Long-term blood pressure changes in renal homotransplantation.

Long-term blood pressure changes were studied in 50 patients who had undergone renal homotransplantation. Excluded were those subjects with arterial stenosis of the transplanted kidney, acute or rapidly progressive rejection, or recurrent glomerulonephritis, as well as those retaining their own diseased kidney(s). The blood pressure after the end of the first year was stable and, therefore, was utilized as the reference blood pressure for this study. One year after transplantation, hypertension was observed in 20% of the patients. Mean blood pressure was positively correlated with age (P less than .01), body weight (P less than .001), and serum creatinine level (P less than .001), and negatively correlated with maintenance dose of prednisone (P less than .01). A higher incidence of hypertension was observed in cadaver kidney transplantation than in living related-donor transplantation. The study minimizes the role of glucocorticoids and emphasizes the role of renal factors in the mechanism of the long-term blood pressure changes.

False-positive HIV antigens related to emergence of a 25-30 kD protein detected in organ recipients.

OBJECTIVE: The routine screening of organ donors for HIV-1 since 1985 has markedly reduced the risk of acquiring infection in organ recipients. However, commercial HIV-1 p24-antigen assays reveal false-positive reactivity in certain recipients. This observation will be discussed here. METHODS: Post-transplantation sera collected sequentially from different organ recipients were tested for HIV antigen: 79 samples were from 14 kidney recipients, 57 from seven bone-marrow allografts and 18 from two heart recipients. Neutralization assays to determine specificity were performed on reactive samples. Immunoblots prepared from sera containing high levels of antigens were tested by Western blot using polyclonal anti-HIV sera. RESULTS: Abbott HIV-1-EIA kits detected non-neutralizable antigens in early post-transplantation sera from 12 kidney, five bone-marrow and two heart recipients. Using in-house immunoblots prepared from positive non-neutralizing antigen sera, a 25-30 kD protein was detected and shown to be the cause of the false HIV antigen cross-reactivity. CONCLUSION: False-positive HIV antigens related to the emergence of a 25-30 kD protein in early post-transplantation sera are detectable in transplant recipients.

Hemolytic uremic syndrome. Recurrence after renal transplantation. Groupe Coopératif de l'Ile-de-France (GCIF).

Hemolytic uremic syndrome (HUS) is an uncommon cause of end-stage renal failure in adults, and few data are available concerning the outcome of renal transplantation in these patients. We conducted this retrospective multicentric study to appreciate the outcome of adult renal transplant recipients whose primary disease was HUS. Sixteen patients, transplanted between 1975 and 1995, were included in the study. In each case, initial diagnosis of HUS was documented by a kidney biopsy. These 16 patients received a total of 25 allografts: 1 graft for 9 patients, 2 grafts for 5 patients, and 3 grafts for 2 patients. Nine patients (56%) developed definite clinical and pathologic evidence of recurrence on at least 1 graft. Four additional patients (25%) demonstrated only some clinical or pathologic evidence of recurrence which could not be distinguished from acute vascular rejection. Three patients had no sign of recurrence of the initial disease. The 1-year graft survival rate was 63% and the 5-year graft survival rate was 18.5%. In the group of patients with proven or possible recurrence (n = 13), the 1-year and 5-year graft survival rates were 49% and less than 10%, respectively. The recurrence was an early event, occurring before the end of the first month after transplantation in half the cases. The recurrence rate was 92% in non-nephrectomized patients and 50% in patients with bilateral nephrectomy. In the literature, 71 adult patients with primary HUS had received a total of 90 kidney grafts. Among them, 54% had a recurrence on their graft, which was diagnosed in 52% of the kidney transplants. It is note-worthy that when data from the literature are pooled with our results, the rate of recurrence appears to be significantly lower in binephrectomized patients than in patients with their native kidneys at the time of transplantation (5 of 14 versus 27 of 35 patients, respectively, p = 0.0155). By univariate analysis, no other risk factor for recurrence could be identified. Treatment with cyclosporine A did not influence the recurrence rate. We conclude that recurrence of HUS after renal transplantation is a frequent, early, and severe complication, leading rapidly to graft loss. Prospective studies are needed to confirm that bilateral nephrectomy prior to transplantation decreases the rate of recurrence.

Recurrence of Fabry's disease in a renal allograft eleven years after successful renal transplantation.

