to drug dose changes.

De novo gastric cancer after liver transplantation is clinically rare, and radical resection remains the only potentially curative treatment. However, post-transplant anatomical distortion and extensive intra-abdominal adhesions increase surgical complexity, while long-term immunosuppression elevates the risks of perioperative infection and organ dysfunction. Furthermore, chemotherapy and immune checkpoint inhibitors may precipitate graft rejection. We report a 68-year-old man who underwent liver transplantation 18 years earlier for HBV-related hepatocellular carcinoma (T1aN0M0), meeting the Milan criteria. Preoperatively, serum HBV DNA was 2.3 × 10[3] IU/mL. He received entecavir and basiliximab induction, followed by early triple immunosuppression and long-term tacrolimus maintenance. During follow-up, HBV DNA remained undetectable, liver function was stable, and no transplant-related complications occurred. Eighteen years after transplantation, he presented with upper abdominal pain. Imaging and endoscopy demonstrated cT4N1M0 gastric adenocarcinoma of the antrum with hepatic parenchymal invasion. Following multidisciplinary discussion, laparoscopic D2 radical gastrectomy with Roux-en-Y reconstruction, partial hepatectomy, and ultra-tension-reducing abdominal wall closure were performed. The postoperative course was uneventful. This case suggests that multidisciplinary, standardized perioperative management can enable safe radical laparoscopic gastrectomy in selected liver transplant recipients.

Calcineurin inhibitors (CNIs) remain the cornerstone of immunosuppression after liver transplantation (LT) but contribute to chronic renal failure, increasing long-term morbidity and mortality. Strategies to minimize CNI exposure and preserve renal function are necessary to improve long-term outcomes in high-acuity LT recipients. We conducted a single-center, prospective, randomized trial of adult LT recipients requiring pre-LT renal replacement therapy (RRT). Patients were randomized to: (1) basiliximab induction and delayed tacrolimus starting postoperative day (POD) 5 (BAS); (2) basiliximab induction, tacrolimus starting POD5, and everolimus starting POD31, followed by tacrolimus minimization (BAS-EVR); (3) standard immunosuppression (control). RRT independence, renal function, rejection, graft and patient survival, and adverse events were assessed. Seventy patients were analyzed (BAS n=30; BAS-EVR n=28; control n=12). Median MELD was 40, and 55.7% of patients required mechanical ventilation or vasopressor support pre-LT. Overall, 68.6% of patients achieved RRT independence by 24 weeks: 73.3% (BAS), 75.0% (BAS-EVR), and 41.7% (control). Basiliximab (p =0.04) and shorter duration of pre-LT RRT (p =0.02) were significantly associated with RRT independence; basiliximab remained significant after adjusting for duration of pre-LT RRT [OR 3.87 (95% CI 1.01-14.74), p =0.048]. Among patients who achieved RRT independence, median eGFR trended higher in the BAS-EVR group (67 mL/min/1.73 m 2) than in BAS (52 mL/min/1.73 m 2) and control groups (50 mL/min/1.73 m 2) at 24 weeks. Patient and graft survival were comparable across groups. Adverse events were similar, although diarrhea (p =0.004) and acute kidney injury (p =0.01) were more frequent in the BAS-EVR group. Basiliximab induction therapy with delayed tacrolimus promotes RRT independence in high-acuity LT recipients. Addition of everolimus to minimize tacrolimus may further preserve renal function without compromising graft or patient survival.

