Transient elastography assessment of liver allograft fibrosis in pediatric transplant recipients

TE measures liver stiffness to assess fibrosis. Its use in post‐transplant patients was reported in few small pediatric studies. We evaluated TE ability to predict liver graft fibrosis in a large cohort while comparing it to the performance of APRI and FIB‐4. We also investigated the effect of graft type on LSMs. Patients at Boston Children's Hospital who underwent LT and LSM ≤ 1 year from biopsy (2007‐2018) were eligible. Ninety‐four patients (45%M) aged 1‐21 years (89% < 18 years; 13% < 2 years) were eligible. Median time between transplant/biopsy and LSM was 5.1 years and 52 days, respectively. Thirty‐nine percent received whole‐liver grafts, 54% TV grafts, and 6% as part of MV. At LSM, median ALT was 25 [IQR 16‐33] IU/L. Twenty‐one percent had METAVIR ≥ F2. LSM was statistically higher among those with significant fibrosis (METAVIR ≥ F2) compared to those with METAVIR F0/F1 (median [IQR] 7.5 [4.6, 13.6] vs 5.1 [4.0, 6.4] kPa, respectively) (P = .005 by Wilcoxon rank‐sum test). APRI and FIB‐4 distributions were not different across METAVIR stages. The AUROC for LSM was 0.71 (95% CI 0.56‐0.85) with an optimal cut‐point of 6.5 kPa. Graft type had no influence on the AUROC for LSM. TE is useful for assessing significant graft fibrosis in children and young adult LT recipients and performs better than APRI and FIB‐4. TV grafts demonstrate similar correlation with histology as whole‐liver grafts.     

AST‐to‐platelet ratio index in non‐invasive assessment of long‐term graft fibrosis following pediatric liver transplantation

Long‐term graft fibrosis occurs in the majority of pediatric liver transplant recipients. Serial biopsies to monitor graft health are impractical and invasive. The APRI has been evaluated in pediatric liver disease, but not in the context of post‐transplantation fibrosis. We aimed to investigate the validity of APRI as a predictor of long‐term graft fibrosis in pediatric liver transplant recipients. This was a retrospective, observational study of a cohort of children who underwent liver transplantation at King's College Hospital between 1989 and 2003, with a relevant dataset available. Protocol liver biopsies were performed at 10‐yr follow‐up and fibrosis was graded using the Ishak scoring system, with S3‐6 denoting “significant fibrosis.” APRI was calculated concurrently with biopsy. A total of 39 asymptomatic patients (20 males; median age at transplant, 1.43 yr) underwent protocol liver biopsies at a median of 10.39 yr post‐transplantation. APRI was associated with significant fibrosis (p = 0.012). AUROC for APRI as a predictor of significant fibrosis was 0.74 (p = 0.013). The optimal cutoff APRI value for significant fibrosis was 0.45 (sensitivity = 0.67; specificity = 0.79; PPV = 0.67; NPV = 0.79). APRI appears to be a useful non‐invasive adjunct in the assessment of significant graft fibrosis in the long‐term follow‐up of pediatric liver transplant survivors.     

Late allograft fibrosis in pediatric liver transplant recipients: Assessed by histology and transient elastography

Late allograft fibrosis in LT recipients can cause graft dysfunction and may result in re‐transplantation. TE is a non‐invasive tool for the assessment of liver fibrosis. We aimed to evaluate the prevalence of allograft fibrosis in pediatric LT recipients, identify factors associated with allograft fibrosis, and determine the diagnostic value of TE, compared to histology. All children who underwent LT for ≥3 years were included. TE was performed for LSM in all patients. LSM of ≥7.5 kPa was considered as abnormal and suggestive of allograft fibrosis. Percutaneous liver biopsy was performed when patients had abnormal LSM and/or abnormal LFTs. Histological fibrosis was diagnosed when METAVIR score ≥F1 or LAF scores ≥1. TE was performed in 43 patients and 14 (32.5%) had abnormal LSM suggestive of allograft fibrosis. Histological fibrosis was identified in 10 of the 15 patients (66.7%) who underwent percutaneous liver biopsy and associated findings included chronic active HBV infection (n = 3), and late acute rejection (n = 3). Multivariate analysis showed that graft age was significantly associated with allograft fibrosis (OR = 1.22, 95% CI: 1.05‐1.41, P = 0.01). In conclusion, late allograft fibrosis is common in children undergoing LT for ≥3 years and associated with graft age. HBV infection and late acute rejection are common associated findings. Abnormal TE and/or LFTs may guide physicians to consider liver biopsy for the detection of late allograft fibrosis in LT children.     

