Pre-transplant end-stage renal disease-related immune risk profile in kidney transplant recipients predicts post-transplant infections.

BACKGROUND: End-stage renal disease (ESRD) is associated with premature aging of the T-cell system. Nevertheless, the clinical significance of pre-transplant ESRD-related immune senescence is unknown. METHODS: We studied whether immune risk phenotype (IRP), a typical feature of immune senescence, may affect post-transplant infectious complications. A total of 486 patients were prospectively studied during the first year post transplant. IRP was defined as positive cytomegalovirus serology with at least 1 of the following criteria: CD4/CD8 ratio <1 and/or CD8 T-cell count >90th percentile. RESULTS: We found that 47 patients (9.7%) had pre-transplant IRP. IRP+ patients did not differ from IRP- patients for any clinical characteristics, but exhibited more pronounced immune senescence. Both opportunistic infections (43% vs. 6%, P < 0.001) and severe bacterial infection (SBI) (40% vs. 25%, P = 0.028) were more frequent in IRP(+) patients. In multivariate analysis, IRP was predictive of both opportunistic infection (hazard ratio [HR] 2.97 [95% confidence interval {CI} 1.53-5.76], P = 0.001), and SBI (HR 2.33 [95% CI 1.34-3.92], P = 0.008). Acute rejection rates were numerically much lower in IRP+ patients. A total of 418 patients (86%) had biological evaluation 1 year post transplant. Among 41 IRP+ patients, 35 (85%) remained IRP+ 1 year post transplant. CONCLUSION: Pre-transplant IRP is associated with an increased risk of post-transplant infection.

Cardiac troponin-I on diagnosis predicts early death and refractoriness in acquired thrombotic thrombocytopenic purpura. Experience of the French Thrombotic Microangiopathies Reference Center.

BACKGROUND: Cardiac involvement is a major cause of mortality in patients with thrombotic thrombocytopenic purpura (TTP). However, diagnosis remains underestimated and delayed, owing to subclinical injuries. Cardiac troponin-I measurement (cTnI) on admission could improve the early diagnosis of cardiac involvement and have prognostic value. OBJECTIVES: To assess the predictive value of cTnI in patients with TTP for death or refractoriness. PATIENTS/METHODS: The study involved a prospective cohort of adult TTP patients with acquired severe ADAMTS-13 deficiency (< 10%) and included in the registry of the French Reference Center for Thrombotic Microangiopathies. Centralized cTnI measurements were performed on frozen serum on admission. RESULTS: Between January 2003 and December 2011, 133 patients with TTP (mean age, 48 ± 17 years) had available cTnI measurements on admission. Thirty-two patients (24%) had clinical and/or electrocardiogram features. Nineteen (14.3%) had cardiac symptoms, mainly congestive heart failure and myocardial infarction. Electrocardiogram changes, mainly repolarization disorders, were present in 13 cases. An increased cTnI level (> 0.1 µg L(-1) ) was present in 78 patients (59%), of whom 46 (59%) had no clinical cardiac involvement. The main outcomes were death (25%) and refractoriness (17%). Age (P = 0.02) and cTnI level (P = 0.002) showed the greatest impact on survival. A cTnI level of > 0.25 µg L(-1) was the only independent factor in predicting death (odds ratio [OR] 2.87; 95% confidence interval [CI] 1.13-7.22; P = 0.024) and/or refractoriness (OR 3.03; 95% CI 1.27-7.3; P = 0.01). CONCLUSIONS: A CTnI level of > 0.25 µg L(-1) at presentation in patients with TTP appears to be an independent factor associated with a three-fold increase in the risk of death or refractoriness. Therefore, cTnI level should be considered as a prognostic indicator in patients diagnosed with TTP.

Complement genes strongly predict recurrence and graft outcome in adult renal transplant recipients with atypical hemolytic and uremic syndrome.

