Ofatumumab in post‐transplantation recurrence of a pediatric steroid‐resistant idiopathic nephrotic syndrome

Treatment of SRNS is a challenge. Antiproliferative agents and depleting antibodies have been reported to be effective. However, these agents are not always successful, and use of ofatumumab could provide a different treatment option. Our patient was diagnosed with a SRNS at 5 years of age. She developed ESRD, with FSGS. This was cause for a first renal transplantation. The NS relapsed, leading to loss of the graft, and a second renal transplantation was performed. Due to the recurrence of the NS, IAds were initiated and led to a complete remission. Our patient remained dependent on IAds, however, despite treatments with calcineurin inhibitors, corticosteroids, rituximab, and abatacept. Ofatumumab was introduced and led to a remission, thus allowing cessation of the IAd treatment. Another infusion of ofatumumab was administered 8 months after the last one, due to the recurrence of the NS and a renewed increase in B cells. Although it did not result in a complete remission, the proteinuria was stabilized in the absence of IAds. Ofatumumab may be an alternative treatment for post‐transplantation rituximab‐resistant SRNS, although this needs to be confirmed by further studies.     

The effect of peri‐transplant plasmapheresis in the prevention of recurrent FSGS

Many pediatric centers utilize a variety of protocols including preemptive plasmapheresis to prevent the recurrence of FSGS post‐transplant. But the effectiveness of this expensive, time‐consuming process of plasmapheresis in the prevention of FSGS recurrence is still unclear. We retrospectively reviewed all pediatric cases of FSGS in our center that received a kidney transplant and compared the transplant and patient outcomes of those transplanted after 2006 who received pretransplant plasmapheresis to those prior to 2006 who did not. Of the 57 children with FSGS, 31 and 26 were transplanted before and after 2006, respectively. The cohorts differed significantly in keeping with the center immunosuppression protocol changes, and prior to 2006, the recipients were significantly younger. All children with FSGS transplanted after 2006 underwent three and one sessions of 1.0 plasma volume/exchange plasmapheresis with fresh frozen plasma replacement prior to the transplant in living and deceased donors, respectively, in addition to five sessions of every other day post‐transplant pheresis. The incidence (27% vs 26%, P = 1.0) and time to recurrence of FSGS in the kidney allograft (P = .22) were not significantly different in patients that did and did not undergo prophylactic plasmapheresis. We need to re‐evaluate the role of preemptive plasmapheresis in the prevention of FSGS recurrence in a prospective multicenter study.     

Pretransplantation combined therapy with plasmapheresis and rituximab in a second living-related kidney transplant pediatric recipient with a very high risk for focal segmental glomerulosclerosis recurrence

Chikamoto H, Hattori M, Kuroda N, Kajiho Y, Matsumura H, Fujii H, Ishizuka K, Hisano M, Akioka Y, Nozu K, Kaito H, Shimizu M. Pretransplantation combined therapy with plasmapheresis and rituximab in a second living‐related kidney transplant pediatric recipient with a very high risk for focal segmental glomerulosclerosis recurrence.
Pediatr Transplantation 2011. © 2011 John Wiley & Sons A/S. Abstract: Prophylactic PP can provide some protection against post‐transplantation recurrences of FSGS, but it cannot prevent recurrences in all cases. Therefore, new preventive therapies are needed. We report on a 7.9‐yr‐old girl treated with pretransplantation prophylactic combined therapy consisting of four sessions of PP and one dose of rituximab before a second living‐related KTX. The patient had a very high risk of post‐transplantation FSGS recurrence because this had occurred after the first KTX. During the 36 months since the second transplantation, she has had no evidence of proteinuria or significant infectious complications. Although our experience is too preliminary to draw any generalizable conclusions, pretransplantation combined therapy with PP and rituximab might be a possible option for the prevention of FSGS recurrence in very high‐risk recipients undergoing living‐donor KTXs.     