A case of Fabry's disease in a renal transplant recipient with a follow-up period of 11 years is reported. The patient suffered from renal, skin, peripheral nerve lesions, and asymptomatic cardiomegaly. Fabry's disease symptoms disappeared after transplantation. Improvement of renal function was rapidly observed, and it remained satisfactory during the whole posttransplantation period. The patient died of a severe, uncontrolled infection and of biliary peritonitis. Autopsy showed a polyvisceral accumulation of sphingolipids deposits. The engrafted kidney was histologically free of disease. Ultrastructurally, it revealed numerous sphingolipid inclusions in the endothelial cells of capillaries. The explanation of this complication could be attributed to: (1) high circulating levels of plasma substrates locally overwhelming the enzymatic capability of the graft endothelial cells; and (2) the endothelial cells originated from the recipient but not from the donor, an occurrence that has been described after transplantation. Rejection and the newly formed deposits in the endothelial cells may lead to the loss of the engrafted organ. As a consequence of the increasing possibility of organ transplantation, this complication should be detected by studying the blood vessels ultrastructurally in order to evaluate the condition of the transplant.

Diabetes mellitus after renal transplantation: characteristics, outcome, and risk factors.

The incidence and risk factors of posttransplant diabetes mellitus were evaluated in 1325 consecutive renal transplant recipients. Thirty-three (2.5%) patients developed diabetes mellitus requiring insulin therapy. Onset occurred a mean of 5.7 +/- 1.5 months following transplantation. The patients were compared with 33 paired-control kidney recipients. The patients were significantly older than the controls (46.8 +/- 1.9 vs. 40.6 +/- 2.1 years) (P<0.05), and chronic renal failure was more often related to interstitial nephritis (P<0.05). A family history of diabetes mellitus, the body mass index, ethnic origin, HLA phenotype, and the total doses of steroids and cyclosporine were similar in the two groups. The number of patients with at least one rejection episode was significantly higher among the diabetic patients (21 versus 9) but the number of episodes was similar. Diabetes occurred a mean of 1.1 +/- 0.3 months following rejection treatment. Intravenous pulsed prednisolone was always used for anti-rejection therapy. Insulin was withdrawn in 16 cases after a mean of 4 +/- 1 months, independently of steroid dosage reductions. Actuarial patient and graft survival rates were not significantly different, although 6-year outcome tended to be better in the controls (86% versus 93% for patient survival and 67% versus 93% for graft survival). This study suggests that pulsed steroid therapy might be the critical factor in the onset of posttransplant diabetes and that the risk is increased in older patients with chronic interstitial nephrititis.

Development of cytomegalovirus resistance to ganciclovir after oral maintenance treatment in a renal transplant recipient.

The emergence of a resistant strain is a theoretical threat after extensive use of antiviral drugs. We report the emergence of a ganciclovir-resistant cytomegalovirus (CMV) strain in a kidney transplant recipient during oral ganciclovir maintenance treatment. The patient was treated by oral ganciclovir for 2 months after successful treatment of CMV primary infection by intravenous ganciclovir. He developed a new episode of CMV infection with no clinical response to intravenous ganciclovir. The CMV isolate exhibited both phenotypic and genotypic resistance to ganciclovir. The CMV isolate was constituted of a mixture of strains, with and without a mutation at codon 460 of the UL97 gene. The clinical condition improved when mycophenolate mofetil (MMF) was discontinued, and a short course of intravenous globulin was added to ganciclovir. The emergence of the CMV strain could be secondary to more potent immunosuppression provide by MMF or subtherapeutic level obtained during oral ganciclovir treatment. We believe that ganciclovir resistance must be part of the differential diagnosis when a patient relapses or fails to respond to ganciclovir treatment.

A randomized multicenter trial comparing leukocyte function-associated antigen-1 monoclonal antibody with rabbit antithymocyte globulin as induction treatment in first kidney transplantations.

