Increased morbidity from ischemic heart disease in patients with Wegener's granulomatosis

Faurschou, Mikkel; Mellemkjær, Lene; Sørensen, Inge Juul; Thomsen, B.; Dreyer, Lene; Baslund, Bo

doi:10.1002/art.24386

Cited by 140 publications

(87 citation statements)

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“…After 12 months, the major cause of death was cardiovascular disease, presumably related to ESRD. Early cardiovascular events have been previously reported in association with ANCA vasculitis and are postulated to be related to active inflammation as well as underlying atherosclerosis (21)(22)(23).…”

Section: Discussionmentioning

confidence: 96%

“…The renal biopsy specimens of 153 patients were reviewed. The median number of glomeruli examined per biopsy specimen was 16 (IQR, [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26]. The pattern of glomerular injury according to the EUVAS schema was categorized as sclerotic in 32% of cases, focal in 6%, crescentic in 43%, and mixed class in 6%.…”

Section: Cohort Description and Outcomesmentioning

confidence: 99%

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Predictors of Treatment Outcomes in ANCA-Associated Vasculitis with Severe Kidney Failure

Lee

Gasim

Derebail³

et al. 2014

Clinical Journal of the American Society of Nephrology

126

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Background and objectives In ANCA-associated GN, severe renal dysfunction portends a poor prognosis for renal recovery and patient survival. This study evaluated the prognostic factors affecting renal and patient outcomes in patients presenting with severe kidney failure to guide immunosuppressive therapy.Design, setting, participants, & measurements This study retrospectively evaluated clinical and histopathologic characteristics of 155 patients who underwent biopsy between October 1985 and February 2011 (median eGFR at presentation, 7.1 ml/min per 1.73 m 2 ; 87% required hemodialysis), all treated with immunosuppressive medications. Three outcomes of interest were measured: patient survival, renal survival, and treatment response (defined as dialysis-free survival without active vasculitis by 4 months after biopsy). Competing risk, Cox, and logistic regression analyses were conducted for each outcome measure.Results Within 4 months after biopsy, treatment response was attained in 51% of patients, 35% remained on dialysis, and 14% died. In a competing risk analysis, estimated cumulative incidence rates of ESRD and diseaserelated mortality were 26% and 17% at 1 year and 32% and 28% at 5 years, respectively. Cyclophosphamide therapy and treatment response by 4 months were independently associated with patient and renal survival, adjusting for the percentage of normal glomeruli, histopathologic chronicity index score, and baseline clinical characteristics. Only 5% of patients still dialysis dependent at 4 months subsequently recovered renal function. Low chronicity index score (odds ratio [OR], 1.16; 95% confidence interval [95% CI], 1.04 to 1.30, per unit decrease) and baseline eGFR.10 ml/min per 1.73 m 2 (OR, 2.77; 95% CI, 1.09 to 7.01) were significantly associated with treatment response by 4 months. Among cyclophosphamide-treated patients, the likelihood of treatment response was .14% even with highest chronicity index score and eGFR,10 ml/min per 1.73 m 2 .Conclusions Although low baseline renal function and severe renal scarring are associated with lower treatment response rate, no "futility" threshold could be identified. Conversely, continued immunosuppressive therapy beyond 4 months is unlikely to benefit patients who remain dialysis dependent.Clin J Am Soc Nephrol 9: 905-913, 2014.

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Section: Discussionmentioning

confidence: 96%

Section: Cohort Description and Outcomesmentioning

confidence: 99%

Predictors of Treatment Outcomes in ANCA-Associated Vasculitis with Severe Kidney Failure

Lee

Gasim

Derebail³

et al. 2014

Clinical Journal of the American Society of Nephrology

126

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confidence: 76%

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Karlson¹,

Chibnik²,

Tworoger³

et al. 2010

Arthritis & Rheumatism

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to RA onset, being ϳ45% at Ͻ4 years and ϳ5% at Ն8 years (1).At what threshold cut point of sTNFRII were the sensitivity and specificity optimized, as recently reported for anti-CCP by the same research group (4)? In addition, does the optimal threshold cut point vary by time interval before disease onset? The predictive efficacy of such critical limit(s) of sTNFRII could be compared with results of anti-CCP testing (4) or testing for other biomarkers (5). The cut level could also be a specific value for testing the validity of these results in further cohort studies. The authors acknowledged that ultimately, replication of these investigations in other cohorts over time will be the best indication of validity of the reported findings (1). ReplyTo the Editor: We thank Drs. Masi and Aldag for their interest in our report. The authors present a recalculation of our Table 4 results and assumed that we performed a stratified analysis (i.e., assigned controls to time-to-RA groups based on the time interval for their matched case). This was not our analysis. We did not stratify the controls into 3 time-to-RA groups; rather, we performed polytomous logistic regression that allowed us to model the relationship of the biomarkers to the risk of different components of the composite outcome, using the entire control group (Glynn RJ, Rosner B. Methods to evaluate risks for composite end points and their individual components. J Clin Epidemiol 2004;57:113-22).In the case of Table 4, and the example discussed by Drs. Masi and Aldag, we were modeling the relationship between quartiles of sTNFRII and risk of developing RA in time-to-first-symptom groups of Ͻ4 years, 4-Ͻ8 years, or 8-12 years. By using this method we were able to compare our 3 RA outcomes based on time to symptoms with all controls and did not have to stratify the controls into time-to-symptom categories based on their matched cases. This increased our study's power to reveal a significant trend and is one explanation for the discrepancy between our P values and those presented by Masi and Aldag. In addition, they stratified the controls into categories with 25% in each group. The quartiles among controls were created for the primary analysis (our Table 3) for the whole control sample without regard to time to RA onset of the matched case. This yielded 25% of controls in each quartile overall for Table 3, but does not translate into 25% of controls in each quartile stratified by time to RA onset for Table 4, as they assumed in their calculations. This is another explanation for the discrepancies in our results. Masi and Aldag raise the question of whether there was a greater concentration of higher-normal or abnormally elevated-range sTNFRII values within quartile 4, in the time period 0 months-4 years prior to RA symptoms (our Table 4). We included only samples from 4 months prior to RA symptoms; hence, the short time period was 0.3-Ͻ4 years. We investigated for clustering of higher values of sTNFRII in the fourth quartile of cases (0.3-Ͻ4 years pre-RA onset) a...

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“…There are several cases that described patients with GPA and myocardial infarction (MI) [25][26][27][28]. In the Danish National Hospital register patients had an increased rate of MI within five years of diagnosis of GPA when compared to the general population [29].…”

Section: Cardiac Manifestation In Granulomatosis With Polyangiitismentioning

confidence: 99%

Cardiac manifestations in antineutrophil cytoplasmic autoantibody (ANCA) — associated vasculitides

Życińska

Borowiec

2016

Kardiol Pol

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Increased morbidity from ischemic heart disease in patients with Wegener's granulomatosis

Abstract: Compared with the background population, WG patients seem to experience an increased number of both early and late cardiovascular events due to IHD.

Cited by 140 publications

References 32 publications

Predictors of Treatment Outcomes in ANCA-Associated Vasculitis with Severe Kidney Failure

Predictors of Treatment Outcomes in ANCA-Associated Vasculitis with Severe Kidney Failure

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Cardiac manifestations in antineutrophil cytoplasmic autoantibody (ANCA) — associated vasculitides

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