Division of Nephrology and Hypertension, III Medical Department, Coburg General Hospital, Coburg, Germany.
J Nephrol. 2012 Sep-Oct;25(5):636-43. doi: 10.5301/jn.5000107.
The last couple of years have brought some major advances both in our understanding of antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis pathogenesis mechanisms and in its treatment options. Recent discoveries of completely new antigens such as lysosome-associated membrane protein-2 (LAMP-2) have meant a huge step forward, and the fact that this antigen is homologous to proteins of bacterial fimbria caused a shift in the focus regarding underlying pathomechanisms of ANCA vasculitis toward bacterial infections, mainly with Klebsiella or Escherichia species, possibly playing a role in triggering the disease. So nephrology has seen real progress in understanding of glomerulonephritis disease mechanisms - not only regarding primary membranous glomerulonephritis (with the recent identification of the phospholipase A2 receptor being the underlying antigen) but also regarding secondary pauci-immune glomerulonephritis due to ANCA-positive vasculitis.
过去几年,我们在抗中性粒细胞胞浆抗体(ANCA)阳性血管炎发病机制的理解以及治疗选择方面都取得了重大进展。最近发现了一些全新的抗原,如溶酶体相关膜蛋白-2(LAMP-2),这是一个巨大的进步,而且这个抗原与细菌菌毛的蛋白质同源,导致了 ANCA 血管炎的潜在发病机制的研究重点发生了转移,朝着细菌感染的方向发展,主要与克雷伯氏菌或大肠杆菌有关,它们可能在引发疾病方面发挥了作用。因此,肾脏病学在理解肾小球肾炎发病机制方面取得了真正的进展——不仅涉及原发性膜性肾小球肾炎(最近发现的磷脂酶 A2 受体是潜在的抗原),也涉及由 ANCA 阳性血管炎引起的继发性寡免疫性肾小球肾炎。