Preemptive plasmapheresis and recurrence of focal segmental glomerulosclerosis in pediatric renal transplantation

Gonzalez E, Ettenger R, Rianthavorn P, Tsai E, Malekzadeh M. Preemptive plasmapheresis and recurrence of focal segmental glomerulosclerosis in pediatric renal transplantation.
Pediatr Transplantation 2011: 15: 495–501. © 2011 John Wiley & Sons A/S. Abstract: FSGS has a high recurrence rate after renal transplantation. To examine the effects of the use of preemptive and post‐transplant PP on recurrence and graft outcome, we conducted a retrospective study on 34 pediatric patients (mean age 13 ± 5 yr) with biopsy‐proven pretransplant FSGS and who underwent a renal transplantation between 1996 and 2007. Recurrence was defined as a serum albumin level of <3.0 g/L in the presence of nephrotic‐range proteinuria (>40 mg/m²/h). Total response to PP therapy was defined as the resolution of the nephrotic‐range proteinuria and partial response as persistent proteinuria despite PP but not in the nephrotic range. Fifteen patients received a LD renal transplantation and 19 patients received a DD renal transplantation. Nineteen patients received CsA and 14 patients received tacrolimus. Nineteen patients (56%) had FSGS recurrence. There was no difference in the recurrence rate between patients receiving CsA vs. tacrolimus. Among the 15 LD patients, 13 received preemptive PP (1–10 sessions) and seven patients (47%) had subsequent FSGS recurrence. Among the 19 DD patients, four received preemptive PP and 12 (63%) had FSGS recurrence. The number of preemptive PP did not affect the recurrence rate. In a group of patients with a previous graft loss secondary to recurrence, the rate of recurrence was lower than expected (40%) and two of the three patients who did not recur had three or more sessions of preemptive PP. Of the 19 patients with recurrence, 17 were treated with PP therapy and 88% of the patients fully or partially responded. Only five patients had graft loss at three yr post‐transplant: two from FSGS recurrence and three from non‐compliance. These results suggest that preemptive PP does not decrease the rate of recurrence after transplantation but might be beneficial in treating high‐risk patients with documented recurrence. Patients with FSGS recurrence post‐transplant can achieve good graft survival with both LD and DD transplantation.     

Rituximab for post-transplant recurrences of FSGS

Abstract:  A 14-yr-old boy whose primary kidney disease was FSGS developed severe recurrence of proteinuria immediately after a second living-related kidney transplant. Despite pre- and post-operative PP and immunosuppressive treatment consisting of steroids, CycA, daclizumab, and MMF, daily protein excretion and serum creatinine increased. We therefore administered rituximab on the fourth day of transplantation. He received four weekly doses of rituximab (375 mg/m²/dose), which resulted in a rapid clearing of circulating CD19-positive B cells, and remission of proteinuria was achieved six wk after the first rituximab treatment. Graft function was excellent six months after transplantation with proteinuria of 8 mg/m²/h. We conclude that rituximab may be an effective treatment for post-transplant recurrence of FSGS.     

Long‐term effect of rituximab in maintaining remission of recurrent and plasmapheresis‐dependent nephrotic syndrome post‐renal transplantation – Case report

Grenda R, Jarmu?ek W, Pi?tosa B, Rubik J. Long‐term effect of rituximab in maintaining remission of recurrent and plasmapheresis‐dependent nephrotic syndrome post‐renal transplantation – Case report.
Pediatr Transplantation 2011: 15: E121–E125. © 2010 John Wiley & Sons A/S. Abstract: Early recurrence of nephrotic syndrome after renal transplantation is a common serious adverse event in children with severe primary FSGS, affecting long‐term outcome. There is no consensus in terms of uniform management in these cases. We describe the long‐term effect of four unadjusted doses of 375 mg/m² i.v. rituximab, given to a five and a half‐yr‐old, nephrectomized child with immediate recurrence of nephrotic syndrome post‐transplantation and dependency from repeated PF. Rituximab was introduced at three months post‐transplantation after performing 18 sessions of PF and development of established dependency of the disease from plasma exchange. Complete remission of proteinuria was achieved with four doses, and it was maintained during next eight months of follow‐up. Complete B CD₁₉ cell depletion was observed during four months after final dose, followed by severe depletion after eight months. No side effects of therapy were noted. Patient was free from PF, which was stopped while introducing rituximab, remaining non‐proteinuric on triple immunosuppression (CsA, MMF, Pred).     