Adhesion molecules are involved in several steps in the immune response: leukocyte adhesion to the endothelium, transendothelial migration, cooperation between immunocompetent cells, and cytotoxicity. Leukocyte function-associated antigen-1 plays a central role among adhesion molecules. In a multicenter randomized open trial, we compared a monoclonal antibody directed against the alpha chain of LFA-1 (Oduli-momab; IMTIX/Pasteur Mérieux Sérums et Vaccins) with rabbit antithymocyte globulin (rATG; IMTIX/Pasteur Mérieux Sérums et Vaccins), as part of a quadruple sequential protocol in 101 patients receiving a first kidney transplant. Clinical tolerance of anti-LFA-1 mAb was better than that of rATG. Short-term rejection rates (< 15 days) were not significantly different (15% and 16% for anti-LFA-1 mAb and rATG, respectively). However, 11% of the anti-LFA-1 mAb patients experienced rejection during the first 10 days of the treatment course compared with none of the patients treated with rATG. The incidence and severity of acute rejection in the first 3 months was not significantly different between groups. Of the LFA-1 and rATG patients, 96% and 92% of the grafts, respectively, were functioning at 12 months. The incidence and severity of infection, whatever the origin, were comparable in both groups. In addition, it was observed that fewer patients required posttransplantation dialysis in the anti-LFA-1 mAb group (19%, vs. 35% for rATG), although the difference was not statistically significant. Altogether, the beneficial action of this monoclonal antibody on short-term renal function recovery makes it a useful tool in the management of renal patients undergoing kidney transplantation.

Anti-B cell lymphocytotoxic antibodies in kidney transplant recipients.

Serial serum samples from 47 renal allotransplant recipients were screened for antiperipheral blood lymphocyte, anti-B cell, and anti-Daudi cell line antibodies. Various associations of these antibodies were observed in 28 patients. Anti-Daudi did not correlate with graft survival, whereas anti-B, although they were often associated with anti-peripheral blood lymphocyte antibodies, showed the strongest correlation with chronic rejection (P = 0.00002). However anti-B cytotoxicity preceded or was concurrent with the onset of chronic rejection in only 53% of the cases. Antibodies were absent in six of nine patients with irreversible acute rejection, but they usually appeared after transplant nephrectomy. These findings suggest that anti-B cell antibodies may play a role in the rejection process. In 15 of 17 recipients (88%), anti-B cell antibodies occurred during the first trimester after transplantation. These patients showed 20% 1-year graft survival compared with 68% in those without antibodies at that time (P less than 0.005).

Long-term outcome of kidney transplantation in patients with systemic lupus erythematosus: a multicenter study. Groupe Cooperatif de Transplantation d'île de France.

BACKGROUND: The outcome of 60 renal transplantations in 53 patients with end-stage renal disease (ESRD) because of lupus nephritis was studied retrospectively and compared with 106 controls matched for age, sex, maximum panel-reactive antibody (PRA) level, and date of transplantation. METHODS: The patients received their transplants over a 260-month period (21.5 years) between October 1971 and August 1993. The population was predominantly women (90%), and the mean age at the time of the transplantation was 33.2 years (range: 21-54 years). Fifty-six transplants (93%) were from cadaveric donors, and 4 (7%) were from living-related donors; 46 patients (86%) had primary allografts, and 7 (14%) received a second allograft. The duration of disease before transplantation was 93.6+/-6.2 months, and the duration of dialysis before transplantation was 48+/-6 months. RESULTS: No patient had clinically active systemic lupus erythematosus (SLE) at the time of transplantation. The 1-year graft and patient survival rates were 83% and 98%, and the 5-year graft and patient survival rates were 69% and 96%. Actuarial graft and patient survival rates in SLE patients were not significantly different from those of the matched control group. Chronic rejection was the major risk factor for graft loss. Lupus nephritis recurred in the graft of one patient 3 months after transplantation, and there were extrarenal manifestations of SLE in four others. CONCLUSIONS: The present study confirms that patients with SLE can receive transplants with excellent graft and patient survival rates and a low rate of clinical recurrent lupus nephritis.

Is renal transplantation involved in post-transplantation liver disease? A prospective study.

Various lesions of the liver commonly observed in renal transplant recipients are usually considered as a consequence of the transplantation procedures (immunosuppression, drug toxicity, alteration of immune responses to various viruses). A group of 64 patients all treated with corticosteroids and azathioprine was studied prospectively, and serial liver biopsies were performed on the day of transplantation and at 1 and 3 years after transplantation. Chronic hepatitis was already present in 40% of the patients on the day of transplantation and an increase of only 15% in the frequency of this condition was observed 3 years later. The presence of HBsAg in 45% of the patients at the time of transplantation was significantly associated with liver lesions. In about 3% of the cases, transplantation was directly responsible for a liver disease (peliosis hepatitis). During the followup period an evolution from chronic persistent hepatitis to chronic active hepatitis was observed with an abnormally high frequency (25%). We conclude that most of the liver diseases observed in transplant recipients are the consequence of events before transplantation and probably related to hemodialysis.

Hodgkin's disease after transplantation.

