Características clínicas, laboratoriais e histológicas de pacientes com glomerulopatia membranosa após o transplante renal

• Ano de defesa: 2016
• Autor(a) principal: Silva, Artur Quintiliano Bezerra da [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Clinical; Transplante renal; Glomerulopatia membranosa; Proteinúria; Tratamento
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=4698189; http://repositorio.unifesp.br/handle/11600/46497

Introduction: Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in the adult population, accounting for about 20% of cases. MN may occur in the transplanted kidney, either as a recurrent or de novo disease. Objetives: This study has the purpose to describe clinical, laboratorial and immunological characteristics of patients submitted to kidney transplantation that developed MN, and evaluate graft and patient survival in patients with post-transplant MN, as well as survival associated factors. Methods: In a retrospective cohort study of patients who were transplanted between 1983 and 2015 and had the diagnosis of MN in the graft, clinical, laboratorial and histopathological kidney parameters were evaluated. Results: 41 patients with post-transplant MN were identified. Men were predominant (58.5%), in the fourth or fifth decade of life. The etiology of end-stage renal disease (ESRD) was MN in 36.6% of the cases, the median for onset of the first proteinuria was 40 months, for diagnosis of MN was 41.5 months and the average post-transplant follow-up was 108.2 ± 52.8 months. Complete remission was achieved in 31.3% patients and partial remission in 43.9%, recurrence was confirmed in 36.6% and the main cause of graft loss was chronic nephropathy (50%) followed by post transplant MN. A secondary cause of MN was identified in 24%, half of them from malignancies. In renal biopsy, there was a positive but non significant correlation between C3 deposits intensity and proteinuria levels. Death-censored graft survival (DCGV) at 10 years was 58.6%. Conclusion: Post-transplant MN has varied clinical presentation, as well as in the native kidney, but usually presented with subnephrotic proteinuria and progressive graft dysfunction, although it has observed complete remission of proteinuria in about ¼ of the cases in this population. Kidney and patient survivals at 10 years were 53.1% and 88.3%,, respectively, and they were not different of that of the general population transplanted at the same service. The remission of the post-transplant MN occurred either in patients undergoing additional immunosuppressive treatment as in those for whom only renoprotection was introduced or optimized. The remission, even if only partial, was associated with a better renal outcome. The 4 main cause of graft loss in this group was chronic graft nephropathy and not post transplant MN. It was not possible to assess the direct benefit or risk of therapeutic interventions (renoprotection and/or immunosuppression) in transplanted kidney, possibly because of the limitations of the present study design.