Donor-estimated GFR as an appropriate criterion for allocation of ECD kidneys into single or dual kidney transplantation.

It has been suggested that dual kidney transplantation (DKT) improves outcomes for expanded criteria donor (ECD) kidneys. However, no criteria for allocation to single or dual transplantation have been assessed prospectively. The strategy of DKT remains underused and potentially eligible kidneys are frequently discarded. We prospectively compared 81 DKT and 70 single kidney transplant (SKT) receiving grafts from ECD donors aged >65 years, allocated according to donor estimated glomerular filtration rate (eGFR): DKT if eGFR between 30 and 60 mL/min, SKT if eGFR greater than 60 mL/min. Patient and graft survival were similar in the two groups. In the DKT group, 13/81 patients lost one of their two kidneys due to hemorrhage, arterial or venous thrombosis. Mean eGFR at month 12 was similar in the DKT and SKT groups (47.8 mL/min and 46.4 mL/min, respectively). Simulated allocation of kidneys according to criteria based on day 0 donor parameters such as those described by Remuzzi et al., Andres et al. and UNOS, did not indicate an improvement in 12-month eGFR compared to our allocation based on donor eGFR.

Synergistic effect of carbapenem-teicoplanin combination during severe Rhodococcus equi pneumonia in a kidney transplant recipient.

Rhodococcus equi is a bacterial pathogen of domestic animals that can infect immunocompromised patients, especially those with impaired cellular immunity, such as transplant recipients. No standard treatment has been established, but therapy must be prolonged, as relapses are common and can occur at the initial site or distant locations. Here we report a case of R. equi-associated pulmonary abscess in a renal transplant recipient successfully treated with a combination of carbapenem and teicoplanin. This combination was shown to be synergistic. It has minimal side effects in transplant recipients and appears to be an effective initial treatment for this severe infection.

Sirolimus may reduce fertility in male renal transplant recipients.

Assessment of sex hormones in organ transplant recipients suggests that sirolimus may impair testicular function. The aim of this study was to evaluate the frequency and severity of sirolimus-associated alterations in sperm parameters and their impact on fathered pregnancy rate. An observational study was carried out in male patients aged 20-40 years who received a kidney transplant during 1995-2005. Patients were sent a questionnaire by post, and sperm analysis was proposed. The fathered pregnancy rates according to the immunosuppressive regimen were estimated and compared using the Poisson model. Complete information was obtained from 95 out of 116 recipients. Patients treated with sirolimus throughout the post-transplant period had a significantly reduced total sperm count compared to patients who did not receive sirolimus (28.6 +/- 31.2 x 10(6) and 292.2 +/- 271.2 x 10(6), respectively; p = 0.006), and a decreased proportion of motile spermatozoa (22.2 +/- 12.3% and 41.0 +/- 14.5%, p = 0.01). Moreover, the fathered pregnancy rate (pregnancies/1000 patient years) was 5.9 (95% CI, 0.8-42.1) and 92.9 (95% CI, 66.4-130.0) in patients receiving sirolimus-based and sirolimus-free regimens, respectively (p = 0.007). Of six patients in whom sirolimus treatment was interrupted, only three showed a significant improvement in sperm parameters. Sirolimus is associated with impaired spermatogenesis and, as a corollary, may reduce male fertility.

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.

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.

Cytokine mRNA and protein expression in a mixed leukocyte reaction before and after allogeneic transfusions. Groupe Coopératif de Transplantation d'Ile de France.

BACKGROUND: The precise mechanism by which pretransplant blood transfusions may favorably influence the graft outcome in human transplantation remains unknown. Here, we explored whether the mechanism might be related to an alteration of cytokine response to transplantation antigens. METHODS: Eight patients awaiting kidney transplantation were selected to receive a single planned pretransplant blood transfusion. Before transfusion and 7 days after transfusion, peripheral blood mononuclear cells from these patients were isolated and in vitro stimulated in a one-way mixed leukocyte reaction (MLR) by using allogeneic fixed Epstein Barr virus-transformed cells as stimulators. RESULTS: The use of a semiquantitative reverse-transcriptase polymerase chain reaction cycle technique to analyze cytokine mRNAs revealed that allostimulation by donor cells clearly induced accumulation of interleukin (IL)-2, IL-4, interferon (IFN)-gamma, and IL-10 mRNA in peripheral blood mononuclear cells collected both before and after transfusion (eight of eight patients). However, both T helper 1 (IFN-gamma) and T helper 2 (IL-4) cytokine responses were more elevated after transfusion in eight of eight patients, as were IL-2 responses in five of eight patients. Such up-regulation of cytokine responses by transfusion was mostly directed against blood donor cells. Indeed, after stimulation by third-party cells, this up-regulation was both inconstant (two of three patients) and of less intensity, and no change was detected after stimulation by autologous cells (three of three patients). CONCLUSIONS: That IL-2, IL-4, and IFN-gamma responses to donor cells were increased by transfusion was further supported by results on cytokine secretion showing increased levels of IL-2 (P < 0.05), IFN-gamma (P = 0.054), and IL-4 (P < 0.05) proteins in supernatants of posttransfusion MLR as compared with pretransfusion MLR. In contrast, transfusion-induced changes in the amount of IL-10 mRNAs were not obvious and were quite variable from one patient to another.

