RESUMO
We describe a case of rapid onset of vascular calcification coincident with the initiation of warfarin therapy in a kidney transplant recipient. Calcification developed within the media of the blood vessel wall, with relative intimal sparing. Medium and small arteries were affected; however, the aorta was mostly free of calcifications, suggesting a differential response to warfarin between the intima and media and between different vascular beds. In addition, unlike the highly calcified native kidney's vessels, the kidney allograft was not calcified, suggesting local genetically determined mechanisms in preventing vascular calcification. Distal subcutaneous necrosis ultimately led to the patient's death.
Assuntos
Anticoagulantes/efeitos adversos , Calcinose/induzido quimicamente , Transplante de Rim , Doenças Vasculares/induzido quimicamente , Varfarina/efeitos adversos , Anticoagulantes/uso terapêutico , Fibrilação Atrial/tratamento farmacológico , Calcinose/diagnóstico , Evolução Fatal , Humanos , Masculino , Pessoa de Meia-Idade , Tomografia Computadorizada por Raios X , Túnica Íntima/diagnóstico por imagem , Túnica Íntima/patologia , Túnica Média/diagnóstico por imagem , Túnica Média/patologia , Doenças Vasculares/diagnóstico , Varfarina/uso terapêuticoRESUMO
Double negative (DN) T cells are expanded in patients with systemic lupus erythematosus (SLE) and stimulate autoantibody production as efficiently as CD4(+) T cells. In this study, we demonstrate that DN T cells from patients with SLE produce significant amounts of IL-17 and IFN-gamma, and expand when stimulated in vitro with an anti-CD3 Ab in the presence of accessory cells. Furthermore, IL-17(+) and DN T cells are found in kidney biopsies of patients with lupus nephritis. Our findings establish that DN T cells produce the inflammatory cytokines IL-17 and IFN-gamma, and suggest that they contribute to the pathogenesis of kidney damage in patients with SLE.
Assuntos
Movimento Celular/imunologia , Proliferação de Células , Interleucina-17/biossíntese , Rim/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Subpopulações de Linfócitos T/imunologia , Adulto , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/metabolismo , Linfócitos T CD4-Positivos/patologia , Linfócitos T CD8-Positivos/imunologia , Linfócitos T CD8-Positivos/metabolismo , Linfócitos T CD8-Positivos/patologia , Células Cultivadas , Humanos , Imunofenotipagem , Mediadores da Inflamação/metabolismo , Mediadores da Inflamação/fisiologia , Rim/patologia , Lúpus Eritematoso Sistêmico/metabolismo , Lúpus Eritematoso Sistêmico/patologia , Pessoa de Meia-Idade , Subpopulações de Linfócitos T/metabolismo , Subpopulações de Linfócitos T/patologia , Regulação para Cima/imunologiaRESUMO
We discuss a 53-year-old woman with systemic lupus erythematosus who presented with vasculitis, hypocomplementemia and nephritis. Although her serum complement 4 (C4) levels were zero, she had four copies of C4 gene. Renal biopsy revealed membranoproliferative glomerulonephritis and the presence of cryoglobulins, detected by electron microscopy, and significant numbers of T cells in the interstitium. Cryoglobulins were considered responsible for the complete consumption of C4 in the serum the levels of which improved gradually after treatment. T cells in the kidney were found to express CD44 and phosphorylated ezrin/radixin/moiesin which explain why they homed to the kidney inappropriately. The contribution of cryoglobulins and T cells in the expression of kidney pathology is discussed.
