Mireille El-Ters, Umadevi Muthyala, Marie D. Philipneri, Fadi A. Hussein, Krista L. Lentine staining for IgG and C3 deposits. We searched the MEDLINE/PubMed electronic database for publications on ANCA-associated glomerulonephritis with IF staining published in English language from 1983 to 2009 using the MeSH terms “ANCA”, “glomerulonephritis”, and “immune deposits”. The search yielded ten relevant articles that comprised case reports and small case series (Table I). Among 281 biopsies that were described in patients with ANCA-associated glomerulonephritis, 154 biopsies (54%) showed positive IF for IgG, IgM, IgA, and/or complements. The proportion of biopsies with heavy staining could not be ascertained as the degree of positivity was not reported for all cases. In general, the patients were treated with corticosteroids and cyclophosphamide, and some received plasma- pheresis. The majority of the cases showed good response to these regimens. Neumann et al. [4] and Haas and Eustace [2] observed significantly heavier proteinuria and trends towards worse renal function in the subsets with immune deposits. The patholophysiologic role of immune deposits in patients with ANCA-mediated vasculitis is unclear. The hypothesis that immune complexes act synergistically with ANCA to produce more severe glomerulonephritis, as manifest by heavier proteinuria and inferior kidney function, was raised by some authors [2, 4]. There are also reports of predominant mesangial IgA deposits described as concomitant ANCA-associated glomerulonephritis and IgA nephropathy [3, 18]. Findings from several animal studies have lead to the notion that early immune complex deposition may play a role in the initiation of vasculitis and glomerulonephritis [25, 26]. A transient immune deposit was observed in an animal model of ANCA-associated glomerulo- nephritis following injection of rats with myelo- peroxidase [25]. In some models, it was postulated that immune complex deposits disappeared before tissue biopsy was performed. In conclusion, immune deposits may be found in a subset of patients with ANCA-associated glomerulonephritis. Anti-neutrophil cytoplasmic antibody-associated glomerulonephritis is an aggressive disease that warrants prompt diagnosis and treatment. It is important to test for serological markers such as ANCA even in cases with active IF and immune deposits on renal histology. Cases such as ours also raise the question of whether ANCA-associated glomerulonephritis is truly pauci- immune. Perhaps, deposits that appear early in the disease process are commonly degraded, or the observation may represent an overlap of two disease forms. Additional studies are warranted to further understand the definitive role and best treatment of patients with ANCA-associated glomerulonephritis and immune deposits. R e f e r e n c e s 1. Pettersson EE, Sundelin B, Heigl Z. 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