Detection of graft fibrosis by vibration‐controlled transient elastography in pediatric liver transplant recipients

Pediatric liver transplant recipients are at risk of developing graft fibrosis which can affect patient survival. VCTE is a non‐invasive tool that measures LSM and has been shown to correlate with hepatic fibrosis. The aim of this study was to therefore evaluate the ability of LSM to predict fibrosis in pediatric liver transplant recipients with different graft types. We performed a cross‐sectional study evaluating LSM of 28 pediatric liver transplant recipients who underwent a total of 20 liver biopsies within 1 month of LSM. LSM was compared to liver histology as well as graft type: WL or PL. The median LSM of all post‐transplant patients was 5.6 kPa (range = 2.7‐18.3). There was a statistically significant correlation between LSM and METAVIR fibrosis score (P = .001) and LAF score (P < .001). There was no difference in LSM between graft type (P = .088). The AUROC curve for LSM predicting any significant fibrosis (F ≥ 2) was 0.863. A cutoff value of 7.25 had a sensitivity of 71%, specificity of 100%, NPV of 87%, and PPV of 100% for significant fibrosis. LSM by VCTE is feasible in pediatric liver transplant recipients regardless of graft type. We found a significant correlation between LSM and hepatic fibrosis and established a cutoff value that may help determine which patients warrant further evaluation for graft fibrosis.     

Association of post‐transplant donor‐specific HLA antibody with liver graft fibrosis during long‐term follow‐up after pediatric liver transplantation

The aim of this study was to evaluate the significance of post‐transplant DSA as a predictor of liver fibrosis during long‐term follow‐up after pediatric LT. We evaluated the histological findings in 18 LT recipients who underwent liver biopsy after DSA screening. Liver fibrosis was scored based on the METAVIR fibrosis staging. Patients were divided into 2 groups based on histological findings, and clinical characteristics among patients with liver fibrosis were assessed. Of 18 patients, 7 were included in the fibrosis group. No significant between‐group differences were found regarding peritransplant characteristics, including age, sex, primary disease, ABO incompatibility, and immunosuppressive regimen. Episodes of acute rejection and non‐adherence to immunosuppressive drugs were comparable between both groups. The MFI for anti‐DR DSA and positive rate were significantly higher in the fibrosis group (1655 vs 216; P = .019, 86% vs 27%; P = .012, respectively). MFI for anti‐DQ DSA was higher in the fibrosis group, but non‐significantly (2052 vs 384; P = .46). Post‐transplant anti‐DR DSA is associated with graft fibrosis during long‐term follow‐up. This finding seems useful for the implementation of valid histological examinations of liver grafts for patients with higher MFI, especially for anti‐DR DSA, after pediatric LT.     

The use of transient elastography and non‐invasive serum markers of fibrosis in pediatric liver transplant recipients

The use of non‐invasive markers to diagnose liver allograft fibrosis is not well established in children after LTx. TE, FT, and ELF score were performed in 117 liver‐transplanted children (60M, 8.9 [0.5–18.5] yr) and 336 healthy controls. Liver biopsy was available in 36 children. Results of histology and non‐invasive markers were compared using correlation coefficient or Mann–Whitney U‐test as appropriate. TE correlated best with histological degree of fibrosis (r = 0.85 vs. r = 0.04 [FT] or r = ?0.38 [ELF]). Liver stiffness values for transplanted children without fibrosis were significantly higher than those of healthy controls (7.55 [5.4–20.4] kPa vs. 4.5 [2.5–8.9] kPa). Presence of rejection was a potent confounder for the performance of TE. Both TE and FT reflected clinical changes (acute rejection, cholestasis, increasing fibrosis) in a total of 16 patients who underwent serial measurements. TE correlates better with histological degree of fibrosis in liver‐transplanted children than FT or ELF, but an individual baseline value needs to be determined for each patient. Normal or cutoff values for pathological degrees of fibrosis cannot be transferred from non‐transplanted children. Follow‐up studies, preferably with protocol biopsies, might help to improve the diagnostic quality of TE.     

