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1 our understanding of the pathophysiology of anti-GBM disease.
2 autoantibodies from patients with autoimmune anti-GBM disease.
3 humoral response, only a select few develop anti-GBM disease.
4 chemoattractant produced by renal cortex in anti-GBM disease.
5 ratification may assist in the management of anti-GBM disease.
6 ate that the RRS concept is transferrable to anti-GBM disease.
7 es against laminin-521 in the development of anti-GBM disease.
8 l outcomes in ANCA-associated vasculitis, to anti-GBM disease.
9 munopathogenic processes in the two forms of anti-GBM disease.
10 microbial Ag may be sufficient to induce the anti-GBM disease.
11 lead to different clinical manifestations of anti-GBM disease.
12 ransplant anti-glomerular basement membrane (anti-GBM) disease.
13 l study involving 30 patients diagnosed with anti-GBM disease and 30 healthy controls matched for the
14 superoxide dismutase as novel biomarkers of anti-GBM disease and lupus nephritis, with stronger corr
15 NCA-associated vasculitis is transferable to anti-GBM disease and the renal histology is strongly pre
16 nusual combination of c-ANCA antibodies with anti-GBM disease, and this association raises complex qu
17 tcomes in anti-glomerular basement membrane (anti-GBM) disease are sparse, and validated tools to aid
18 ated in the urine and kidneys of mice during anti-GBM disease, as well as in mice with spontaneously
19 iology of anti-glomerular basement membrane (anti-GBM) disease before clinical presentation is unknow
24 ary hemorrhage, another important feature of anti-GBM disease; this was not correlated with the sever
28 e largest assembled cohorts of patients with anti-GBM disease (with 174 patients included in the fina