Atypical hemolytic and uremic syndrome (aHUS) is a severe disease strongly associated with genetic abnormalities in the complement alternative pathway. In renal posttransplantation, few data are available on recurrence risk and graft outcome according to genetic background in aHUS patients. The aim of this study was to identify risk factors for recurrence and transplant outcome and, in particular, the role of complement gene abnormalities. We retrospectively studied 57 aHUS patients who had received 71 renal transplants. A mutation in complement gene was identified in 39 (68%), in factor H (CFH), factor I (CFI), membrane cofactor-protein (MCP), C3 and factor B (CFB). At 5 years, death-censored graft survival was 51%. Disease recurrence was associated with graft loss (p = 0.001). Mutations in complement genes were associated with higher risk of recurrence (p = 0.009). Patients with CFH or gain of function (C3, CFB) mutations had a highest risk of recurrence. M-TOR inhibitor was associated with significant risk of recurrence (p = 0.043) but not calcineurin inhibitor immunosuppressive treatment (p = 0.29). Preemptive plasmatherapy was associated with a trend to decrease recurrence (p = 0.07). Our study highlights that characterization of complement genetic abnormalities predicts the risk of recurrence-related graft loss and paves the way for future genetically based individualized prophylactic therapeutic strategies.

Circulating and intragraft TH17 cells are not increased at the early stage of chronic allograft nephropathy.

Since TH17 cells could play a role in the pathogenesis of allograft nephropathy, we investigated them in peripheral blood and kidney allograft infiltrates. We compared percentages of TH17 cells and IL17A in peripheral blood of 14 kidney allograft recipients and 8 healthy volunteers. Allograft recipients experiencing graft dysfunction and kidney biopsy specimens showing chronic allograft nephropathy (CAN) were distinguished from a "control group," both of which were tested for TH17 and CD15+ staining. Allograft recipients displayed a significantly lower percentage of TH17 cells and IL17A blood levels than healthy volunteers, suggesting effects of the immunosuppressive regimen. No difference in these values was observed between the CAN group and the control group. On kidney allograft biopsies, CD15+ infiltrate was significantly higher in the CAN group than in the control group. In CAN, IL17 secretion might play a chemoattractant role for neutrophils. However, these preliminary data have to be confirmed in larger studies.

Autoantibodies specific for the phospholipase A2 receptor in recurrent and De Novo membranous nephropathy.

Recent findings in idiopathic membranous nephropathy (MN) suggest that in most patients, the disease is because of anti-phospholipase A(2) receptor (PLA(2) R1) autoantibodies. Our aim was to analyze the prevalence and significance of anti-PLA(2) R1 antibodies in recurrent and de novo MN after transplantation. We assessed circulating PLA(2) R1 autoantibodies by a direct immunofluorescence assay based on human embryonic kidney cells transfected with a PLA(2) R1 cDNA, and the presence of PLA(2) R1 antigen in immune deposits. We showed that PLA(2) R1 was involved in 5 of 10 patients with recurrent MN, but in none of the 9 patients with de novo MN. We also showed a marked heterogeneity in the kinetics and titers of anti-PLA(2) R1, which may relate to different pathogenic potential. We provide evidence that some patients with PLA(2) R1-related idiopathic MN and anti-PLA(2) R1 antibodies at the time of transplantation will not develop recurrence. Because PLA(2) R1 autoantibody was not always associated with recurrence, its predictive value should be carefully analyzed in prospective studies.

Renal transplantation in patients with AA amyloidosis nephropathy: results from a French multicenter study.

Although end-stage renal disease related to AA amyloidosis nephropathy is well characterized, there are limited data concerning patient and graft outcome after renal transplantation. We performed a multicentric retrospective survey to assess the graft and patient survival in 59 renal recipients with AA amyloidosis. The recurrence rate of AA amyloidosis nephropathy was estimated at 14%. The overall, 5- and 10-year patient survival was significantly lower for the AA amyloidosis patients than for a control group of 177 renal transplant recipients (p = 0.0001, 0.028 and 0.013, respectively). In contrast, we did not observe any statistical differences in the 5- and 10- year graft survival censored for death between two groups. AA amyloidosis-transplanted patients exhibited a high proportion of infectious complications after transplantation (73.2%). Causes of death included both acute cardiovascular events and fatal septic complications. Multivariate analysis demonstrated that the recurrence of AA amyloidosis on the graft (adjusted OR = 14.4, p = 0.01) and older recipient age (adjusted OR for a 1-year increase = 1.06, p = 0.03) were significantly associated with risk of death. Finally, patients with AA amyloidosis nephropathy are eligible for renal transplantation but require careful management of both cardiovascular and infectious complications to reduce the high risk of mortality.

Injection of donor-derived splenic dendritic cells plus a nondepleting anti-CD4 monoclonal antibody to prolong primary skin graft survival indefinitely and abrogate the production of donor-specific antibodies in the Fischer-to-Lewis rat combination.