Basiliximab treatment for steroid‐resistant rejection in pediatric patients following liver transplantation for acute liver failure

An IL‐2 receptor antagonist, basiliximab, decreases the frequency of ACR in liver transplant (LT) recipients as induction therapy. The aim of this study was to evaluate the effectiveness of basiliximab against SRR as rescue therapy in pediatric LT patients with ALF. Forty pediatric ALF patients underwent LT between November 2005 and July 2013. Among them, seven patients suffering from SRR were enrolled in this study. The median age at LT was 10 months (6–12 months). SRR was defined as the occurrence of refractory rejection after more than two courses of steroid pulse therapy. Basiliximab was administered to all patients. The withdrawal of steroids without deterioration of the liver function was achieved in six patients treated with basiliximab therapy without patient mortality, although one patient developed graft loss and required retransplantation for veno‐occlusive disease. The pathological examinations of liver biopsies in the patients suffering from SRR revealed severe centrilobular injuries, particularly fibrosis within one month after LT. We demonstrated the effectiveness and safety of rescue therapy consisting of basiliximab for SRR in pediatric LT recipients with ALF.     

The histological quantification of alpha‐smooth muscle actin predicts future graft fibrosis in pediatric liver transplant recipients

Activated hepatic stellate cells express cytoplasmic ASMA prior to secreting collagen and consequent liver fibrosis. We hypothesized that quantifying ASMA could predict severity of future fibrosis after LT. For this, 32 pairs of protocol biopsies, that is, “baseline” and “follow‐up” biopsies taken at 1‐ to 2‐year intervals from 18 stable pediatric LT recipients, transplanted between 2006 and 2012 were selected. Morphometric quantification of “ASMA‐positive area percentage” was performed on the baseline biopsy. Histological and fibrosis assessment using Metavir and LAFSc was performed on all biopsies. The difference of fibrosis severity between the “baseline” and “follow‐up” was termed “prospective change in fibrosis.” Significant association was seen between extent of ASMA positivity on baseline biopsy and “prospective change in fibrosis” using Metavir (P=.02), cumulative LAFSc (P=.02), and portal LAFSc (P=.01) values. ASMA‐positive area percentage >1.05 predicted increased fibrosis on next biopsy with 90.0% specificity. Additionally, an association was observed between extent of ASMA positivity and concomitant ductular reaction (P=.06), but not with histological inflammation in the portal tract or lobular area. Hence, ASMA quantification can predict the future course of fibrosis.     

Unique clinical conditions associated with different acinar regions of fibrosis in long‐term surviving pediatric liver grafts

In the majority of long‐term survivors after PLTx, graft fibrosis has been identified. Recently, subtypes of graft fibrosis have been described based on their predominant acinar localization. We aimed to evaluate whether the development of portal, perisinusoidal, and centrilobular distribution of graft fibrosis is related to patient or transplantation‐related parameters. We reviewed the histological features in protocol liver biopsies taken at 1 and 5 years after PLTx of 47 children on a tacrolimus‐based immunosuppressive regimen. Fibrosis was assessed according to the LAFSc. The prevalence of portal fibrosis increased from 31% to 62%, sinusoidal from 68% to 79%, and centrilobular from 76% to 85%. The presence of portal fibrosis was associated with total bilirubin and γGT levels (each P<.02) and tended to be associated with biliary complications (P=.06). Sinusoidal fibrosis was associated with prior rejection episodes (P<.02) and centrilobular fibrosis with the presence of HLA mismatches (P=.02). In conclusion, using the LAFSc, we found a high incidence of progressive fibrosis in the 1‐year and 5‐year protocol biopsies after PLTx. Progression of fibrosis was observed in all acinar compartments, and each of the three locations is associated with different clinical conditions.     

Tacrolimus‐related seizure after pediatric liver transplantation – A single‐center experience

To identify the risk factors for new‐onset seizures after pediatric LT and to assess their clinical implications and long‐term prognosis. The clinical and laboratory data of 27 consecutive children who underwent LT from January 2007 to December 2010 in our center were analyzed retrospectively. Patients were divided into seizures group and a non‐seizures group. Pre‐operative, intra‐operative, and post‐operative data were collected. Seizures occurred in four children, an incidence of 14.8%. All exhibited generalized tonic–clonic seizures within the first two wk after LT. Univariate analysis showed that the risk factors associated with seizures after pediatric LT included gender, pediatric end‐stage liver disease score before surgery, Child–Pugh score before surgery, serum total bilirubin after surgery, and trough TAC level. Multivariate analysis showed that trough TAC level was the only independent risk factor associated with the seizures. All children who experienced seizures survived with good graft function and remained seizure‐free without anti‐epileptic drugs over a mean follow‐up period of 33.7 ± 14.6 months. High trough TAC level was the predominant factor that contributed to seizures in the early post‐operative period after pediatric LT. High PELD and Child‐Pugh scores before LT and high post‐operative serum Tbil may be contributory risk factors for TAC‐related seizures.     