Hodgkin's disease (HD) has seldom been reported after transplantation. Epstein-Barr virus (EBV) is present in about 50% of Reed-Sternberg cells in HD developing in immunocompetent individuals, but is more frequently found in HD of acquired immune deficiency syndrome patients. We report 7 cases of HD that occurred in transplant recipients. Clinical and pathological data and studies of EBV reveal specific features of HD after transplantation. Six patients received kidney transplants and 1 patient received combined kidney and pancreas transplantation. Immunosuppressive therapy consisted of cyclosporine, steroids, azathioprine, and antilymphocyte globulins. One patient received, in addition, anti-CD3 mAb therapy and an EBV+ B cell lymphoma developed. Retrospective EBV serological data from patients were collected. Tumors were classified according to pathology. EBV studies were conducted by immunohistochemical methods with monoclonal antibodies to EBV-latent membrane protein (LMP) or EBV-nuclear antigen 2 (EBNA2), and by in situ hybridization for latent nuclear EBV-early RNAs (EBERs). The mean lapse of time between transplantation and HD was 49 months. Six patients presented with enlarged lymph nodes and 1 patient presented with liver involvement. HD was classified as IA in 2 patients, IIA in 3 patients, IIIB in 1 patient, and IVB in 1 patient. Four patients had primary EBV infection after graft, before HD, and the others reactivated latent EBV infection. Histological subtypes were mixed cellularity in 6 cases and lymphocytic depletion in 1 case. Latent EBV infection was detected with EBERs in all tumors. Reed-Sternberg cells expressed LMP, and were negative for EBNA2 expression. Six patients were treated: 2 patients at stage I received radiotherapy, and relapsed within 1 year with a more advanced stage of HD; chemotherapy was indicated as primary therapy in 5 patients, and as salvage therapy in 2 patients; it was associated with radiotherapy in 4 patients. Immunosuppressive therapy was reduced in all patients. Four patients were alive and in complete remission 18, 25, 31, and 67 months after chemotherapy, with a functioning graft in 3 patients. Two patients died of infection. Mixed cellularity is the most frequent histological subtype observed in HD occurring in transplant patients. EBV is present in all Reed-Sternberg cells. Posttransplant HD shows similarities with human immunodeficiency virus-associated HD. These facts argue for a role of EBV infection and immunosuppression in the progression of HD after transplantation.

Human herpes virus-8 and other risk factors for Kaposi's sarcoma in kidney transplant recipients. Groupe Cooperatif de Transplantation d' Ile de France (GCIF).

BACKGROUND: The exact reasons for the high incidence of Kaposi's sarcoma (KS) after kidney transplantation are still unknown. Immunosuppression is classically considered as the main risk factor, but the relative risk contributed by the patient's geographic origin and by human herpes virus (HHV)-8 infection still has to be determined. METHODS: We carried out a retrospective and a prospective study among kidney transplant recipients (TP) to identify the risk factors for posttransplantation KS. Each of 30 KS patients was matched with two controls to investigate the association with geographic origin, immunosuppressive regimen, HHV-8 antibodies before and after transplantation, and other infections. Among TP with new onset of KS, we prospectively evaluated HHV-8 serology and viremia in response to decreased immunosuppression. RESULTS: African and Middle East origins, past infection with hepatitis B, hemoglobin level <12 g/dl, lymphocyte count <750/mm3 at the time of diagnosis and initial use of polyclonal antilymphocyte sera were risk factors for KS. After multivariate analysis, origin in Africa or Middle East and use of antilymphocyte sera for induction remained as independent risk factors. Sixty-eight percent (17/25) of TP with HHV-8 antibodies before or after transplantation developed KS compared with 3% (1/33) of seronegative TP (P<0.00001). HHV-8 DNA was detectable in seven of nine peripheral blood mononuclear cells (PBMC) and in six of six KS lesions at diagnosis; it became negative in PBMC in three of five patients in parallel with tumor regression. CONCLUSION: African and Middle East geographic origins, HHV-8 infection before and after kidney transplantation, and initial use of polyclonal antilymphocyte sera were independent risk factors for KS. The presence of HHV-8 antibodies before or after transplantation was highly predictive of the emergence of posttransplantation KS and conferred a 28-fold increased risk of KS (odds ratio=28.4; 95% confidence interval: 4.9-279). Detection of HHV-8 DNA within PBMC and KS lesions seems related to tumor burden and evolution.

Induction versus noninduction in renal transplant recipients with tacrolimus-based immunosuppression.

