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Background: Anemia frequently occurs after kidney transplantation, its origin is multifactorial. The objective of this study was to evaluate the frequency of anemia among kidney transplantation patients at 3 months after transplantation and its relationship to inflammatory, oxidative, and nutritional states. Furthermore, we determined serum prohepcidin, a precursor of hepcidin, the main hormone implicated in iron metabolism., Materials and Methods: We performed a transverse retrospective study in 130 patients who underwent kidney transplantation, including 89 men and 41 women. Patients were randomized according to the presence or absence of anemia at 3 months. The patients' inflammatory, oxidative, and nutritional states were evaluated as well as renal function and serum prohepcidin at 3 months., Results: Twenty-four percent of the patients developed anemia at 3 months after transplantation. These patients presented with a greater inflammatory state, a poor nutritional status, and poor renal function. Serum prohepcidin was significantly lower compared with the transplantation patients who did not show anemia., Conclusions: Serum prohepcidin was significantly higher among kidney transplantation patients who did not develop anemia. The inflammatory state may be a determinant of the response to treatment with erythropoiesis-stimulating agents in anemic kidney transplant recipients., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background and Objective: Disorders in bone mineral metabolism are common after kidney transplantation, covering, among other pathologic conditions, secondary hyperparathyroidism. Paricalcitol, a selective vitamin D receptor activator, is indicated in the prevention and treatment of secondary hyperparathyroidism. Recent evidence suggests that paricalcitol is also associated, by mechanisms not yet clarified, with improved patient survival. To clarify these unknown mechanisms, the aim of this study was to determine whether 3 months of treatment with paricalcitol modified the urinary peptidome of kidney transplant patients., Methods: This prospective study included 42 stable kidney transplant patients, randomized in 2 groups: a group treated with 1 μg/d paricalcitol (n=25) and a control group that did not receive paricalcitol (n=17). Urine samples of all patients were collected at baseline and after 3 months. The proteomic approach was based on magnetic bead technology coupled to MALDI-TOF mass spectrometry., Results: Paricalcitol treatment produced significant changes in urinary peptidome of kidney transplant patients. Variations in urinary peptides were independent of the degree of proteinuria and of the decrease in parathyroid hormone levels., Conclusions: With this preliminary study, we obtained a profile of urinary peptides in which changes occurred due to treatment with paricalcitol. The identification of proteins to which these peptides belong may improve our knowledge about the possible pleiotropic effects of paricalcitol., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Background: Cardiovascular disease is the leading cause of death in renal transplant (RT) patients. Both traditional and emerging risk factors, some of which are controversial, have been described in the pathogenesis of cardiovascular disease. Carotid ultrasound (CUS) is considered to be an excellent diagnostic tool for subclinical atherosclerosis., Objective: To evaluate the relationship between biomarkers of inflammation, growth factors, metalloproteinases, and the development of subclinical atherosclerosis diagnosed by using CUS., Methods: We studied 93 RT patients (aged 54±12 years; 67.9% men; 13.5% with pre-RT diabetes mellitus). The following biomarkers were determined in the patients' blood hours before RT: C-reactive protein (CRP) and serum amyloid A using nephelometry; interleukin (IL) 2, 6, 8, and 10 and soluble IL-2 receptor, tumor necrosis factor (TNF) α, vascular endothelial growth factor (VEGF), epidermal growth factor, and monocyte chemotactic peptide using chemoluminescence; and pregnancy-associated plasma protein (PAPP)A using ELISA. A CUS was carried out during the first month after RT., Results: Carotid intima-media thickness (IMT) was elevated in 51% of the patients, and 50.5% of the patients had atherosclerotic plaque. Both plaque (P=.004) and IMT (P=.001) correlated with age, and