Pediatric liver transplantation for neonatal‐onset Niemann‐Pick disease type C: Japanese multicenter experience

Niemann‐Pick disease type C (NPC) is a rare autosomal recessive inherited disease characterized by lysosomal accumulation of free cholesterol in macrophages within multiple organs. Infantile‐onset NPC often presents with jaundice and hepatosplenomegaly from birth, but these symptoms usually improve during early childhood, and it rarely progresses to liver failure. We report three cases from different hospitals in Japan; the patients developed neonatal‐onset NPC, and liver transplantation (LT) was performed as a life‐saving procedure. LT was performed at 19 days, 59 days, and 4 months of age, respectively. The last patient was diagnosed with NPC before LT, while the first two patients were diagnosed with neonatal hemochromatosis at LT. In these two patients, the diagnosis of NPC was made more than a year after LT. Even though oral administration of miglustat was started soon after the diagnosis of NPC, all patients showed neurological regression and required artificial respiratory support. All patients survived more than one year after LT; however, one patient died due to tracheal hemorrhage at 4.5 years of age, and another one patient was suspected as recurrence of NPC in liver graft. In conclusion, while LT may be a temporary life‐saving measure in patients with neonatal‐onset NPC leading to liver failure, the outcome is poor especially due to neurological symptoms. A preoperative diagnosis is thus critical.     

Determinants of large drain losses early after pediatric liver transplantation

The goal of this study was to evaluate postoperative ascites to correlate it with graft dysfunction and other complications. We therefore reviewed the files of patients transplanted between 2009 and 2014 to correlate drain losses with indication, patient and organ size, PELD, graft type, GRWR, NRBW, NGWD, cold ischemia time, histologically proven graft dysfunction, and surgical complications. Of 120 LTs in 104 patients, 48 (40%) were complicated by graft dysfunction, 43 (36%) by surgical complications, and 25 (21%) by cellular rejection. Large drain losses correlated with younger age (P=.05), graft dysfunction (P<.01), surgical complications (P<.01), chylous ascites (P=.05); there was no association with PELD, GRWR, NRBW, or NGWD. Graft dysfunction was predicted by >20 mL/kg/d of ascites at age 0‐2 years (AUROC 0.671), and >10 mL/kg/d above 2 years (AUROC 0.710). The measurement of drain losses after pediatric LT could be used as a non‐invasive marker of graft dysfunction. Younger recipients tend to develop larger amounts of ascites, and its persistence is associated with early complications.     

Hepatopulmonary syndrome associated with nodular regenerative hyperplasia after liver transplantation in a child

HPS is a significant complication of portal hypertension in children with chronic liver disease and is an established indication for LT. It is characterized clinically by the triad of pulmonary vascular dilatation causing hypoxemia in the setting of advanced liver disease. NRH, a cause of non‐cirrhotic portal hypertension, is characterized by diffuse benign transformation of the hepatic parenchyma into small regenerative nodules with minimal or no fibrosis. Development of NRH and HPS in pediatric LT recipients has not been reported, although occasional cases have been reported in adult LT recipients. In this report, we discuss a case of a three‐yr‐old male who developed HPS, two yr after LT. Pulmonary and cardiac causes for hypoxemia were ruled out by appropriate investigations including a chest X ray, echocardiogram, cardiac catheterization, and a CT angiographic study. The diagnosis of HPS was confirmed via bubble echocardiogram that demonstrated intrapulmonary shunting. Open liver biopsy revealed marked NRH. The patient underwent liver retransplantation that resulted in complete reversal of his pulmonary symptoms and normal oxygen saturations within three months after LT.     