We have previously shown that injection of donor-derived Fischer rat OX62+ dendritic cells plus an anti-CD4 monoclonal antibody generates donor-specific CD4+CD25+FoxP3+ regulatory T cells in Lewis rats spleens. The regulatory T cells indefinitely prolonged the survival of skin graft from Fischer rat and abrogated the antidonor antibody response. We have now shown that an injection of 2 × 10(6) donor-derived OX62+ dendritic cells plus 2 mg nondepleting anti-CD4 monoclonal antibody (W3/25) at 28 days before grafting induced indefinite skin graft survival in this combination; whereas an injection on day -1 prolonged it only to 50 days. This effect is donor specific. In both cases, we suppressed the antidonor antibody response. It is likely that the efficacy of this protocol is, at least in part, dependent on induction of donor-specific regulatory T cells, as suggested by previous data. The 28 days necessary to obtain tolerance of allogenic skin grafts may be due to the time required for the host to induce proliferation of donor-specific regulatory T cells.

[Role of percutaneous arterial embolization in renal pathology]. / Place de l'embolisation artérielle percutanée en pathologie rénale.

Therapeutic embolization in renal pathology is used for various conditions in cancerology, traumatology, urology, nephrology and for iatrogenic complications of percutaneous manoeuvers. Any department of vascular radiology may be requested to use this technique, especially in emergent traumatology or palliative cancerology. The authors study the various conditions that may benefit from these procedures and give the highlights of the main indications and the main types of embolic agents used. Complications, side effects and the major precautions are also reviewed.

[Management of lithiasis of kidney transplant]. / Prise en charge de la lithiase sur rein transplanté.

INTRODUCTION: Urolithiasis in kidney transplants is rare but not exceptional (0,20-3%). Dealing with it is complex: abstention, lithotripsy or surgery? The aim of this study is to find out what can be done about it. METHOD: A retrospective study about 420 kidney transplants performed in our institution between 1990 et 2005 revealed nine cases of lithiasis. Among the factors leading to lithiasis were urinary flow obstruction in six cases and hyperparathyroidy in three cases. RESULTS: Five grafts with calculi whose diameter do not exceed 5mm were kept under medical supervision. Two of them were in chronic rejection without residual diuresis. Extra shockwawe lithotripsy was performed for a 13 mm diameter calical calculi. Two percutaneous extraction were performed: one for a 20mm diameter "pyelic" calculi and one for three kidney stones and among them one was 12 mm. A 20mm calculi was extracted by open pyelotomy during the repairing of the ureteral anastomosis on a Bricker diversion. CONCLUSION: Consequently, dealing with calculi on kidney transplants is similar to dealing with a unique native kidney.

Renal insufficiency, a frequent complication with age in oral-facial-digital syndrome type I.

The oral-facial-digital syndrome type I (OFD I) is characterized by multiple congenital malformations of the face, oral cavity and digits. A polycystic kidney disease (PKD) is found in about one-third of patients but long-term outcome and complications are not well described in the international literature. Renal findings have been retrospectively collected in a cohort of 34 females all carrying a pathogenic mutation in the OFD1 gene with ages ranging from 1 to 65 years. Twelve patients presented with PKD - 11/16 (69%) if only adults were considered -with a median age at diagnosis of 29 years [IQR (interquartile range) = (23.5-38)]. Among them, 10 also presented with renal impairment and 6 were grafted (median age = 38 years [IQR = (25-48)]. One grafted patient under immunosuppressive treatment died from a tumor originated from a native kidney. The probability to develop renal failure was estimated to be more than 50% after the age of 36 years. Besides, neither genotype-phenotype correlation nor clinical predictive association with renal failure could be evidenced. These data reveal an unsuspected high incidence rate of the renal impairment outcome in OFD I syndrome. A systematic ultrasound (US) and renal function follow-up is therefore highly recommended for all OFD I patients.

Vitamin D metabolite-mediated hypercalcemia with suppressed parathormone concentration in Pneumocystis jiroveci pneumonia after kidney transplantation.