Success with plasmapheresis treatment for recurrent focal segmental glomerulosclerosis in pediatric renal transplant recipients

FSGS recurs in approximately 30% of transplanted kidneys and may lead to graft loss. We retrospectively examined the efficacy of early and intensive PP without additional IS in pediatric kidney transplant patients with recurrent FSGS at our center. Seven of 24 patients (29%) had nephrotic proteinuria and histologic evidence of FSGS recurrence within 1–5 days post‐transplantation. PP was initiated early after transplantation and initially performed daily until sustained decline in proteinuria. PP frequency was then individually tapered according to proteinuria. Recurrent FSGS in all seven patients responded to a four‐ to 32‐wk course of PP. Two of seven patients had a second recurrence of FSGS, and both recurrences remitted after an additional 3–6 wk of PP. Median observation period was 4.5 yr (0.8–16.3 yr). Complete remission of recurrent FSGS has been sustained in all seven patients, and all patients have stable graft function with recent plasma creatinine <1.5 mg/dL in six of seven patients. Most recent urine protein/creatinine is 0.13–0.61 mg/mg in six of seven patients. One patient has heavy proteinuria secondary to chronic allograft nephropathy 16 yr post‐transplant. Intensive and prolonged PP, when initiated early in the post‐operative period, is effective in treating recurrent FSGS and preventing graft loss without the use of additional immunosuppressants.     

HLA desensitization with bortezomib in a highly sensitized pediatric patient

The proteasome inhibitor bortezomib has been used with variable success in the treatment of AMR following heart transplant. There is limited experience with this agent as a pretransplant desensitizing therapy. We report a case of successful HLA desensitization with a bortezomib‐based protocol prior to successful heart transplantation. A nine‐yr‐old boy with dilated cardiomyopathy, not initially sensitized to HLA (cPRA of zero), required three days of ECMO, followed by implantation of a Heartmate II LVAD. Within six wk, the patient developed de novo class I IgG and C1q complement‐fixing HLA antibodies with a cPRA of 100%. Two doses of IVIG (2 g/kg) failed to reduce antibody levels, although two courses of a novel desensitization protocol consisting of rituximab (375 mg/m²), bortezomib (1.3 mg/m² × 5 doses), and plasmapheresis reduced his cPRA to 0% and 87% by the C1q and IgG assays, respectively. He underwent heart transplantation nearly two months later. The patient is now >one yr post‐transplant, is free of both AMR and ACR, and has no detectable donor‐specific antibodies by IgG or C1q. Proteasome inhibition with bortezomib and plasmapheresis may be an effective therapy for HLA desensitization pretransplant.     

Preventing recurrence of focal segmental glomerulosclerosis following renal transplantation: a case report

While the recurrence of FSGS in a primary renal transplant has been well studied, strategies to prevent subsequent recurrence in later transplants, has not been well formulated. This is important considering that one center's experience with adults reported an initial recurrence rate of 57% with reoccurrence of 37% in subsequent transplants. However, renal function was maintained in 62% (1). In pediatrics, data from a single-center reported 100% recurrence of FSGS in the second allograft after an initial recurrence of 52% (2). Two commentaries reviewing such data, one each in adults and pediatrics, suggested that the benefits of living-related donation might not be realized in patients with FSGS because of this frequent recurrence (3, 4). Here, we report a patient who was considered to be at very high risk for post-transplant recurrence of FSGS, because of the established risk factors, who was successfully retransplanted after a course of pretransplant plasmapheresis, followed by post-transplant plasmapheresis and the use of cyclosporine. Eighteen months post-transplant, he has no proteinuria and his serum creatinine is 1.2 mg/dL.     

Recurrence of focal segmental glomerulosclerosis in renal allograft: An in‐depth review

Vinai M, Waber P, Seikaly MG. Recurrence of focal segmental glomerulosclerosis in renal allograft: An in‐depth review.
Pediatr Transplantation 2010: 14: 314–325. © 2010 John Wiley & Sons A/S. Abstract: Focal segmental glomerulosclerosis is a major cause of chronic kidney disease requiring transplantation in children. Recurrence rate in the renal allograft transplantation is as high as 50%. Recurrence of FSGS is associated with renal dysfunction and early graft loss. To date, there is no established therapy for recurrent FSGS after renal transplant. We have reviewed the current English literature in order to summarize current practices with emphasis on graft outcome. We conclude that despite multiple approaches to the post transplant management of recurrent FSGS, none have been shown to be consistently beneficial. Currently, pheresis combined with high dose anti‐calcineurin with or without rituximab seems to be the most promising. Further controlled studies are needed to define the optimal therapeutic regimens to treat recurrent of FSGS.     