Obliterative portal venopathy: A histopathologic finding associated with chronic antibody‐mediated rejection in pediatric liver allografts

The significance of post‐transplant HLA DSA and chronic AMR in LT is an emerging field of study. Although OPV has previously been described as a histopathologic finding in DSA‐positive adult LT recipients, it was not included in the recent Banff criteria for chronic AMR. Our aim was to describe the association between OPV and chronic AMR in pediatric LT recipients. A retrospective review of 67 liver biopsies performed between November 2014 and April 2016 in 45 pediatric LT recipients identified four patients with OPV. Clinical status, liver biochemistry, the presence of DSA, and available non‐HLA antibody testing, as well as histopathologic features of chronic AMR, were assessed. All four patients with OPV had class II DSA and histopathologic features of chronic AMR based on the Banff criteria. Two patients were noted to have non‐HLA antibodies. Three patients are undergoing treatment with IVIG but have persistent DSA. Two patients have graft failure and are awaiting retransplantation. In conclusion, OPV is a histopathologic finding associated with chronic AMR in pediatric LT recipients. Further studies are needed to elucidate whether OPV is reversible and/or amenable to medical therapy.     

Liver transplantation for urea cycle disorders in pediatric patients: A single‐center experience

LT has emerged as a surgical treatment for UCDs. We hypothesize that LT can be safely and broadly utilized in the pediatric population to effectively prevent hyperammonemic crises and potentially improve neurocognitive outcomes. To determine the long‐term outcomes of LT for UCDs, charts of children with UCD who underwent LT were retrospectively reviewed at an academic institution between July 2001 and May 2012. A total of 23 patients with UCD underwent LT at a mean age of 3.4 yr. Fifteen (65%) patients received a whole‐liver graft, seven patients (30%) received a reduced‐size graft, and one patient received a living donor graft. Mean five‐yr patient survival was 100%, and allograft survival was 96%. Mean peak blood ammonia (NH₃) at presentation was 772 μmol/L (median 500, range 178–2969, normal <30–50). After transplantation, there were no episodes of hyperammonemia. Eleven patients were diagnosed with some degree of developmental delay before transplantation, which remained stable or improved after transplantation. Patients without developmental delay before transplantation maintained their cognitive abilities at long‐term follow‐up. LT was associated with the eradication of hyperammonemia, removal of dietary restrictions, and potentially improved neurocognitive development. Long‐term follow‐up is underway to evaluate whether LT at an early age (<1 yr) will attain improved neurodevelopmental outcomes.     

Liver transplantation for neonatal‐onset citrullinemia

Citrullinemia or ASS deficiency in its classical form presents in the neonatal period with poor feeding, hyperammonemia, encephalopathy, seizures, and if untreated can be fatal. Despite advances in medical therapy, neurocognitive outcomes remain suboptimal. LT has emerged as a potential management option. A retrospective single‐center review identified 7 children with a median age of 1.1 years (range, 0.6‐5.8) at referral. Five children presented clinically, and 2 were treated prospectively from birth due to positive family history. All patients received standard medical and dietary therapy prior to LT. The indications for LT were frequent metabolic decompensations in 4, elective in 2, and ALF in 1. The median age at LT was 2.4 years (range, 1.3‐6.5). Five patients received 6 left lateral segment grafts, one a live unrelated donor left lateral segment as an APOLT graft, and one a cadaveric whole liver graft as APOLT. One child required retransplantation due to hepatic artery thrombosis. Graft and patient survival were 86% and 100%, respectively. Median follow‐up is 3.1 years (range, 0.1‐4.1), and the median age at follow‐up is 5.5 years (range, 4.0‐9.8). There have been no metabolic decompensations in 6 children, while 1 patient (with APOLT) developed asymptomatic hyperammonemia with no clinical or histological signs of liver injury, requiring additional medical therapy. Our medium‐term experience following LT in citrullinemia is favorable, demonstrating a positive transformation of the clinical phenotype.     