Pneumocystis jiroveci pneumonia (PJP) is a severe complication in immunocompromised hosts including transplant recipients. Hypercalcemia (HCa) is not a classic symptom of the disease. However, HCa (mean [SD; range], 2.90 [0.20; 2.71-3.17] mmol/L) was detected in 5 patients with PJP at diagnosis. The HCa was associated with decreased concentrations of circulating parathormone (PTH), from 294 (292) ng/L 3 to 6 months previously to 20 (23.5; 7-53) ng/L. Concentrations of 1,25-(OH)2 vitamin D, measured in 3 patients, were in the high normal range (54.66 [7.23; 225-66] microg/L), whereas 25-(OH) vitamin D concentrations were low (13.9 [2.17; 20-60] microg/L). After treatment with trimethoprim-sulfamethoxazole for 21 days, 4 patients recovered and 1 died. Calcium and PTH concentrations rapidly returned to normal (2.36 [0.05] mmol/L and 89 [29.7] ng/L, respectively) at 2 months after the acute phase of the disease. Although fewer than 10 cases of PJP-associated HCa have been reported to date, it is possible that this association is more frequent than previously thought because our cases were detected during 2 years. As in other granulomatous disease-induced HCa, including fungal infections, it is likely that endogenous extrarenal production of 1-alpha-hydroxylase by activated macrophages and by interferon-gamma involved in granuloma formation results in increased conversion from 25-(OH) vitamin D to 1,25-(OH)2 vitamin D and, consequently, in transient HCa and suppression of PTH secretion. Fortuitous detection of HCa in transplant recipients with pulmonary symptoms must raise suspicion of PJP or fungal infection.

Injection of donor-derived OX62+ splenic dendritic cells with anti-CD4 monoclonal antibody generates CD4+CD25+FOXP3+ regulatory T cells that prolong allograft skin survival indefinitely and abrogate production of donor-specific antibodies in a rat model.

OBJECTIVE: To examine in a rat model the ability of donor dendritic cells and anti-CD4 monoclonal antibody (mAb) to generate donor-specific CD4+CD25+ regulatory T cells (Tregs) and to evaluate the capacity of these Tregs to prolong skin allograft survival and abrogate the production of donor-specific antibodies after skin grafting. MATERIALS AND METHODS: OX62+ (nonplasmacytoid) splenic dendritic cells were isolated from Fischer rats using magnetic beads and injected (2 x 10(6)) into Lewis rat recipients with or without treatment with a nondepleting anti-CD4 (W3/25) mAb. After 4 weeks, splenic CD4+CD25+FOXP3+ T cells were harvested using magnetic beads from conditioned animals and injected (1 x 10(6)) into naïve Lewis recipients (day 1) before they received a skin graft from a Fischer (n = 4) or a third-party (Norway; n = 4) donor rat. Donor-specific antibodies were detected in recipient blood using flow cytometric cross-matches with donor lymphocytes from day 0 to day 30 after grafting. RESULTS: After injection of conditioned CD4+CD25+FOXP3+ T cells, Lewis recipients accepted skin grafts from Fischer donors indefinitely (>100 days) but rejected third-party skin grafts. Donor-specific antibodies were detected at low levels in only 1 recipient receiving conditioned Tregs before grafting. Naive Tregs did not prolong skin graft survival. CONCLUSION: These preliminary data suggest that splenic dendritic cells in combination with an anti-CD4 mAb induce donor-specific Tregs that indefinitely prolong allogeneic skin graft survival and inhibit donor-specific antibody production. Experiments are under way to determine whether this protocol can inhibit chronic lesions after heart transplantation in this model.

Recurent and de novo membranous glomerulopathy after kidney transplantation.

The aim of this study was to compare the clinical characteristics of recurrent and de novo membranous glomerulopathy (MG) among a cohort of 614 recipients transplanted between 1989 and 2006. Lupus nephritides were excluded. The diagnosis was established on protocol biopsies performed 1, 2, 4, or 8 years after transplantation or because of proteinuria/nephrotic syndrome and/or an increased serum creatinine level. HCV infection, cryoglobulinemia, monoclonal gammopathy, skin cancers, Kaposi sarcoma, diabetes mellitus, anti-HLA antibodies, and graft survival were not significantly different between the groups. Seventeen MG were diagnosed in 15 patients (2.45% of the whole group), including 6 recurrent MG (35%) and 11 de novo MG (75%). Recurrent MG occurred earlier than de novo MG (15.58 +/- 19.13 vs 49.27 +/- 32.71 months). Recipients with de novo MG were more frequently infected with HCV, which seemed to be the main etiologic factor for de novo MG, and may be linked to a Th2 polarization of the immune response.