Rituximab treatment for recurrence of nephrotic syndrome in a pediatric patient after renal transplantation for congenital nephrotic syndrome of Finnish type

Congenital nephrotic syndrome (CNS) of the Finnish type due to mutation in the NPHS-1 gene results in massive proteinuria due to structural abnormality in the glomerular slit diaphragm, and is usually refractory to immunosuppressive therapy. Patients eventually require bilateral nephrectomy and renal replacement therapy, with transplantation being the ultimate goal. Post-transplant recurrence of nephrotic syndrome occurs in about 25% of children and is thought to be immune-mediated secondary to antibodies formed against the nephrin protein in renal allograft. Conventional therapy with calcineurin inhibitors (CNI), cyclophosphamide and corticosteroids with or without plasmapheresis often fails to achieve remission resulting in graft loss in 12-16%. There is limited experience with use of rituximab (RTX) in pediatric organ transplant recipients. We report the first case of post-transplant recurrence of nephrotic syndrome in a 4-yr-old child with CNS due to NPHS-1 mutation in whom CNI, corticosteroid and cyclophosphamide therapy was unsuccessful, but who achieved remission after depletion of B cells with RTX, associated with a decrease in the level of anti-nephrin antibodies. The child remains in remission 5 yr following treatment. Our experience suggests that activated B cells may play a pivotal role in the recurrence of nephrosis after renal transplantation in children with CNS.     

Early post‐transplant hyperbilirubinemia is a possible predictive factor for developing neurological complications in pediatric living donor liver transplant patients receiving tacrolimus

The cause of post‐transplant CNI‐NCs is multifactorial and not ascribed solely to CNI toxicity. A total of 90 children (aged <20 years) who underwent LDLT were evaluated to investigate the predictive factors associated with CNI‐NCs. Twelve patients (13.3%) developed CNI‐NCs after LDLT (age range, 2‐15 years). The symptoms of CNI‐NCs were seizures, VD, and stupor. The median onset of CNI‐NCs was 10 days (range, 5‐30 days) post‐transplant. In the univariate analysis, higher recipient age at LDLT, donor age and recipient's BW, lower actual GV/SLV and TAC dosage/BW, and higher mean T‐Bil and sodium level for 7 days after transplantation were independently significantly associated with TAC‐NCs. Multivariate analysis showed that the T‐Bil level in the first week after LDLT was the only significant independent predictive factor for TAC‐NCs (HR, 1.588; 95% CI, 1.042‐2.358; P=.031). In conclusion, CNI‐NCs occurred most frequently in children over 5 years and were associated with hyperbilirubinemia for 7 days post‐transplant, regardless of TAC levels. The transplant team should refer to a neurologist to define the diagnosis and to collaborate to resolve the neurological problems.     

Isolated abdominal nocardiosis in a pediatric renal transplant recipient

Nocardia infection after RT is uncommon. The most common modes of exposure are inhalation of dust containing nocardia or contaminated soil/water and surgical instruments. Isolated abdominal nocardiosis following RT has not been reported. We report an 11‐year‐old female who developed nocardia abscesses of the abdomen post‐RT. ESRD was secondary to FSGS and she had received multiple immunosuppressive agents prior to transplant. Induction immunosuppression consisted of thymoglobulin and maintenance was with tacrolimus, mycophenolate, and prednisone. There were construction activities in the hospital ward during her hospital stay. Due to immediate recurrence of FSGS in the allograft, she received plasma exchange, rituximab, and IVIG. Anti‐infective prophylaxis consisted of TMP‐SMX, valganciclovir, and nystatin. She developed multiple loculated fluid collections in the abdomen 6 weeks later. Histology of lesions demonstrated suppurative caseating granulomatous inflammation and the AFB culture showed Nocardia farcinica. With the reduction of immunosuppressive agents along with usage of TMP‐SMX, imipenem‐cilastatin, and linezolid, she had a partial recovery after 9 months with persistent small abscesses but remained asymptomatic clinically. There was no evidence of nocardia infection in lungs and brain. Repeat AFB culture from the lesions was negative. Allograft function remained stable throughout. She remains on oral TMP‐SMX therapy. We postulated that she could have acquired nocardia either from the contaminated air particles in the hospital from the construction activities or reactivation of nocardia from prior colonization. Nocardia infection should be suspected in immunocompromised patients with unexplained fever and abdominal pain.     