A child with unresectable biliary rhabdomyosarcoma: 48‐month disease‐free survival after liver transplantation

We describe here a two‐yr‐old boy with biliary RMS successfully treated by chemotherapy and LT. The child presented with obstructive jaundice at 20 months of age. A mildly vascularized, non‐calcified, partially cystic lesion was visualized in the left hepatic lobe. Solid infiltration of the common bile duct and of both left and right hepatic ducts was suspected. Liver biopsy suggested a botryoid‐type embryonal RMS originating from the biliary tract. After extrahepatic spread of the tumor was excluded, a biliary drain was applied and neoadjuvant chemotherapy was started. After the treatment, although reduced in volume, the mass was still unresectable without aggressive surgery and gross residual disease. LT with a reduced segment II/III graft was performed four months after diagnosis. The patient received six cycles of adjuvant chemotherapy, and he is alive and recurrence‐free 48 months post‐transplantation. A posteriori, the transplant might have possibly been avoided with an aggressive resection with biliary reconstruction. Nevertheless, although the risk of the transplant has to be balanced against the chemoresponsiveness of the tumor, the four‐yr disease‐free survival of this patient suggests that, when coupled with effective chemotherapy, transplantation might be considered a potential treatment for unresectable biliary RMS.     

De novo hepatitis B virus infection after pediatric liver transplantations with hepatitis B core antibody‐positive donors: A single‐center 20‐yr experience

DNHB is common in countries with high prevalence of hepatitis B, and therefore, contracting hepatitis B after LT with HBcAb⁺ grafts is a major concern. We studied DNHB in 247 children (aged <18 yr) who underwent LT from 1994 to 2013. Sixty‐six of 247 recipients received HBcAb⁺ donor grafts. The incidence of DNHB was 5.7% (14 of 247 children) and that in HBcAb⁺ donor grafts was 19.7% (13 of 66 children). The incidence of DNHB without LAM prophylaxis was 31.3% (nine of 29 children), while that with prophylaxis was 10.8% (four of 37 children). LAM prophylaxis negatively correlated with DNHB by Cox regression analysis (p = 0.028, odds ratio = 0.258). Among 13 DNHB patients with HBcAb⁺ donor grafts, eight recovered from DNHB and four showed the emergence of LAM resistance. There was no DNHB‐related graft failure. This study showed that HBcAb⁺ donor graft was associated with development of DNHB, and use of LAM prophylaxis decreased the incidence of DNHB with HBcAb⁺ graft.     

Transplantation for infantile nephronophthisis with loss‐of‐function mutation in NPHP3: Lesson from a case

The choice of KT only or CLKT for infantile NPHP with mild liver fibrosis is understudied. A 5‐year‐old girl was transferred to our center for KT due to ESRD. Her primary disease was infantile NPHP with compound heterozygous NPHP3 mutations: c.458A>C(p.Q153P)/missense mutation and c.2032A>T(p. K678X)/nonsense mutation. The patient had elevated liver enzymes and biopsy‐proven liver fibrosis. As liver synthesis was acceptable, only KT was performed. However, liver fibrosis progressed at 1.5 years after transplantation, manifested with portal hypertension and hypersplenism. Common causes for portal hypertension were excluded, and the progression was attributed to NPHP. AMR attacked allograft at about 2 years post‐transplant. To solve both the liver and the kidney problems, CLKT was performed. Her liver and kidney function recovered initially, but she unfortunately died of pneumonia and subsequent intracranial hemorrhage two weeks later. Nonsense mutation in NPHP3 gene may be correlated with rapid progression of liver disease in infantile NPHP. More studies are required to determine the role of CLKT in these cases; however, combined transplantation may improve long‐term graft and patient survival.     

Survival outcomes scores (SOFT,BAR, and Pedi‐SOFT) are accurate in predicting post‐liver transplant survival in adolescents

SOFT and BAR scores utilize recipient, donor, and graft factors to predict the 3‐month survival after LT in adults (≥18 years). Recently, Pedi‐SOFT score was developed to predict 3‐month survival after LT in young children (≤12 years). These scoring systems have not been studied in adolescent patients (13–17 years). We evaluated the accuracy of these scoring systems in predicting the 3‐month post‐LT survival in adolescents through a retrospective analysis of data from UNOS of patients aged 13–17 years who received LT between 03/01/2002 and 12/31/2012. Recipients of combined organ transplants, donation after cardiac death, or living donor graft were excluded. A total of 711 adolescent LT recipients were included with a mean age of 15.2±1.4 years. A total of 100 patients died post‐LT including 33 within 3 months. SOFT, BAR, and Pedi‐SOFT scores were all found to be good predictors of 3‐month post‐transplant survival outcome with areas under the ROC curve of 0.81, 0.80, and 0.81, respectively. All three scores provided good accuracy for predicting 3‐month survival post‐LT in adolescents and may help clinical decision making to optimize survival rate and organ utilization.