the increase of IMT was progressive, on both the left and the right side. Pre-RT CRP, IL-8, TNF-α, VEGF, MCP-1, and PAPP-A were significantly more elevated in patients with plaque. In the multivariate analysis adjusted for clinical variables, age (odds ratio [OR], 1.05; 95% confidence interval [CI], 1.01-1.10; P=.04), CRP (OR, 7.5; 95% CI, 2.05-27.3; P=.002), IL-8 (OR, 4.73; 95% CI, 1.27-17.6; P=.02), and PAPP-A (OR, 4.45; 95% CI, 1.22-16.2; P=.023) were independent markers of the presence of plaque., Conclusions: Age, CRP, IL-8, and PAPP-A, and not growth factors, are markers of carotid atheromatous plaque in RT patients., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Background: Chronic allograft nephropathy (CAN), a major complication in renal transplant patients, is an important cause of graft loss. Inflammation as measured in the pretransplant and posttransplant phases, using various markers, has been associated with worse renal function and a greater risk of cardiovascular disease and of long-term graft loss., Objective: The objective of our study was to evaluate whether worsening inflammation in the first 3 months postoperatively was a risk factor for developing CAN., Patients and Methods: We performed a cross-sectional study in 207 patients. The following markers of inflammation (MIF) were determined pretransplant and at 3 months after grafting: C-reactive protein (CRP) (mg/L), interleukin (IL)-6 (pg/mL), IL-10 (pg/mL), tumor necrosis factor (TNF)-α (pg/mL), and its soluble receptor (ng/mL), soluble-IL2R (UI/mL), pregnancy-associated plasma protein A (PAPP-A; mUI/L), and IL-4 (pg/mL). We also calculated the ratio at 3 months versus the pre value of MIF., Results: CAN was diagnosed after the first year in 23 patients (11.3%) always by renal biopsy performed for clinical indications. Patients with CAN showed worse inflammation, eg, MIF ratios over one, with statistically significant differences for the ratios of TNF-α and PAPP-A (P=.032 and P=.051 respectively). Upon multivariate logistic regression analysis, using CAN as the dependent variable and age, sex, donor age, months on dialysis, acute tubular necrosis, acute rejection, and MIF ratios as covariates, we observed that an acute rejection episode (OR=13.03; CI=2.8-60.9; P=.001), CRP ratio (OR=1.36; CI=1.07-1.73; P=.013), and PAPP-A ratio (OR=1.80; CI=0.92-3.53; P=.005) were independent markers of CAN., Conclusions: Among other factors, inflammation may determine the onset of CAN as diagnosed by renal biopsy., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Objective: Patients on dialysis display increased inflammation (IF) and oxidative stress (OS). Diabetes mellitus (DM) may increase both processes. The role of transplantation in this situation is unknown. Herein we have assessed the evolution of IF and OS following grafting and its relationship to a prior diagnoses of DM and to kidney function at 1 year., Patients and Methods: This prospective study included 131 dialysis patients who underwent transplantation of mean age 54 +/- 12 years, including 68% men with 19.5% showing prior DM. The following markers of IF and OS were determined prior to and at 3 months after grafting: C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), soluble TNFalpha receptor (sTNFalpha-R), soluble IL-2 receptor (sIL-2R), oxidized LDL (oxLDL), and anti-oxLDL antibodies (oxLDLab). The evolution (ratio) of these markers was assessed by dividing the values at 3 months by the prior ones. Modification of Diet in Renal Disease (MDRD) was determined at 12 months., Results: Patients with prior DM were older (P = .034). There were no differences in the pregrafting phase between diabetics and nondiabetics in relation to IF or OS. IF and OS showed a worse evolution postgrafting among patients with prior DM. At 1 year postgrafting renal function was greater in patients without prior DM (P = .022). There was an inverse correlation between the ratios of markers and kidney function at 1 year postgrafting: TNFalpha: r = -.235 (P = .012); sIL-2R: r = .441 (P < .001); and sTNFalpha-R: r = .225 (P = .017)., Conclusions: In the pregrafting phase, there were no differences between patients with or without DM in terms of IF and OS. These differences appeared in the postgrafting phase: patients with DM showed greater IF and OS, an increase that may explain the poor kidney function observed at 1 year among patients with DM.