Tubulopathy and pancytopaenia with normal pancreatic function: a variant of Pearson syndrome.

Out of a series of 30 French patients with Pearson syndrome, we report on two patients with an atypical presentation, which include growth deficiency, pancytopaenia, tubulopathy and absence of exocrine pancreas dysfunction. Patient 1, a 4-year-old boy with a past history of pancytopaenia and transient metabolic acidosis at 13 months of age, presented at 2(1/2) years of age with severe tubulopathy of de Toni-Debré-Fanconi type, growth retardation, metabolic lactic acidosis and mild cytolysis. Despite normal exocrine pancreatic function, study of mitochondrial DNA revealed a 3.5 kb deletion. Patient 2 had a personal history of pancytopaenia requiring blood transfusions at 11 months of age and presented with severe intractable proximal and distal tubulopathy at 2 years of age. Exocrine pancreatic deficiency could not be evidenced and post-mortem studies revealed a 4.9 kb deletion of the mitochondrial DNA. A review of the literature revealed three patients presenting with Pearson syndrome and tubulopathy with normal pancreatic function and highlights delay in diagnosis in those three patients. The series of 30 French patients with Pearson syndrome also revealed that tubulopathy was present in 7/30 cases (23%), with variable outcome. In conclusion, Pearson syndrome should be screened for in children presenting with the association of growth retardation, anaemia/pancytopaenia, lactic acidosis and tubulopathy, even in the absence of exocrine pancreatic deficiency.

Management of post-biopsy renal allograft arteriovenous fistulas with selective arterial embolization: immediate and long-term outcomes.

AIM: To evaluate the outcomes after transcatheter embolization of percutaneous biopsy-related arteriovenous fistulas in renal allografts. MATERIALS AND METHODS: All post-biopsy renal-transplant vascular injuries referred for embolization between June 1999 and October 2006 were reviewed retrospectively. There were six male and six female patients with a mean age of 49.8 years (range 25-67 years); nine patients were symptomatic, three asymptomatic. Colour Doppler ultrasound (CDUS) and angiography showed one intra-renal arteriovenous fistula in 10 patients and two in two patients, combined with a pseudoaneurysm in six patients. Superselective embolization using a single catheter or coaxial microcatheter was performed with 0.035'' coils or 0.018''microcoils, respectively, in all 12 cases. 24-h creatinine clearance values before (the day of biopsy) and after (7-14 days; 3 months) the procedure were compared using the Wilcoxon signed-rank test. Physical examination and CDUS were performed after 1, 6, and 12 months, and yearly thereafter. Mean follow-up was 33.6 months. RESULTS: Complete definitive occlusion of the fistula was achieved consistently with a single procedure. No procedure-related complications occurred. Renal infarction was minor in all patients (0-10% in nine and 10-20% in three). Symptoms resolved completely. Creatinine clearance values obtained before and after embolization were not statistically different (p=0.168;.889 respectively). No late recurrences were reported. CONCLUSION: Transcatheter embolization with coaxial or single-catheter techniques was effective and safe for treating post-biopsy arteriovenous fistulas in renal transplants. The loss of renal parenchyma was minimal and no mid-term deterioration of allograft function was noted. The long-term survival of the renal allograft seemed to be not affected by embolization.

Detection of Foxp3+ cells on biopsies of kidney transplants with early acute rejection.

This retrospective study was conducted to examine whether the presence of Foxp3+ cells in biopsies of kidney transplants displaying early acute rejection (AR) predicted the outcome of the episode. Seventeen biopsies showing AR included in this study were obtained at 42 +/- 30 days after transplantation. Lesions were graded according to the Banff classification. Foxp3 staining was performed on paraffin-embedded sections with a monoclonal antibody after antigen retrieval. We evaluated relationships between the number and the location of Foxp3+ cells, the type of rejection, and the serum creatinine value at 1 year. Foxp3+ cells were detected in 11 of 17 biopsies with AR (9.5 +/- 13.3 cells/mm(2)). These elements were mixed with other interstitial inflammatory cells. Intraepithelial tubular Foxp3+ cells were seen in 9 biopsies (1.5 +/- 2.5 cells/mm(2)). Foxp3+ cells were associated with borderline lesions (25.5 +/- 22.4/mm(2)); type 1 AR (7.18 +/- 9/mm(2)) and type 2 AR (1.99 +/- 3.46/mm(2)). The average number of cells per field was not different in C4d(+) and C4d(-) AR (6 +/- 8.35 vs 8.5 +/- 14.7/mm(2)). Graft loss within the first year was higher among the group of recipients without Foxp3+ cells (3/6) than those with Foxp3+ cells (0/11). All AR with intraepithelial tubular Foxp3 cells had favorable outcomes. Foxp3 has been proposed as a relevant marker of CD4(+)CD25(+) regulatory T cells. This study showed that Foxp3+ cells can be detected in kidney transplant biopsies with AR. The absence of Foxp3+ cells, especially in epithelial tubular cells, might indicate a poor prognosis following an AR episode.