Cytotoxic T lymphocyte changes after HLA-DR match and HLA-DR mismatch blood transfusions.

In the present study, we analyzed transfusion-induced cytolytic T lymphocyte (CTL) changes in patients who received either a one-HLA-DR-match or a zero-HLA-DR-match pretransplant blood transfusion. Twenty-four nonimmunized naive patients awaiting kidney transplantation received one planned, HLA-typed blood transfusion. The frequencies of CTL precursors (CTLp) directed against blood donor cells and controls were evaluated before and sequentially at days 7, 28, and 60 after transfusion. Results showed that sharing one HLA-DR between donor and recipient did not prevent CTL sensitization. Indeed, (1) An increase of donor-specific CTLp frequencies was observed in 8 of 11 patients who received a zero HLA-DR match (71%), as well as in 9 of 13 patients who received a one-HLA-DR-match (69%) transfusion. (2) This increase occurred with similar kinetics in the two groups, as it was highly significant 7 days after transfusion (P=0.002 and P=0.0035 in the first and second groups, respectively) but transient; CTLp frequencies returned to pretransfusion levels by day 60 after transfusion in both groups. (3) Finally, the magnitude of this increase was similar in the DR-match and DR-mismatch groups. Thus, if it is confirmed, in clinical practice, that one DR match between the blood donor and the patient would improve the tolerance effect of pretransplant blood transfusion, this phenomenon is unlikely to be related to the prevention of CTL sensitization.

Evidence that antihuman tumor necrosis factor monoclonal antibody prevents OKT3-induced acute syndrome.

We have used an antihuman tumor necrosis factor monoclonal antibody, CB006 (murine IgG1), to prevent the OKT3-induced acute clinical syndrome. This syndrome is due to the massive, although transient release in the circulation of various cytokines (TNF, interferon gamma, interleukin 2, interleukin 6) and represents one important side effect linked to in vivo use of OKT3. Fourteen kidney allograft recipients undergoing prophylactic OKT3 therapy were treated with CB006 in a single i.v. injection of either 0.4 mg/kg (group I, 7 patients) or 2 mg/kg (group II, 7 patients), 1 hr before the first OKT3 administration. Nineteen consecutive patients formed a historical control group. None of the CB006-pretreated patients showed any of the common, severe OKT3-associated symptoms (hypotension, respiratory distress, or neurotoxicity), which were observed in 10% of the historical controls. In addition, CB006-treated patients showed a lower frequency of pyrexia (> or = 39 degrees C) and gastrointestinal symptoms. None of the CB006-treated patients presented severe vomiting or diarrhea, defined as repeated episodes inducing significant fluid and electrolyte loss. Two out of the 7 patients in group I and group II had mild transitory diarrhea. Mild single vomiting episodes occurred in 2 group I patients and 3 group II patients. At variance in all controls, gastrointestinal symptoms were long lasting and associated with major prostration due to electrolyte and fluid loss. Importantly, CB006-treated patients who presented mild symptoms had detectable bioactive circulating TNF, showing incomplete inactivation of OKT3-induced TNF by CB006. CB006 was perfectly well tolerated, did not induce xenosensitization, and did not affect the biological or clinical effectiveness of OKT3.

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.

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.

How to deal with the hyperimmunized potential recipients.

End-stage renal disease (ESRD) patients with high levels of anti-HLA panel reactive antibodies (PRA) represent an increasing group in which sensitization, induced by pregnancies, previous transplants, and blood transfusions, considerably delay the opportunity to receive a graft. Currently, more than 50% of the 4700 patients awaiting transplantation in France are sensitized, of which 33% are defined as hyperimmunized (PRA greater than = 80%), and only 9.5% of the total number of transplants have been done in highly sensitized recipients. The magnitude of this problem, similar in Europe and North America, explains why more active strategies for managing hyperimmunized patients have been introduced during the past decade. Clearly, the simplest is finding of a well-matched organ that does not carry the HLA antigens against which the recipient has generated antibody, but that is limited by the number of shared grafts. The second is the development of a new cross-matching technique prior to transplantation. Attempts at immunoregulation of secreting B cell clones have been carried out using either hypertransfusions or injection of polyclonal Ig. Finally, removal and prevention of the resynthesis of HLA antibodies is a most attractive approach using immunoadsorption (IA) system with sepharose-bound protein-A columns. In our unit, fifteen ESRD patients with high levels of PRA were treated with IA. Infectious complications were not observed after IA and transplantation, and the procedure was well tolerated. In spite of the use of adjunctive immunosuppressive treatment with cyclophosphamide and prednisolone, this method produced only variable effects in lowering PRA levels, and was hampered by high de novo resynthesis of anti-HLA antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Incidence and consequences of post-transplantation lymphoproliferative disorders.