Statins are prescribed to reduce posttransplant dyslipidemia, which is frequent among kidney graft recipients. Their efficacy to reduce cholesterol levels has been accompanied by pleiotropic effects. Proteomics is the study of the expressed complement of proteins in tissues or biological fluids. It includes the identification of changes in proteins that occur in various states, eg, after drug administration. Our study objectives were: (1) to analyze the effect of atorvastatin (10 mg/d) on lipid profile, renal function, proteinuria, and inflammation parameters, such as C-reactive protein (CRP), and (2) to use proteomics to ascertain whether this treatment modified the patients' urinary peptide profiles seeking to understand the molecular actions of the drug. Urinary peptide profiles, lipids, renal function parameters (creatinine clearance), proteinuria, and CRP were determined in 39 patients at baseline and at 12 weeks after atorvastatin treatment (10 mg/d). The peptide fraction of each sample acquired using magnetic beads was analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Our results showed that treatment with atorvastatin produced a significant reduction in lipid profile, but did not modify renal function (creatinine clearance), proteinuria, or CRP. The proteomic study showed that statin treatment did not produce significant changes in the urinary peptidome, although there was a tendency for some peptides to increase or decrease after the treatment.

Hepcidin is a hormone that regulates the intestinal absorption of iron and its release from the reticuloendothelium. The objective of this study was to determine the use of hepcidin for kidney disease patients with a diagnosis of iron deficiency pretransplantation by evaluating the soluble transferrin receptor (sRTfR-F) index as a marker for iron deficiency. This transverse study of 164 pretransplant patients determined hematometry and conventional markers related to iron metabolism, as well as soluble transferrin receptor (sTfR), its index (sTfR-F), and serum hepcidin concentrations. The following markers of inflammation (MIF) were also assessed C-reactive protein (hs-CRP), interleukin-6 (IL-6), soluble IL-2 receptor (sIL-2R), tumor necrosis factor-alpha (TNF-alpha), and soluble TNF-alpha receptor (s-TNF-alphaR). Among the studied patients, 11.4% showed an absolute iron deficiency with ferritin concentrations < 100 ng/mL, a mean hepcidin value of 120.7 +/- 38.5 ng/mL, and a mean sTfR-F value of 1.03 +/- 0.3; 18.2% of patients displayed a ferritin > 800 ng/mL with mean hepcidin and sTfR-F values of 147.5 +/- 36.6 ng/mL and 0.54 +/- 0.2, respectively. Iron deficiency was not observed in the other patients when considering the conventional markers: ferritin > 100 ng/mL and transferrin saturation (ST) > 20%. However, this study showed that determination of hepcidin concentrations together with M/F improved the identification of iron deficiency in pretransplant patients by 21.6%.

