RESUMEN
Atypical non HLA antibodies are increasingly recognised as causes of immunological injury in allotransplantation. In this report we describe a non HLA sensitized male renal allograft recipient who developed acute vascular rejection on a "for cause" biopsy (Banff v2, g2, ptc 3) at day 4 post first renal allograft in the presence of elevated angiotensin II type 1 receptor antibodies (AT1R-Ab level 14.1). The acute rejection was treated with pulse corticosteroid therapy, anti-thymocyte globulin (ATG × 6), plasma exchange (1.5 plasma volume replacement x6) and oral candesartan. Serum creatinine improved and follow up biopsy confirmed resolution of rejection following treatment. AT1R-Ab should be considered when rejection is diagnosed in the absence of HLA antibodies.
Asunto(s)
Autoanticuerpos/sangre , Rechazo de Injerto/inmunología , Trasplante de Riñón/efectos adversos , Receptor de Angiotensina Tipo 1/inmunología , Enfermedad Aguda , Administración Oral , Corticoesteroides/administración & dosificación , Adulto , Aloinjertos , Bloqueadores del Receptor Tipo 1 de Angiotensina II/administración & dosificación , Suero Antilinfocítico/administración & dosificación , Bencimidazoles/administración & dosificación , Biopsia , Compuestos de Bifenilo , Rechazo de Injerto/diagnóstico , Rechazo de Injerto/terapia , Humanos , Inmunosupresores/administración & dosificación , Masculino , Intercambio Plasmático , Quimioterapia por Pulso , Receptor de Angiotensina Tipo 1/efectos de los fármacos , Índice de Severidad de la Enfermedad , Tetrazoles/administración & dosificación , Factores de Tiempo , Resultado del Tratamiento , Regulación hacia ArribaRESUMEN
Monoclonal gammopathy of renal significance is defined as any B cell or plasma cell clonal lymphoproliferation which neither causes tumor complications nor meets any current hematological criteria for specific therapy, with one or more kidney lesions related to the produced monoclonal immunoglobulin, such as amyloidosis. A 50-year-old male presented with heavy proteinuria and blood tests showing IgA and Lambda paraproteinemia. Light microscopy showed mesangial eosinophilic ground substance extending into the capillary loops, and positive staining within the glomeruli and vessel walls for amyloid P immunohistochemistry was also noted. Immunofluorescence showed positive staining for IgA and Lambda in the mesangia and capillary loops. Electron microscopy exhibited organized fibrils measuring 4-5 nm in diameter in the mesangia, glomerular basement membranes and vessel walls. We interpreted the overall findings as atypical renal amyloidosis with IgA and Lambda deposition on immunofluorescence. Further amyloid typing using laser microdissection-liquid chromatography and mass spectrometry will be useful.