BACKGROUND: The aim of this study was to compare the efficacy and safety of induction treatment with antithymocyte globulins (ATG) followed by tacrolimus therapy with immediate tacrolimus therapy in renal transplant recipients. METHODS: This 12-month, open, prospective study was conducted in 15 centers in France and 1 center in Belgium; 309 patients were randomized to receive either induction therapy with ATG (n=151) followed by initiation of tacrolimus on day 9 or immediate tacrolimus-based triple therapy (n=158). In both study arms, the initial daily tacrolimus dose was 0.2 mg/kg. Steroid boluses were given in the first 2 days and tapered thereafter from 20 mg/day to 5 mg/day. Azathioprine was administered at 1-2 mg/kg per day. RESULTS: At month 12, biopsy-confirmed acute rejections were reported for 15.2% (induction) and 30.4% (noninduction) of patients (P=0.001). The incidence of steroid-sensitive acute rejections was 7.9% (induction) and 22.2% (noninduction)(P=0.001). Steroid-resistant acute rejections were reported for 8.6% (induction) and 8.9% (noninduction) of patients. A total of nine patients died. Patient survival and graft survival at month 12 was similar in both treatment groups (97.4% vs. 96.8% and 92.1% vs. 91.1%, respectively). Statistically significant differences in the incidence of adverse events were found for cytomegalovirus (CMV) infection (induction, 32.5% vs. noninduction, 19.0%, P=0.009), leukopenia (37.3% vs. 9.5%, P<0.001), fever (25.2% vs. 10.1%, P=0.001), herpes simplex (17.9% vs. 5.7%, P=0.001), and thrombocytopenia (11.3% vs. 3.2%, P=0.007). In the induction group, serum sickness was observed in 10.6% of patients. The incidence of new onset diabetes mellitus was 3.4% (induction) and 4.5% (noninduction). CONCLUSION: Low incidences of acute rejection were found in both treatment arms. Induction treatment with ATG has the advantage of a lower incidence of acute rejection, but it significantly increases adverse events, particularly CMV infection.

[New immunosuppressive drugs and diabetes]. / Nouveaux immunosuppresseurs et diabète.

Glucocorticoïds, calcineurin inhibitors (especially tacrolimus) and the combination of both are responsible for the occurrence of diabetes mellitus after organ transplantation. These drugs induce both insulin resistance and insulinopenia. Risks factors are well identified: high doses of immunosuppressive drugs, genetic background, age and weight excess. Long-term consequences seem to be as deleterious as those of other types of diabetes mellitus. Modulating the doses of immunosuppressive drugs is efficient in decreasing insulin requirement in transplant recipients but only individualization of immunosuppression taking risks factors into account will permit to decrease the incidence of this side-effect.

Hand-assisted laparoscopic live donor nephrectomy in a patient with renal artery aneurysm.

Among the transplantation teams there is an increasing interest in laparoscopic live donor nephrectomy. For technical reasons, the use of the left kidney is recommended. However, considering the shortage of organ donors, it is likely that right-side laparoscopic live donor nephrectomy will need to be considered in selected donors, even those with vascular anomalies. Here we report the first case of right-side live donor laparoscopic nephrectomy in a patient with a renal artery aneurysm. Arteriography showed a 3-cm saccular aneurysm of the main right renal artery located at the bifurcation of the secondary branches and associated with an inferior polar artery coming directly from the aorta. The patient was placed in the lumbotomy position. An 8-cm midline incision was made above the umbilicus to insert the HandPort system (Smith & Nephew S.A., 72019 Le Mans Cedex2, France). Four additional trocars were introduced. Dissection of the renal artery was carried out beyond the level of relieving the aneurysm behind the vena cava. The main and polar arteries were clipped, and the renal vein was stapled. The kidney was removed through the HandPort and perfused cold ex vivo. The warm ischemia time for the kidney was 1 min, and the total operative time was 280 min. Vascular abnomalies were corrected ex vivo. The postoperative course of the donor was uneventful. At 6 months after transplantation, the graft function was normal. The hand-assisted approach is of particular value on the right side where the dissection must be carried out behind the vena cava. The HandPort may save few precious minutes over the sac extraction technique of the standard laparoscopic procedure.

Demonstration of a passive Heymann nephritis-like mechanism in a human kidney transplant.