Post-transplant lymphoproliferative disorder (PTLD) is a recognized severe complication arising in allograft recipients treated with immunosuppressive drugs. Although not common, PTLD is one of the most frequent tumours among graft recipients, comprising 15-25% of neoplasms, compared with 5% in the general population. The introduction of cyclosporin A (CyA) in the early 1980's and the very potent new immunosuppressants such as anti-CD3 monoclonal OKT3 and FK506 have been associated with a significant rise in the incidence of PTLD and with their earlier presentation. The incidence of this malignancy varies with the organ transplanted (1-2% of renal transplant recipients) and with the nature and severity of the accompanying immunosuppressive regimen. While the precise etiology of PTLD is still unclear, significant advances have been made recently in the understanding of its pathogenesis. Most PTLD tumour cells present an activated B-cell phenotype and an unrestricted pattern of latent EBV gene products. It is generally accepted that Epstein-Barr virus (EBV) infection or reactivation and intensive anti-T lymphocyte regimens play a major role in the genesis of PTLD. They include a spectrum of EBV-related disorders ranging from lymphoid hyperplasia to frank malignant non-Hodgkin's lymphoma. Although different therapeutic attempts have been proposed, optimal treatment remains elusive. The mortality rate for monoclonal lymphomas was reported to be as high as 80%. Infusion of anti-B monoclonal antibodies seems to be a promising modality. Different preventive approaches have been proposed, including EBV sero-negative donor/recipient matching and careful monitoring of EBV infection. Cautious use of anti-rejection treatment in combination with prophylactic antiviral therapy is recommended.

Post-transplantation polyomavirus infections.

Increasing attention has been recently accorded to BK and JC viruses (BKV and JCV). Both these human polyomavirus (HPV) are members of the papovavirus family which includes the simian virus SV 40. BKV and JCV infect more than 60% of the population worldwide. After primary infection, they remain harboured in the kidneys and may become reactivated in situations of immune impairment. HPV were first described in 1971. BKV was isolated in a renal transplant patient with ureteral stricture and JCV in a patient with progressive multifocal leukoencephalopathy (PML). BKV was known to be involved in post-bone marrow transplantation (BMT) hemorrhagic cystitis. In renal transplantation, BKV and JCV were initially found in the post-transplant ureteric stricture and PML. They are now recognised as a possible cause of transplant interstitial nephritis, mimicking rejection (satisfying the Banff criteria for acute rejection) or drug toxicity. In HPV nephritis there is a mixed interstitial inflammatory infiltrate with focal tubular injury; the tubular epithelium shows marked anisonucleosis, nuclear atypia and basophilic or amphophilic intranuclear inclusions. Tubulitis is frequent. DNA hybridisation or gene amplification by polymerase chain reaction usually demonstrate HPV. Although histology with viral nucleic acid detection may be helpful in differentiating viral infection and rejection, confusion between these complications may lead to either anti-rejection therapy, with the risk of over-immunosuppression, or reduction of immunosuppression, with the risk of graft loss. Confusion may also arise with inclusions of other viruses, such as cytomegalovirus, herpes virus and adenovirus. Reactivation of BKV and JCV infection was demonstrated in respectively 22.2% and 10.9% of renal transplant recipients and 55% and 6.7% of BMT patients. Unfortunately, no routine screening is available for these viruses, so this complication is probably underestimated. No specific therapy of HPV infection is currently available.

Confirmation of the interaction between cyclosporine and the calcium channel blocker nicardipine in renal transplant patients.

We report seven cases out of eight reversible raises (350% of mean increase) of cyclosporine (CsA) plasma levels in patients receiving the new calcium channel blocker nicardipine (Loxen-Sandoz) and CsA after renal transplantation. Nicardipine was introduced 3 to 36 weeks post transplantation in 7 cases of hypertension and 1 case of angina pectoris. CsA plasma levels raised considerably 1 to 30 days after nicardipine introduction and returned to pretreatment levels 1 to 7 days after withdrawal. Serum creatinine increased in 1/8 patients. These data suggest that nicardipine interferes with CsA metabolism and this interaction is reversible after nicardipine discontinuation. These findings point out the fact that at least some calcium channel blockers need to be cautiously used in patients receiving CsA.