Refractory autoimmune hemolytic anemia after intestinal transplant responding to conversion from a calcineurin to mTOR inhibitor

AIHA is a rare and serious complication of solid organ transplantation. Herein, we report four cases of warm or mixed AIHA in pediatric patients following combined liver, small bowel and pancreas transplant. The hemolysis was refractory to multiple treatment modalities including steroids, rituximab, IVIG, plasmapheresis, cytoxan, discontinuation of prophylactic penicillin, and a change in immunosuppression from tacrolimus to cyclosporine. All patients had resolution or marked improvement of hemolysis after discontinuation of maintenance of CNI and initiation of sirolimus immunosuppression. One patient developed nephrotic syndrome but responded to a change in immunosuppression to everolimus. Three of the four patients continue on immunosuppression with sirolimus or everolimus without further hemolysis, evidence of rejection or medication side effects. Based on our experience and review of similar cases in the literature, we have proposed a treatment algorithm for AIHA in the pediatric intestinal transplant patient population that recommends an early change in immunosuppressive regimen from CNIs to sirolimus therapy.     

De novo hepatocellular carcinoma post‐multivisceral transplantation in a child

De novo hepatocellular carcinoma (HCC) post‐transplantation in patients without viral hepatitis is extremely rare, with only three reported adult cases in the English literature. Here, we present a case of de novo HCC that developed in a 7‐year‐old female, who at 8 months of age received a liver, small bowel, spleen, and pancreas transplantation 6.5 years ago for gastroschisis and total parenteral nutrition (TPN)‐related cirrhosis. The post‐transplant course was complicated by Epstein‐Barr virus (EBV) infection, post‐transplant lymphoproliferative disease, and subsequent development of multifocal EBV‐associated post‐transplant smooth muscle tumors (EBV‐PTSMT) in the small bowel 1 year and 10 months after transplantation, respectively. This was managed by reducing immunosuppression with rituximab and EBV‐specific cytotoxic T‐cell therapy. She was noted to have a new lesion in her transplanted liver graft 6.5 years post‐transplantation that was diagnosed as HCC. The HCC was resected, and the patient remained clinically stable for 7 months. At that time, recurrence of the HCC was discovered on MRI. She passed away 6 months after. To the best of our knowledge, this is the first reported occurrence of de novo HCC post‐transplantation in the pediatric population that is unrelated to viral hepatitis in either recipient or donor.     

Eltrombopag (thrombopoietin‐receptor agonist) and plasmapheresis as rescue therapy of acute post‐renal transplant immune thrombocytopenia in a child with Schimke immuno‐osseous dysplasia—case report

SIOD is rare disorder related to SMARCAL1 or SMARCAL2 gene mutation, including (among other comorbidities) T‐cell immunodeficiency, nephrotic syndrome, and renal failure. Up to 22% of primary patients may develop various autoimmune disorders. We report the case of 11‐year‐old male with SIOD, who presented ITP at 2 years after renal transplantation with decrease in platelet count (from normal) to 56 000/μL and then (gradually) to 2000/μL. There was no effect of iv. methylprednisolone/dexamethasone. As the presence of antibodies against GPIIb/IIIa, GPIb, and GPIaIIa platelet glycoproteins was confirmed, patient was given 50 g of IVIG and then was put on plasmapheresis; however, both showed poor direct effect. As we were afraid to give rituximab (due to expected overimmunosuppression), we prescribed the oral TPO‐receptor agonist (eltrombopag). Patient responded after 17 days of therapy, to the final dose of 50 mg/d (approx. 2 mg/kg). The antiplatelet antibodies disappeared after four plasmapheresis. Overall, the therapy was continued for 7 weeks and was stopped at platelet count of 433 000/μL. Platelet count remained stable in 8‐month follow‐up. Combination of plasmapheresis and TPO‐receptor agonist was effective in post‐renal transplant acute ITP in patient with SIOD.     