Introduction: Proteinuria and dyslipidemia are nonimmune risk factors implicated in the deterioration of kidney function and associated with an increased risk of accelerated atherogenesis. Statin therapy, used for cholesterol reduction, has shown a renoprotective effect in animal models, particularly in cases of proteinuria. This may occur through lipid-independent mechanisms, such as improved endothelial dysfunction/vascular biology, reduced inflammatory cytokine production (transforming growth factor-beta 1 [TGF-beta1]), and regulation of fibrogenic responses. We studied mechanisms of action of agents, such as statins, to change proteinuria, inflammatory parameters, and TGF-beta1 plasma levels in relation to vascular tone., Methods: Fifty-six kidney transplant recipients (30 men and 26 women of overall mean age 54 +/- 13 years) were treated posttransplantation with atorvastatin (10 mg/d) for 12 weeks without renin-angiotensin-system blockade drugs. Inflammatory variables, biochemical parameters, lipid profile, renal function, and TGF-beta1 levels were determined at baseline and at 3 months. Vascular stiffness was evaluated using pulse wave velocity (PWV)., Results: Baseline TGF-beta1 plasma levels were higher among transplant recipients than healthy controls, namely 8.12 ng/mL (range, 5.82-13.12) to 2.55 (range, 1.78- 4.35) (P < .01). Furthermore, the levels remained higher after the treatment with atorvastatin, namely, 7.59 (range, 4.97-12.35) to 2.55 (range, 1.78-4.35) ng/mL (P < .01). Atorvastatin treatment significantly decreased total cholesterol as well as low-density lipoprotein cholesterol plasma levels, but did not modify mean blood pressure (MBP), proteinuria, creatinine clearance, or inflammatory factors. Reduction in TGF-beta1 plasma levels was statistically significant among patients with PWV >9.75 (m/s) (pathology reference value) namely, from 10.7 ng/mL (range, 7.02-13.98) to 6.7 (range, 3.96-11.94) (P = .038). Among older patients, atorvastatin significantly decrease TGF-beta1 plasma levels: from 9.5 ng/mL (range, 6.45-14.44) to 5.65 (range, 3.63-9.48; P < .05). The decreased TGF-beta1 was not related to changes in lipid profiles., Conclusions: Atorvastatin (10 mg/d) improved the lipid profile and moreover among older patients with worse PWV (>9.75 m/s), TGF-beta1 levels were significantly reduced. Our results suggested that statins displayed potent actions distinct from their hypolipidemic effects.

This study assessed the performance of three methods for estimating glomerular filtration rate (GFR) in kidney transplant patients: the Cockcroft-Gault formula, the modification of diet in renal disease (MDRD) method, and the four-variable modification of diet in renal disease (four-variable MDRD), both as an overall estimate and as related to clinical disease stage. We analyzed data from 136 renal transplant patients including 84 men in an overall age range of 28 to 76 years. Patients were categorized into three groups according to GFR as determined by the arithmetical mean of the last four creatinine clearance determinations after outlying values had been excluded: group 1, estimated GFR of <30 mL/min (n = 26); group 2, estimated GFR of 30 to 60 mL/min (n = 63);, and group 3, estimated GFR >60 mL/min (n = 33). Fourteen patients were excluded from the analysis because of a high variability between their creatinine clearance determinations. Estimated GFRs using the Cockroft-Gault, MDRD, and four-variable MDRD formulae were compared with GFRs as measured by creatinine clearance. Statistically significant correlations were observed for all three formulae for the overall series and for individual clinical groups. Hence, we concluded that all equations had a similar capacity to predict the GFR. In addition, because of the clear, significant correlation between the MDRD and the four-variable MDRD (r = .992; P = .0001), we believe that the four-variable MDRD can substitute for the MDRD for clinical purposes.

Background: Renal insufficiency and renal transplant (RT) provoke a microinflammatory state that leads to increased atherosclerosis. It is not fully known whether calcineurin inhibitors (CNIs) play a role in the inflammation observed in these patients or whether any differences exist between CNIs., Objectives: The study aimed to establish differences in the inflammatory state of two groups treated with cyclosporine microemulsion (CyA) or tacrolimus (TC)., Patients and Methods: This prospective study included 81 RT patients divided into two groups according to the CNI: CyA group, n = 35 versus TC group, n = 46. The markers of inflammation (MIF) were determined preRT and at 3 and 12 months' postRT: C-reactive protein (CRP), serum amyloid protein A (SAA), interleukin-6 (IL-6), soluble interleukin-2 receptor (sIL-2R), tumor necrosis factor-alpha (TNF-alpha), and pregnancy-associated plasma protein A (PAPP-A). Samples were collected in stable patients in the absence of rejection, active infection, or inflammatory processes., Results: No significant differences existed between the markers of inflammation in the two treatment groups prior to transplantation. At 3 months' posttransplant, patients treated with CyA showed significantly higher levels of IL-6 (P = .05), SAA (P = .03), and sIL-2R (P = .008) compared with patients treated with TC. These differences were maintained for IL-6 (P = .03) and sIL-2R (P = .027) at 12 months' posttransplant. A multivariate analysis at 3 months showed that only age [OR 10.1; CI (95% 2.6-38.4); P = .001], SAA [OR 4.8; IC (95% 1.4-16.5); P = .015], and sIL-2R [OR 4.9; IC (95% 1.5-16.2); P = .009] were independent predictors of the CNI used. At 12 months, age [OR 3.7; IC (95% 0.9-14.2] and sIL-2R [OR 6.04; IC (95% 1.5-23); P = .006] continued to be independent predictors., Conclusions: Patients treated with CyA displayed significantly higher levels of inflammatory markers (IL-6, SAA, sIL-2R) at 3 and 12 months' posttransplantation, independent of age, gender, time on dialysis, diabetes mellitus (preRT and de novo postRT), and renal function measured by serum creatinine.

