Antibrush border antibody disease: a case report and literature review

• Autor(a) principal: Almeida, Jose Bruno de
• Data de Publicação: 2021
• Outros Autores: Brito, Laíse Pereira Arcoverde Fechine, Guedes, Felipe Leite, Vale, Pedro Henrique Cavalcante, Santos, Rivaldo Pereira, Martins, Sílvia Queiroz Santos, Dantas, Gleiko Yuri de Figueredo, Wanderley, David, Araújo, Stanley de Almeida, Silva, Gyl Eanes Barros
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRN
• Texto Completo: https://repositorio.ufrn.br/handle/123456789/54343; https://doi.org/10.1016/j.xkme.2021.04.015
• topic: anti-brush border antibody disease; auto-antibodies; autoimmunity; chronic kidney disease; kidney biopsy; megalin

Anti-brush border antibody (ABBA) disease, also called anti–low-density lipoprotein receptor-related protein 2 (anti-LRP2) nephropathy, occurs due to the formation of antibodies against brush border antigens of the renal proximal convoluted tubule. We report a case of ABBA disease in a male farmer in his 30s who presented with 2 years of polyuria, dysuria, nocturia, and urinary urgency. He described a history of long-term occupational exposure to pesticides and silica, evolving into possible pneumoconiosis, and prior pulmonary tuberculosis. At presentation, he had reduced kidney function (serum creatinine 3.6 mg/dL) with hyponatremia, hypokalemia, hypophosphatemia, a normal anion gap, metabolic acidosis, and respiratory acidosis, and 2.2 g/day of urine proteinuria. The kidney biopsy was consistent with ABBA, showing amorphous immune-deposits in the tubular basement membrane and strong positivity on indirect immunofluorescence in the brush border of the proximal tubules. The trigger for production of ABBA is still unknown, but it may be associated with chronic conditions such as pulmonary tuberculosis and occupational exposures such as silica and pesticides, as seen in the patient in this report. Most cases do not respond to immunosuppression, and the prognosis is poor.