Extended follow‐up of pediatric liver transplantation patients receiving once daily calcineurin inhibitor

We describe longitudinal results in a cohort of pediatric liver transplant patients successfully minimized to once daily CNI monotherapy for longer than five yr and assess changes in liver biochemistries and liver histology. A retrospective chart review of all pediatric liver transplant patients at a single center was performed. Biopsies and serum biochemistries (AST, ALT, total bilirubin, direct bilirubin, INR, creatinine) are reported at time points: PM, five‐yr, seven‐yr, and nine‐yr post‐minimization. Biopsies were assessed for inflammation and fibrosis using Ishak and Batts grading systems. Successful minimization to daily CNI monotherapy was defined as normal liver enzymes with no episodes of rejection. Thirty‐three patients have successfully remained on once daily CNI for >5 yr, and 19/33 of these patients have serial liver biopsies available for review. We report on the clinical and histological findings of these 19 patients. All 19 patients continue to have normal liver biochemistries. On post‐minimization biopsies, fibrosis progressed by ≥2 stages in one patient (5.3%) despite normal liver biochemistries. Carefully selected patients can tolerate minimization to once daily CNI monotherapy as few have progression of fibrosis.     

Liver transplantation in a child with multifocal hepatocellular carcinoma hepatitis C and management of post‐transplant viral recurrence using boceprevir

HCV infection is the leading cause of liver transplantation in the adult population in the United States. HCV infection occurs in 0.2–0.4% of the pediatric population and progression to HCC is uncommon. Liver transplantation for HCV in children is rare. In this report, we present a case of pediatric patient with HCV and multifocal HCC at the age of 13 who underwent successful liver transplantation. While good graft function was initially observed, at one month after transplant, he experienced significant hepatitis C recurrence. He was treated with low‐accelerating dose regimen antiviral therapy of PEG‐IFN and RBV, followed by addition of a protease inhibitor, boceprevir, which led to viral clearance. To our knowledge, this is the first case report describing the post‐transplant course of a child transplanted for HCV and HCC, and the first pediatric case report on using the triple therapy for management of post‐liver transplant recurrence of HCV. This case report demonstrates the need for increased vigilance of surveillance for HCC during childhood.     

Efficacy of rituximab therapy in children with refractory nephrotic syndrome: a prospective observational study in Shanghai

Background

Idiopathic nephrotic syndrome is the most common glomerular disease in children. This study was undertaken to observe the efficacy and side-effects of rituximab (RTX) in treating children with different types of refractory primary nephrotic syndrome.

Methods

Twelve patients with steroid dependent nephrotic syndrome (SDNS), frequently relapsing nephritic syndrome (FRNS), and steroid resistant nephrotic syndrome (SRNS) were enrolled in our study. There were obvious drug side-effects, and proteinuria remained difficult to control. RTX was administered at a dose of 375 mg/m² body surface area, once or twice weekly.

Results

The male to female ratio was 3:1, and the onset age was 1.6–8.9 years. There were 9 patients with steroid sensitive nephrotic syndrome (SDNS or FRNS), and 3 patients with SRNS. There were 7 patients with minimal change disease (MCD), 3 patients with focal segmental glomerular sclerosis (FSGS), 1 with focal proliferative glomerulonephritis, and 1 without renal biopsy. The total effective treatment rate of RTX was 91.67%, and for 77.78% of the patients, steroid dosage could be reduced. Six months before and after RTX infusion, the mean steroid dosage was significantly decreased (P=0.014) and the recurrence number was significantly reduced (P<0.001). The results were better in MCD patients than in FSGS patients (P=0.045). There was no significant difference between FRNS/SDNS and SRNS patients (P=0.175). During RTX administration, 3 patients developed skin rashes, 1 developed hypotension, and 1 developed a fever. One patient experienced a persistent decrease in serum immunoglobulin level but without serious infection.

Conclusion

RTX was effective in the treatment of refractory nephrotic syndrome, and it could significantly reduce the use of steroid and immunosuppressants.     

Use of belatacept to maintain adequate early immunosuppression in calcineurin‐mediated microangiopathic hemolysis post‐renal transplant

We report a 17‐yr‐old boy who developed a microangiopathic hemolytic anemia presumed secondary to tacrolimus shortly following a living‐related donor renal transplant. This was initially managed by plasmapheresis. Reinstitution of calcineurin inhibition using cyclosporine led to recurrence of hemolysis, so an alternative agent was needed. He was commenced on monthly intravenous belatacept, with no further recurrence of the hemolysis, and subsequent stable graft function. Modulation via CTLA‐4 offers an alternative immunosuppressive tactic if current regimens produce graft threatening adverse effects. The method of administration and frequency of dosage of belatacept also lends itself well to the high‐risk period of adolescence and transition. We propose that belatacept may therefore also have utility in difficult cases complicated by poor concordance, common in the adolescent age group.