Need for hepatocellular carcinoma screening before renal transplantation in HBs +, HBe +, western African.

We report a case of fulminant hepatocellular carcinoma discovered 50 days after renal transplantation. The recipient was a young Senegalese, hepatitis B virus chronic carrier. The pre-transplant check-up was normal, and the tumor was latent until its dramatic expression. Progression of hepatitis B liver disease occurs in immuno-suppressed renal transplant recipients, which often leads to chronic active hepatitis, cirrhosis and hepatocellular carcinoma, with a high risk of death due to liver disease. The early discovery of the tumor in this patient emphasizes the necessity for complete hepatic screening before transplantation in african, hepatitis B virus chronic carrier recipients. Moreover, the accumulation of risk factors for hepatocellular carcinoma: hepatitis B virus, food mycotoxins (aflatoxin), parasitic infestation and immunosuppression with transplantation is stressed.

Single-center experience with cyclosporine therapy for kidney transplantation: analysis of a twenty-year period in 1200 patients.

Since the introduction of cyclosporine (CyA) in our center in February 1983, 1267 kidney transplant patients have received an immunosuppressive regimen based on CyA, usually in association with azathioprine and steroids and following an induction therapy in three quarters of patients. The aim of this study was to retrospectively analyze our 20-year experience with CyA and examine the evolution of therapy during this period. Induction treatment has been less commonly used during the past 5 years. Even in the early years of our experience, CyA doses were low (under 6 mg/kg per day at 3 months after transplantation). Acute tubular necrosis was observed in 39.4% of patients. The incidence of acute rejection episodes has dramatically decreased since 1984, but the frequency of steroid-resistant rejection has remained constant (around 20%). The first year of transplantation, 32.7% of patients had arterial hypertension. De novo diabetes mellitus occurred in 2.5% of patients. An incidence of 11.8% of malignancies was observed. Skin cancer and lymphomas accounted for 50% and 12% of neoplasms. Five-year graft and patient survivals were 70% and 87%, respectively. Renal function remained remarkably constant during the first 10 years of follow-up with a mean creatinine of 150 micromol/L. Chronic allograft nephropathy resulted in 43% graft losses. In conclusion, CyA has been well tolerated in our patients. However, the occurrence of chronic allograft nephropathy was a major concern in our cohort.

[Multivisceral Kaposi's disease and encrusted pyelitis in a renal transplantation recipient]. / Maladie de Kaposi multiviscérale et pyélite incrustée chez un transplanté rénal.

Immunosuppression therapy carries inherent risks involving the occurrence of infections and neoplasms. Whereas therapeutic advancement have reduced its frequency, encrusted pyelitis reappears in kidney-transplanted patients and may lead to detransplantation. It is related to chronic urological infections and not inevitably favored by endoscopic explorations. Kaposi's sarcoma is the third cause of tumor in renal-transplanted patients. It is rarely multivisceral and develops exceptionally in the transplant. We report the case of a 60 year-old woman who developed an encrusted pyelitis and a Kaposi's sarcoma in a kidney which was transplanted 14 months earlier.

[Blood transfusion before kidney transplantation, is it indicated?]. / Transfusions sanguines avant transplantation rénale quel intérêt?

The beneficial effect of blood transfusions on the prognosis of renal transplantation has been recognized since 1972, and has led transplant centres to adopt a systematic transfusion policy in end-stage renal disease patients requiring a graft. By the end of the eighties, the dramatic improvement in the results of transplantation, the disappearance of transfusions prescribed in haemodialyzed patients after recombinant human erythropoietin became available and finally the evidence of the transfusion risk have raised questions both on transfusion policy, and even on the reality of the transfusion effect itself. The consequence has been great discrepancy in the current policies of different renal transplantation centres: some countries (USA, Great Britain, Scandinavia, Southern Europe) have nearly abandoned transfusion protocols, while others (Benelux, France) remain confident in their transfusion policy. The effect of transfusions on 1-year graft survival has not been detected since 1988 in multicentre international registry reports. However, recent studies have suggested that transfusions could still have a positive effect, especially on specific endpoints, such as the acute rejection incidence observed after transplantation. Moreover, clinical and biological data show that the transfusion effect and its mechanism could depend on the HLA compatibility between the blood donor and the recipient. This justifies current and further clinical and biological investigations on the topic, in order to evaluate the possible current persistent interest of the transfusion policy before transplantation, and to elucidate the biological mechanisms of this unique attempt at immunomanipulation.