Assuntos
Hipersensibilidade Imediata/complicações , Deficiência de IgA/etiologia , Falência Renal Crônica/complicações , Diálise Renal , Corticosteroides/uso terapêutico , Angioedema/etiologia , Relação CD4-CD8 , Tamponamento Cardíaco/cirurgia , Comorbidade , Emergências , Hemodiafiltração , Humanos , Hipersensibilidade Imediata/tratamento farmacológico , Hipotensão/etiologia , Deficiência de IgA/sangue , Deficiência de IgA/tratamento farmacológico , Imunoglobulina E/imunologia , Falência Renal Crônica/terapia , Linfopenia/etiologia , Pessoa de Meia-Idade , Pericardiocentese , Diálise Renal/efeitos adversos , Desequilíbrio Hidroeletrolítico/etiologiaRESUMO
AA (secondary) amyloidosis is one of the most severe and uncommon complications of several rheumatic disorders and chronic infections such as tuberculosis (TB). Successful treatment depends on the control of the underlying inflammatory process, what can lead to an improvement or a regression in organ dysfunction. If the disorder persists, it has been reported in some cases of AA amyloidosis secondary to rheumatic diseases, that the use of biologic therapy is so far the only opportunity to reduce the development of AA amyloidosis and to reverse established deposits. We report herein a case of a latent TB infection complicated by a life-threatening AA amyloidosis presented as nephrotic syndrome. After an adequate antituberculostatic treatment, AA amyloidosis remained active and Tocilizumab (TCZ) was started with a dramatic resolution of the proteinuria, stabilization of the amyloid deposits and improvement in general condition.