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Résumé Les infections et les néoplasies sont les conséquences attendues du traitement immunosuppresseur, qui diminue les réponses cellulaires et humorales de façon non spécifique. Les infections étaient surtout fréquentes et sévères durant la période précoce après la transplantation (première année). Leur diagnostic rapide et précoce, leur prévention systématique et leur prise en charge ont beaucoup bénéficié ces dernières années de nouveaux outils de diagnostic (biologie moléculaire) et du développement des médicaments antiviraux et antifongiques, aboutissant à une baisse très significative des infections et de la mortalité de cause infectieuse dans cette population. Cependant, de nouveaux agents infectieux (BK virus, parvovirus, virus de l’hépatite E, ou Chigunkunya, West Nile et autres dans certaines régions) sont venus enrichir la liste des infections du patient transplanté. Les complications néoplasiques sont surtout dues au cumul et à la durée de l’immunosuppression, et surviennent souvent en phase tardive (après la première année). Ces néoplasies sont viro-induites et concernent essentiellement la peau et le tissu lymphoïde, mais l’incidence des cancers non cutanés est également augmentée. Mise à part la réduction de l’immunosuppression qui demeure essentielle, leur prise en charge était similaire à celle des patients non transplantés, avec des résultats médiocres ; les néoplasies sont actuellement la troisième cause de décès chez les transplantés. L’introduction récente d’immunosuppresseurs ayant des propriétés antitumorales et antiprolifératives (inhibiteurs de mTor) bouleverse le paysage : non seulement l’incidence des cancers est plus faible chez les patients recevant des mTor comme immunosuppression d’entretien, mais l’introduction de mTor peut stopper ou ralentir l’évolution de la maladie de Kaposi ou de certains cancers cutanés déjà diagnostiqués. Infections and malignancies are the expected complications of immunosuppressive therapy, which non-specifically impairs cellular and humoral immune responses in renal transplant recipients. Infections were usually frequent and severe during the early post-transplant period (first year). Recent diagnostic methods (molecular biology) and availability of new antivirals, antifungal and antibiotic drugs made rapid diagnosis and systematic preventive strategies much easier and this resulted in a significant reduction of infections and infectious death in this population. However, new infectious agents like BK polyomavirus, hepatitis E virus, parvovirus (as well as Chigunkunya, West Nile and others in particular areas) were recently recognized as responsible of aggressive infections in the immunocompromised host. Malignancies are also common after transplantation, due to the intensity and duration of immunosuppression. Skin cancers and lymphoproliferative disorders are the most common and are undoubtedly caused by viral infections, but incidence of non-skin cancers is also increased. After reduction of immunosuppression, treatment is similar to non-transplant patients: Results are usually poor and cancer is now the third cause of death in transplant recipients. Due to their anti-proliferative and anti-tumoral properties, incidence of de novo cancer significantly decreased in patients receiving mTor inhibitors as maintenance immunosuppression; furthermore, in patients already diagnosed with Kaposi sarcoma or recurrent skin cancers, introduction of mTor was associated with stabilisation and/or regression of malignant lesions. [ABSTRACT FROM AUTHOR]