Recurrence of IgA nephropathy with crescents in kidney transplants.

Crescentic IgA nephropathy is an uncommon finding in native kidneys (3%-5%) and in renal transplants. This study was performed to determine the frequency of relapsing crescentic IgA nephropathy after kidney transplantation. Over a 15-year period, 42 patients (25 men, 17 women) of age range 17 to 59 years with biopsy-proven IgA nephropathy in their native kidneys were entered into this retrospective study, because they had undergone kidney transplantation and had sequential allograft biopsies during their follow-up. Mean follow-up after transplantation was 8.9 years (range, 1-15 years). In their native kidneys, 5 patients (12%) had more than 20% crescents, and only 2 (5%) had more than 50% of glomeruli involved. As expected, 52.4% of recipients showed recurrent mesangial IgA deposits in their kidney grafts. The 2 patients with diffuse crescentic IgA nephropathy in their native kidneys experienced acute graft dysfunction at 15 and 47 months. Graft biopsy showed recurrent IgA deposits with cellular crescents in 30% and 20% of glomeruli, respectively. Despite corticosteroid pulse therapy, graft failures occurred 2 and 27 months later. No crescentic proliferation was observed during follow-up in any other case. Only 5 other grafts failed because of chronic allograft nephropathy, without any relationship to the relapse of IgA deposits. These data suggested for the first time that only diffuse crescentic IgA nephropathy in the native kidneys was associated with the occurrence of crescents in the kidney transplants, a finding that raises the possibility of a particular subgroup of IgA nephropathies.

Rheumatoid arthritis-induced pseudotumoral AA amyloidosis of the bladder with vesico-peritoneal fistula.

Rheumatoid arthritis-induced AA amyloidosis of the bladder is rare, with fewer than 25 cases reported so far. This localization may be life-threatening with a mortality rate of about 60%, most often due to massive hematuria or multiorgan failure as a result of systemic amyloidosis. We report the case of a 72-year-old woman with a long history of rheumatoid arthritis who developed gross hematuria that induced severe anemia. Ultrasonography and tomodensitometry revealed a large mass localized in the upper part of the bladder. Cystoscopy showed a congestive inflammatory area with a large vesicoperitoneal fistula. Biopsies revealed amyloidosis, and immunohistochemical staining of the specimens defined the process as AA amyloidosis. The amyloid deposits were also found in the rectum, duodenum, uterus and kidneys. This case of rheumatoid arthritis-induced AA amyloidosis of the bladder is characterized by its pseudotumoral aspect and the existence ofa vesico-peritoneal fistula: only 2 cases have been reported so far. Treatment was symptomatic, and the patient died from cachexia. The pseudotumoral forms of AA amyloidosis, including amyloidosis of the bladder, deserve an early correct diagnosis. Otherwise, an incorrect diagnosis, especially cancer, may prompt inappropriate treatments.

Long-term results of monoclonal anti-Il2-receptor antibody versus polyclonal antilymphocyte antibodies as induction therapy in renal transplantation.

We compared the influence of induction therapy on 5-year patient and graft survival as well as on renal function in 100 kidney graft recipients at low immunological risk treated with antilymphocyte globulin (n = 50) versus anti-IL-2R monoclonal antibody (n = 50) in a prospective multicenter study. Long-term immunosuppressive treatment included cyclosporine, mycophenolate mofetil, and a short course of steroids in all patients. Five year graft (86% vs 86%) and patient (94% vs 94%) survivals were identical in both study arms. Moreover, neither serum creatinine or proteinuria were significantly different between the two groups. Our results showed that the choice of the induction therapy seemed to not have a major impact on long-term outcomes among renal recipients at low immunological risk.