Since calcineurin inhibitors (CNI) have been introduced, they have become the cornerstone of immunosuppression for renal transplant patients, but their cardiovascular and neurological toxicities, and primarily their renal toxicity, have brought about an increased effort to find combinations of immunosuppressants that are either CNI-free or that use minimum doses of these drugs. The weight of immunosuppression therefore lies with drugs that have a better toxicity profile. The POP observational transverse study including 213 renal transplant patients was designed to study CNI minimization strategies. The mean time of transplant evolution to the time of reduction was 9.9 +/- 11.8 months. The acute rejection rate to the start of reduction was 9.4%. Almost all the patients were undergoing treatment with CNI + mycophenolate mofetil (MMF) + steroids in the immediate posttransplantation period. When reduction was chosen, all patients were undergoing treatment with MMF (mean dose at the start of reduction = 1490.7 +/- 478.0 mg/d). Among the cohort, 66.7% of patients were being treated with tacrolimus (mean C0 levels 13.3 +/- 6.6 ng/mL) and 33.3% with cyclosporine (mean C0 levels 192.2 +/- 94.0 ng/mL; mean C2 levels 1097.5 +/- 457.6). The main reasons for withdrawal were nephrotoxicity (55.9% of the cases), as well as prevention of adverse effects (21.6%). The mean target CNI dose reduction was 41.4% +/- 21.45% in the tacrolimus group and 28.6 +/- 10.0% in the cyclosporine group. In conclusion, CNI toxicity, primarily renal toxicity, makes reduction of these drugs based on the use of full MMF doses an alternative to manage renal transplant patients.

Everolimus (Eve) has shown good efficacy and safety profiles in clinical trials in combination with low doses of cyclosporine but there is limited experience in other modes, especially with calcineurin inhibitor elimination. We developed a retrospective study to analyze its clinical use after approval in Europe in 2005. Herein we have presented the results of a series of 272 patients followed for the first 6 months after Eve introduction. In 93.8% of cases Eve was introduced after the first month posttransplantation (conversion use), and 6 months after introduction, the CNI had been eliminated in 75% of cases. The main indication for Eve introduction was the diagnosis of a malignant neoplasm (42%), whereas the combined indication of prevention and/or treatment of toxicity, especially nephrotoxicity, accounted for 46.3% of cases. Initial doses were low (1.37 mg/d), but were progressively increased up to 2 mg/d at 6 months. Renal function remained unchanged during the follow-up period, whereas proteinuria moderately increased. Only 5 cases (2%) of acute rejection episodes were observed with excellent patient and graft survivals at 6 months after conversion. Further analysis of this extensive series of patients with a longer follow-up is needed.

