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Master Thesis

Traitement et évolution du syndrome néphrotique idiopathique cortico-résistant de l’enfant : étude d’une cohorte monocentrique de 68 patients traités par anticalcineurines

Abstract : Idiopathic nephrotic syndrome (NS) is the major acquired glomerular disease of children. His main treatment is corticosteroids, but 10-20% of patients are steroid-resistants. For these patients, prognosis depends on decreasing of proteinuria, with a systematic progression to end-stage renal disease (ESRD) in the absence of remission. The introduction of calcineurin inhibitors (CNI) has changed their prognosis. The outcome of this study was the observation of the sequence of treatments and evolution of a single-center retrospective cohort of children followed for idiopathic NS with initial steroid-resistance, since CNI introduction. Between 1987 and 2013, 68 patients were followed for idiopathic steroid-resistant NS. All patients were treated with CNI. For 41 patients (60%), this treatment was sufficient to allow a complete remission (CR). With additional treatments, a CR was achieved in 47 patients (69%). Immunoadsorptions and rituximab were involved in obtaining this RC, respectively for 50% and 33% of treated patients. Of these patients in CR, 26 (55%) had relapses. Rituximab allowed no subsequent relapse in 28% of treated patients. An evolution to ESRD had occurred in 16 patients (23.5%). Post-transplant recurrence occurred in 88%, with graft loss in 31% of transplanted patients. Despite an improved prognosis with the introduction of CNI, idiopathic steroid-resistant NS remains a severe disease, and it is essential to continue research of new treatments for multi-drug resistant patients and prevention of post-transplant recurrence.
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Master Thesis
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  • HAL Id : dumas-01513852, version 1

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Juliette Bouchereau. Traitement et évolution du syndrome néphrotique idiopathique cortico-résistant de l’enfant : étude d’une cohorte monocentrique de 68 patients traités par anticalcineurines. Médecine humaine et pathologie. 2016. ⟨dumas-01513852⟩

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