Résumé Le virus BK (BKv) est un virus ubiquitaire dont la séroprévalence se situe aux alentours de 80 % dans la population générale. Après une primo-infection asymptomatique, le BK virus reste quiescent chez les sujets sains, et la réactivation survient dans un contexte de diminution de l’immunité. Le pouvoir pathogène de ce virus s’exprime principalement chez le transplanté rénal, chez qui il peut occasionner dans environ 5 % des cas une néphropathie tubulo-interstitielle spécifique, causant la perte du greffon chez environ 20 à 30 % des patients infectés. Depuis les années 1990, son incidence augmente avec l’utilisation de nouveaux traitements immunosuppresseurs puissants. La clé de voûte de la prise en charge thérapeutique de cette infection virale, voire celle de la néphropathie associée, est la baisse de l’immunosuppression qu’il convient alors de contrebalancer avec le risque de survenue d’un rejet immunologique. Plusieurs types de traitements adjuvants ont été proposés dans des études non contrôlées (fluoroquinolones, léflunomide, immunoglobulines intraveineuses, cidofovir), sans preuve d’efficacité suffisante jusqu’à maintenant pour en recommander l’usage en première intention. La fréquence élevée de l’infection et sa gravité potentielle sont des arguments en faveur de la mise en place de stratégies préventives, au moins chez les sujets à risque, mais là encore, aucune n’a fait la démonstration de son efficacité de manière formelle. Une nouvelle transplantation est possible après la perte d’un greffon lié à une néphropathie à BKv, sous réserve d’un suivi rapproché de la virémie. BK virus is near ubiquitous, with a seroprevalence of around 80% in the general population. Subsequent to an asymptomatic primary infection, BK virus then remains dormant in healthy subjects. Reactivation occurs in immunocompromised people. BKv is pathogenic mainly among patients who have received a kidney transplant, in whom the virus can cause specific tubulo-interstitial nephritis and even result in graft failure among approximately 20 to 30% of nephritic cases. Since the mid 90s, incidence has increased with the use of new powerful immunosuppressor treatments. The cornerstone of BK virus infection or BK virus-associated nephropathy treatment is a decrease of the immunosuppressive regimen, which must then be offset with the risk of rejection. The use of several adjuvant therapies has been submitted (fluoroquinolones, leflunomide, intravenous immunoglobulins, cidofovir), with no sufficient proof enabling the recommendation of first-line prescription. The high frequency of this infection and its potential harmfulness argue for the use of prevention strategies, at least among patients presenting risk factors. Retransplantation is safe after a first kidney allograft loss caused by BK-virus nephropathy, on condition that a screening for viremia is frequently conducted. [ABSTRACT FROM AUTHOR]

Infections and malignancies are the expected complications of immunosuppressive therapy, which non-specifically impairs cellular and humoral immune responses in renal transplant recipients. Infections were usually frequent and severe during the early post-transplant period (first year). Recent diagnostic methods (molecular biology) and availability of new antivirals, antifungal and antibiotic drugs made rapid diagnosis and systematic preventive strategies much easier and this resulted in a significant reduction of infections and infectious death in this population. However, new infectious agents like BK polyomavirus, hepatitis E virus, parvovirus (as well as Chigunkunya, West Nile and others in particular areas) were recently recognized as responsible of aggressive infections in the immunocompromised host. Malignancies are also common after transplantation, due to the intensity and duration of immunosuppression. Skin cancers and lymphoproliferative disorders are the most common and are undoubtedly caused by viral infections, but incidence of non-skin cancers is also increased. After reduction of immunosuppression, treatment is similar to non-transplant patients: Results are usually poor and cancer is now the third cause of death in transplant recipients. Due to their anti-proliferative and anti-tumoral properties, incidence of de novo cancer significantly decreased in patients receiving mTor inhibitors as maintenance immunosuppression; furthermore, in patients already diagnosed with Kaposi sarcoma or recurrent skin cancers, introduction of mTor was associated with stabilisation and/or regression of malignant lesions., (Copyright © 2016 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.)

BK virus is near ubiquitous, with a seroprevalence of around 80% in the general population. Subsequent to an asymptomatic primary infection, BK virus then remains dormant in healthy subjects. Reactivation occurs in immunocompromised people. BKv is pathogenic mainly among patients who have received a kidney transplant, in whom the virus can cause specific tubulo-interstitial nephritis and even result in graft failure among approximately 20 to 30% of nephritic cases. Since the mid 90 s, incidence has increased with the use of new powerful immunosuppressor treatments. The cornerstone of BK virus infection or BK virus-associated nephropathy treatment is a decrease of the immunosuppressive regimen, which must then be offset with the risk of rejection. The use of several adjuvant therapies has been submitted (fluoroquinolones, leflunomide, intravenous immunoglobulins, cidofovir), with no sufficient proof enabling the recommendation of first-line prescription. The high frequency of this infection and its potential harmfulness argue for the use of prevention strategies, at least among patients presenting risk factors. Retransplantation is safe after a first kidney allograft loss caused by BK-virus nephropathy, on condition that a screening for viremia is frequently conducted., (Copyright © 2015 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.)