Introduction: The prevalence of diabetes mellitus (DM) is greater among patients with solid organ transplants than in the general population, although the factors associated with posttransplant DM (PTDM) are unknown., Objectives: The objective of this study was to estimate the prevalence of and assess the risk factors for PTDM., Patients and Methods: We included outpatients with functioning isolated solid organ allografts (kidney, liver, heart, and lung). We collected demographic and posttransplant clinical data that included DM diagnostic ADA criteria, DM treatment, DM family history, presence of hepatitis C virus (HCV), immunosuppression treatment, hypertension, and dyslipidemia., Results: A total of 2178 patients included, 1410 kidney recipients, 489 liver transplants, 207 heart transplants, and 72 lung recipients. Seventeen and four-tenths percent of the patients who did not have DM prior to transplantation, developed PTDM (median time: 79 days). A greater prevalence was observed among patients with a family history, HCV, and tacrolimus treatment (with or without steroids P < .05). By logistic regression analyses, OR for these factors were 1.51, 1.65, and 1.38, respectively. Of those patients who did not suffer PTDM, 55.2% showed basal blood glucose values under 100 mg/dL; only 68% presented with a hemoglobin Alc under 6., Conclusions: The prevalence of PTDM among kidney recipients was higher than that in the general population. DM family history, HCV positive, and tacrolimus were risk factors associated with this entity.

This prospective study evaluated the relationship between inflammation and oxidative stress in a group of dialysis patients just before and 3 months after kidney transplantation and compared the results with a control group of healthy subjects. The oxidative stress markers determined were different F2-isoprostane isomers. The inflammatory markers included C-reactive protein, interleukin-6, tumor necrosis factor-alpha, and pregnancy-associated plasma protein A. Forty-three patients were the study group and 50 healthy subjects from a hospital blood bank as controls. The results showed levels of inflammatory and oxidative stress markers to be higher in the dialysis patients than in the control group, although they improved following kidney transplantation. Finally, significant correlations were observed between F2-isoprostane isomers and inflammatory markers.

Introduction: Various studies describe the pleiotropic antiinflammatory and antioxidant effects of atorvastatin, in addition to its hypolipemic effects. It has been suggested that statins modify glucose homeostasis via their antiinflammatory effects. A further hypothesis suggests that the incidence of posttransplantation diabetes is lower in statin-treated patients. This study sought to ascertain whether atorvastatin modifies glucose homeostasis, adiponectin, and inflammatory markers in kidney transplant recipients., Patients and Methods: Sixty-eight kidney transplant recipients (41 men, 27 women; mean age, 53 +/- 12 years) with stable renal function and dyslipidemia were treated with atorvastatin (10 mg/d) for 12 weeks. Glucose, insulin, homeostasis model assessment (HOMA-IR) index, adiponectin, tumor necrosis factor (TNF)-alpha, and serum C-reactive protein (CRP) concentrations were determined at baseline and at 3 months. The lipid profile, renal function parameters (creatinine, creatinine clearance, and proteinuria), as well as GOT, GPT, and CK were determined at baseline and at 3 months., Results: Treatment with atorvastatin achieved a statistically significant decrease in lipid profile. After 3 months of treatment, 74.6% of patients had total cholesterol and 78.7% low-density lipoprotein (LDL) cholesterol concentrations within reference range (<5.2 and 3.3 mmol/L, respectively). Furthermore, 47.5% of patients attained an LDL concentration <2.59 mmol/L. A greater reduction in total cholesterol (P = .05) and LDL cholesterol (P = .04) was achieved in patients with creatinine clearance <60 mL/min. Atorvastatin did not modify glucose homeostasis parameters, adiponectin, TNF-alpha, or CRP. At baseline and after 3 months of treatment, an inverse correlation was found between adiponectin and glucose, insulin, HOMA- IR index, and creatinine clearance, and a positive correlation was found between adiponectin and high-density lipoprotein (HDL) cholesterol., Conclusion: Atorvastatin at a dose of 10 mg/d in kidney transplant recipients does not modify glucose homeostasis or alter inflammatory markers, despite its hypolipemic effects. Its efficacy to reduce total cholesterol and LDL cholesterol was greater in patients with worse renal function.

