Anti-glomerular basement membrane (anti-GBM) disease accompanied by vasculitis that was not positive for antineutrophil cytoplasmic antibodies to myeloperoxidase and proteinase 3: a report of two cases and the incidence of anti-GBM disease at one institution

Nakabayashi, Kimimasa; Fujioka, Yasunori; Arimura, Yoshihiro; Fukuoka, Toshihito; Marumo, Tomohumi; Umino, Michiru; Kamiya, Yasushi; Okai, T; Tsurumaki, Shigeru; Nagasawa, Toshihiko; Yamada, Akira

doi:10.1007/s10157-011-0435-z

Cited by 4 publications

(3 citation statements)

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“…For example, incidence figures from the literature are variable. Table 3 summarizes the results of prior studies that have described the incidence of anti-GBM disease (8)(9)(10)(11)(12)(13)(14)(15). Although there may be natural variation in disease rates among the populations studied, obvious differences in study methods may account for the different figures reported.…”

Section: Discussionmentioning

confidence: 99%

“…Although there may be natural variation in disease rates among the populations studied, obvious differences in study methods may account for the different figures reported. In half of these studies, an incidence rate could not be calculated because the population at risk was not specified (12,13,15) or could only be estimated (11). Studies of renal biopsy registries have reported comparatively lower incidence rates of approximately 0.6 pmp per year (10,14).…”

Section: Discussionmentioning

confidence: 99%

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Spatial and Temporal Clustering of Anti-Glomerular Basement Membrane Disease

Canney¹,

O’Hara²,

McEvoy³

et al. 2016

CJASN

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Background and objectives An environmental trigger has been proposed as an inciting factor in the development of anti-GBM disease. This multicenter, observational study sought to define the national incidence of anti-GBM disease during an 11-year period (2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014) in Ireland, investigate clustering of cases in time and space, and assess the effect of spatial variability in incidence on outcome.Design, setting, participants, & measurements We ascertained cases by screening immunology laboratories for instances of positivity for anti-GBM antibody and the national renal histopathology registry for biopsy-proven cases. The population at risk was defined from national census data. We used a variable-window scan statistic to detect temporal clustering. A Bayesian spatial model was used to calculate standardized incidence ratios (SIRs) for each of the 26 counties.Results Seventy-nine cases were included. National incidence was 1.64 (95% confidence interval [95% CI], 0.82 to 3.35) per million population per year. A temporal cluster (n=10) was identified during a 3-month period; six cases were resident in four rural counties in the southeast. Spatial analysis revealed wide regional variation in SIRs and a cluster (n=7) in the northwest (SIR, 1.71; 95% CI, 1.02 to 3.06). There were 29 deaths and 57 cases of ESRD during a mean follow-up of 2.9 years. Greater distance from diagnosis site to treating center, stratified by median distance traveled, did not significantly affect patient (hazard ratio, 1.80; 95% CI, 0.87 to 3.77) or renal (hazard ratio, 0.76; 95% CI, 0.40 to 1.13) survival.Conclusions To our knowledge, this is the first study to report national incidence rates of anti-GBM disease and formally investigate patterns of incidence. Clustering of cases in time and space supports the hypothesis of an environmental trigger for disease onset. The substantial variability in regional incidence highlights the need for comprehensive country-wide studies to improve our understanding of the etiology of anti-GBM disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Spatial and Temporal Clustering of Anti-Glomerular Basement Membrane Disease

Canney¹,

O’Hara²,

McEvoy³

et al. 2016

CJASN

View full text Add to dashboard Cite

show abstract

“…Anti-GBM disease is caused by autoantibody against glomerular and alveolar basement membrane, and is pathologically distinct from arteritis [1]. However, anti-GBM disease accompanied by arteritis was reported soon after the establishment of the concept of anti-GBM disease [2,3], and after the generalization of ANCA assay, a substantial proportion (21.2-45.8%) of anti-GBM disease has been found to be positive for ANCA (Table 1) [4][5][6][7][8][9][10][11]. Therefore, ANCA is supposed to be responsible for the arteritis accompanied anti-GBM disease, and ANCA-positive anti-GBM disease is termed ''double positive'' disease.…”

Section: Introductionmentioning

confidence: 99%