The underlying mechanism of human extramembranous glomerulonephritis (EMGN) is generally thought to involve circulating immune complexes. Data presented here suggest that "in situ" formation of immune deposits may also be important in the pathogenesis of EMGN. We describe a patient with a "de novo" EMGN in a kidney transplant a few months after the graft placement. Before transplantation, the patient's serum contained antibodies reacting in vitro with rat kidney brush-border, but serum concentration of these antibodies rapidly decreased prior to the onset of proteinuria. No circulating immune complexes were detected on serial serum samples from the patients. Antibodies which were eluted from the kidney transplant biopsy were shown to react with the brush-border of the proximal convoluted tubule of rat kidney. We postulate that "in situ" formation of immune complexes within the glomerular capillary walls, and not circulating immune complexes, is the pathogenic mechanism responsible for the glomerular lesions of this case of EMGN.

Prostaglandins and hypertension in chronic renal diseases.

The role of prostaglandin A (PG A) in the pathogenesis of renal hypertension has been studied. The concentration of endogenous PG A was measured in the peripheral plasma by radioimmunoassay in patients with chronic renal disease and in control subjects. The mean plasma concentration of PG A1 equivalents was as follows: 1. normotensive healthy volunteers (n=23): 115 +/- 15 pg/ml 2. patients in terminal renal failure on regular hemodialysis a) anephric patients (n=6): 51+/- 21 pg/ml b) patients retaining their own kidneys, all but one with hypertension (n=9): 231 +/- 51 pg/ml (P less than 0.01 versus control) 3. patients with chronic renal disease a) with hypertension (n=7): 204 +/- 60 pg/ml (P less than 0.01 versus control) b) without hypertension (n=11): 136 +/- 30 pg/ml. Renal hypertension was associated with high levels of PG A in peripheral blood. This increase is probably a secondary adaptative mechanism for the excretion of a greater fraction of the glomerular filtrate at a lower blood pressure. PG A may represent a circulating "antihypertensive hormones".

Distinct phenotypic composition of diffuse interstitial and perivascular focal infiltrates in renal allografts: a morphometric analysis of cellular infiltration under conventional immunosuppressive therapy and under cyclosporine A.

Phenotypic analysis of interstitial mononuclear cell infiltrates was undertaken in 40 transplant renal specimens obtained from 38 patients in order to assess the influence of immunosuppressive therapy. Thirteen patients were given conventional immunosuppressive treatment (azathioprine and prednisone) and the other 25 received cyclosporine. The immunostaining was performed using seven antileucocyte antibodies by alkaline phosphatase-anti-alkaline phosphatase method. Interstitial infiltrates were distributed in two patterns: diffuse infiltrates and periglomerular/perivascular aggregates. The phenotypic composition was distinct in these two patterns: in diffuse infiltrates, monocytes/macrophages (EBM 11) represented the predominant inflammatory cell and were associated with a minor component of T cells (T 11). In contrast, aggregates had a major T lymphocyte phenotype in addition with few foci of B cells. T4 subset of T lymphocytes always predominated over T8 subset. The repartition and the proportion of each cell type were not significantly different in rejecting and not rejecting grafts and were not affected by the immunosuppressive regimen.

[Allogeneic immune response after blood transfusion in patients awaiting renal transplantation]. / Réponse immune allogénique après transfusion sanguine chez des malades en attente de transplantation rénale.

To investigate the mechanisms of the beneficial effect of blood transfusions (BT) on subsequent kidney transplant survival, we studied the influence of 3 planned BT on lymphocyte reactivity and on lymphocytotoxic antibody (LT) production in previously non-transfused uremic patients. A sustained and non-specific decrease in mixed lymphocyte reactivity (MLR) was observed in approximately 60% of the cases, whereas other patients had only a transient decrease but otherwise normal or even increased responses. Neither the pre-BT degree of immune responsiveness nor the clinical status of the patients had any influence on this phenomenon. Similarly, hepatitis B seroprophylaxy or vaccination did not interfere with this BT effect. Anti-HLA, LT, which are potentially harmful for the transplant, were noted in 13% of cases, while 13% additional cases displayed "cold" anti-B lymphocyte LT which do not have the same prognostic value. In some instances, suppression of cellular reactivity developed concurrently with LT production, which indicates that there is no interaction between cellular and humoral responses induced by BT.

[Is ligation of the remaining native ureter at the time of renal transplantation always harmless?]. / La ligature de l'uretère propre restant, lors des transplantations rénales, est-elle toujours anodine?

Three cases of nephrectomy after transplantation with uretero-ureteral anastomosis are presented: this anastomosis in transplantation looks to be anodyne when the transplant keeps normal function. Complications become when appears a degradation of the renal function.