Purpose: Children have been reported to be at greater risk for hepatic artery thrombosis when compared to adults due to small arterial size, nonuse of intraoperative microscope, and postoperative hypercoagulable state., Methods: We evaluated arterial anastomosis type, intraoperative field magnification, and hepatic artery complications and how they were managed. All patients underwent ultrasound, anticoagulation consisted of 41 mg aspirin once a day, and 35 patients received alprostadil (PGE) for the first 7 days after transplantation. No patients were administered intravenous heparin following liver transplantation., Results: Of the 74 livers transplanted, 36 grafts (48.6%) were whole organ transplants and 38 grafts (51.4%) were partial livers. We observed HAT in 1 of 74 (1.35%) transplants in our pediatric liver transplant population. The only patient with HAT was a young girl with a history of biliary atresia. The occurrence of a hepatic artery thrombosis on day 7 was caused by the migration of an intimal plaque dissection within the artery graft. She was emergently taken back into the operating room for graft revision. This individual currently has a survival time of 426 days following her last transplant., Conclusions: Hepatic artery thrombosis may be minimized in pediatric liver transplantation without the use of microsurgery. Anticoagulation utilizing ASA and alprostadil is sufficient to avoid HAT. Accurate use of ultrasound is crucial to avoid this complication. Graft and patient salvage is possible with expedient surgical treatment; microsurgery, anticoagulant therapy, site of arterial inflow, and recipient size and weight.

Background: Due to the early age that pediatric patients with autoimmune hepatitis (AIH) are transplanted, it is theorized that older AIH patients may have different outcomes than pediatric patients following liver transplantation., Methods: This is a retrospective review of both the adult and pediatric liver transplant programs consisting of 56 patients. Rejection and recurrence of AIH were determined by biopsy., Results: The autoimmune patient having rejection episodes had a 1.76-fold increase in relative risk to develop autoimmune recurrence when compared to patients without rejection [RR = 1.76; 95% CIRR (1.08, 2.86)]. The pediatric group had a 6.62-fold increase in relative risk to develop colitis following liver transplantation [RR = 6.62; 95% C.I.R.R. (1.36, 32.13); P =.02]. Mean days to recurrence of AIH were similar in both groups (1364 +/- 1074 vs 936; P = NS). There were more hospitalized days in the pediatric group compared to the adults (20.5 +/- 13.3 days vs 51.7 +/- 22.2 days, P =.039). OKT-3 was rarely used (n = 5) in either group (9.3% vs 7.7%, P = NS) and was not correlated with which patients would be weaned from steroids or recurrence., Conclusions: Based on this review, pediatric patients were more likely to develop ulcerative colitis following liver transplantation and they incurred longer hospital stays than adults. The adult group was more likely to be weaned from steroids, with AIH recurrence unrelated to weaning.

Background: Biliary complications in pediatric liver transplantation (PLT) are associated with increased morbidity and mortality., Methods: Prospectively, data was collected on 89 consecutive liver transplants performed in 82 children. Eighty-nine consecutive PLTs were tracked for transplant type (partial versus whole), recipient age/weight, duct anastomosis type, surgical technique, and biliary complications. Treatments of biliary complications (surgical versus interventional radiology) were also evaluated., Results: Forty-six children (51.7%) received partial transplants and 43 (48.3%) children received whole organs. The average age for whole liver transplanted children was 8.95 +/- 6.62 years and average weight was 36.2 +/- 28.7 kg; for those receiving partial livers, 3.19 +/- 3.52 years and 14.1 +/- 13.0 kg. Duct-to-duct anastomosis was performed for 26 grafts and Roux-en-Y choledochojejunostomy for 63 grafts. Biliary complications occurred in 10 of 89 (11.2%) grafts. Complications included anastomotic strictures in four (40%), bile leak in five (50%), intraparenchymal biloma in one (10%). The complication rate for whole organs was 1/43 (2.3%) and 9/46 (19.6%) for partial organ (P =. 015). No difference in complication rates were seen in type of ductal anastomosis (7.7% vs 12.7%, P = NS). Reoperation for biliary complication was necessary in only 2/10 (20%) of grafts., Conclusions: Technical advances have reduced the incidence of biliary complications in PLT. Partial liver grafts have a statistically higher risk of biliary complication than whole grafts. Most biliary complications can be managed with radiological intervention without surgical exploration. Pediatric biliary complications are not associated with graft loss.