Introduction ABO-incompatible kidney transplantation (ABOiKT) has emerged as a viable option whenever there is non-availability of a compatible donor. Traditionally considered a contraindication due to the high risk of antibody-mediated rejection, advancements in desensitization protocols, immunosuppressive therapy, and post-transplant monitoring have significantly improved the outcomes. In this study, we have detailed our experience of ABOiKT performed in a tertiary care hospital in North India. Methodology It was a single-center retrospective cohort study. All consecutive ABOiKT performed from 2014 to 2021 were screened. Recipients younger than 15 years of age, with dual-organ transplants, and with highly sensitized transplants were excluded from the study. Three years of follow-up data from the hospital records were collected and analyzed. The primary objective was to study the incidence of biopsy-proven acute rejections (BPARs), and secondary objectives were to study the incidence of graft loss and infectious complications. Results A total of 93 ABOiKTs meeting the inclusion and exclusion criteria were included in the study. Fourteen (15.1%) kidney transplant recipients (KTRs) experienced BPAR, the majority of which were antibody-mediated (10 out of 14; 71.42%). Overall, 8 (8.6%) KTRs experienced graft loss. The rejection-free survival at six months, one year, and three years was 84 (90.3%), 83 (89.2%), and 79 (84.9%), respectively. Correspondingly, graft survival at six months, one year, and three years was 90 (96.8%), 87 (93.5%), and 85 (91.4%), respectively. Urinary tract infection was the most common infection encountered in 35 (37.6%) cases. There was no significant difference in incidence of acute rejection or graft loss between the two cohorts with basiliximab/nil or rabbit antithymocyte globulin as the induction agent. In regression analysis, anti-A/B antibody titer or the type of induction agent used did not predict acute rejection; however, delayed graft function was significantly associated with rejection episodes (OR: 43.33, 95% CI: 4.54-413.27, p<0.05). Conclusions With careful recipient selection and vigilant post-transplant monitoring, patient and graft outcomes can be improved substantially after ABOiKT. This approach offers a promising solution to reduce waiting times and expand the donor pool for potential KTRs.

The use of Janus Kinase (JAK) inhibitors with concomitant maintenance immunosuppressive therapy (IST) for the solid organ transplant (SOT) population presents significant challenges due to intensified immunosuppression resulting in an increased risk of opportunistic infections and malignancies coupled with limited clinical experience among transplant providers. A 48-year-old man presented with end-stage kidney disease secondary to IgA nephropathy requiring commencement of haemodialysis. He had a concurrent diagnosis of primary myelofibrosis (PMF), which did not require treatment at presentation. A year later, he underwent a living-donor kidney transplant from an HLA-identical sibling. The patient received induction IST with basiliximab and methylprednisolone, followed by standard maintenance therapy with tacrolimus and mycophenolate mofetil. The latter was reduced in dose due to underlying PMF. In the months following transplantation, he experienced worsening PMF parameters and was commenced on the JAK2 inhibitor, ruxolitinib. This was complicated by development of detectable BK Polyomavirus DNA (BKPyV-DNAemia), prompting adjustment of his immunosuppression regimen and dose reduction of ruloxlitinib. His course was further complicated by renal allograft rejection. Ruxolitinib was subsequently discontinued, and he transitioned to the second-generation JAK inhibitor fedratinib, which led to improvement in PMF parameters and stabilization of both graft function and BKPyV-DNAemia. This case highlights the therapeutic challenges inherent in integrating JAK inhibitors into established immunosuppression regimens in solid organ transplantation. It underscores the difficult balance between preserving graft tolerance and mitigating the risk of opportunistic infections such as BKPyV-DNAemia, while emphasising the need for close monitoring of net immunosuppression in this setting.

Uterus transplantation (UTx) is an emerging therapeutic option for women with absolute uterine factor infertility, requiring intensive immunosuppression that increases susceptibility to opportunistic infections such as cytomegalovirus (CMV). Evidence guiding CMV management in UTx remains limited. The authors report a case of CMV reactivation in a 34-year-old woman with Mayer-Rokitansky-Küster-Hauser syndrome who underwent successful living-donor UTx. The patient received induction with methylprednisolone and basiliximab, followed by maintenance immunosuppression with tacrolimus, azathioprine, and prednisone. Antiviral prophylaxis with ganciclovir/valganciclovir was administered for three months. After prophylaxis discontinuation, routine surveillance detected CMV DNAemia approximately five months post-transplant, leading to treatment with valganciclovir and temporary postponement of embryo transfer. Following viral clearance, embryo transfer was successfully performed. During early pregnancy, low-level CMV DNAemia recurred. Given concerns about antiviral teratogenicity, management focused on the reduction of immunosuppression, including tacrolimus dose adjustment and discontinuation of azathioprine, with close monitoring via cervical biopsies. CMV DNAemia resolved spontaneously without antiviral therapy, and no rejection episodes or CMV disease occurred. This case highlights the complex balance between infection control and graft preservation in UTx recipients, particularly during pregnancy. It suggests that individualized reduction of immunosuppression may be a safe and effective strategy for managing CMV reactivation when antiviral therapy is contraindicated. Additionally, it supports the concept that the uterine graft may exhibit relatively low immunogenicity. Further studies are needed to define optimal immunosuppressive thresholds and standardized CMV management protocols in this unique transplant population.