Predictive value of IgG autoantibodies against C1q for nephritis in systemic lupus erythematosus.

Siegert, C. E. H.; Daha, Mohamed R.; Tseng, Chi-Wei; Coremans, I.; Es, Leendert A. van; Breedveld, F. C.

doi:10.1136/ard.52.12.851

Cited by 127 publications

(102 citation statements)

References 26 publications

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“…Furthermore, the appearance of circulating antibodies to Clq-CLR has served as a harbinger for flares of lupus glomerulonephritis (18,19). In the present study, antibodies to Clq-CLR were recovered from the glomeruli of 4 of 5 patients with proliferative or inflammatory lesions at autopsy.…”

Section: Discussionmentioning

confidence: 52%

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Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

Mannik

Wener

1997

Arthritis & Rheumatism

104

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Objective. To determine if antibodies to the collagen-like region of Clq (Clq-CLR) are present in the glomerular immune deposits of patients with systemic lupus erythematosus (SLE).Methods. Kidney tissues were obtained at autopsy, glomeruli were isolated, and glomerular basement membrane fragments were prepared. Antibodies were extracted with low pH or with DNase.Results. The concentrations of antibodies to Clq-CLR recovered from the glomeruli were 150-fold higher per unit of IgG than that found in the serum or in the serum and interstitial fluid entrained in glomeruli. Antibodies to Clq-CLR were recovered from glomeruli of 4 of 5 patients with proliferative glomerulonephritis at autopsy.Conclusion. This is the first demonstration that antibodies to Clq-CLR are deposited and concentrated in the renal glomeruli of patients with SLE. These antibodies, thus, have the potential of contributing to the pathogenesis of lupus glomerulonephritis.

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Section: Discussionmentioning

confidence: 52%

“…Several independent investigations have established the high prevalence of autoantibodies to Clq-CLR in patients with proliferative lupus glomerulonephritis (14)(15)(16)(17). In addition, increasing levels of these autoantibodies is known to herald the flare of glomerulonephritis in patients with SLE (18,19).…”

mentioning

confidence: 99%

Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

Mannik

Wener

1997

Arthritis & Rheumatism

104

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“…Antibodies with specificities other than for DNA have been associated with renal disease in other studies of SLE (12)(13)(14). Therefore, we tested the sera for the presence of antibodies to histones, IgG, and C1q.…”

Section: Resultsmentioning

confidence: 99%

An in vitro assay for detection of glomerular binding IgG autoantibodies in patients with systemic lupus erythematosus.

Budhai

Oh²,

Davidson³

1996

J. Clin. Invest.

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The deposition of anti-dsDNA antibodies in the glomerulus is believed to play a critical role in the pathogenesis of nephritis in SLE. However, an absolute correlation between serum levels of anti-dsDNA antibodies and renal disease has not been found. Recently a glomerular binding assay (GBA) has been developed to detect IgG binding to isolated rat glomeruli. We have used the GBA to study sera from four groups of SLE patients: (A) ϩ anti-dsDNA antibodies, active nephritis; (B) Ϫ anti-dsDNA antibodies, active nephritis; (C) ϩ anti-dsDNA antibodies, no nephritis; and (D) Ϫ anti-dsDNA antibodies, no nephritis. The serum antids-DNA antibodies in group A and group C patients could not be distinguished on the basis of isotype, charge, or crossreactivity with histones. Nevertheless, the mean intensity of glomerular immunofluorescence was significantly higher in group A than in the three other patient groups and distinguished between patients with serum anti-dsDNA antibodies who had nephritis and those without clinically apparent nephritis. GBA reactivity was unaffected by DNase treatment of sera, but was partially inhibited by preincubation with dsDNA. These findings are consistent with the hypothesis that some anti-dsDNA antibodies cross-react with glomerular components and that the presence of this crossreactivity is associated with, and may be responsible for, the development of nephritis. In addition, we have identified a group of SLE patients with renal disease and typical renal histopathology and immune deposits who do not have serum anti-dsDNA antibodies or antibodies that directly bind to glomeruli in the GBA. The mechanism of renal immune deposition in these patients remains to be determined. ( J. Clin. Invest. 1996. 98:1585-1593.) Key words: systemic lupus erythematosus • glomerulonephritis • anti-DNA antibodies

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“…The clinical performance of anti-C1q for detecting renal flare was similar to that of C3, C4, and ADNA (43)(44)(45)(46)(47). Unlike C3 and C4, prospective studies found that anti-C1q levels began to increase 4 to 6 mo before renal flare (12,43) and became significantly different than baseline 2.3 mo before flare (12). Positive predictive values of 50 to 71% for impending flare were calculated.…”

Section: Antibodies To Complement Component C1qmentioning

confidence: 99%

Biomarkers for Lupus Nephritis

Rovin¹,

Zhang²

2009

Clinical Journal of the American Society of Nephrology

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Current treatment of severe lupus nephritis is unsatisfactory in terms of both outcome and toxicity. To improve the efficacy and decrease the adverse effects of immunosuppression, it would be ideal to be able to predict the course and pathology of lupus nephritis and adjust therapy appropriately. This will require biomarkers that reflect disease activity. Recently, significant effort has been put into identifying biomarkers that can anticipate impending lupus renal flare, forecast development of chronic kidney disease, or reflect kidney histology at the time of flare. Although these biomarkers are potentially useful, to date none has been clinically validated in a large, prospective cohort of patients with SLE. This article reviews the current status of lupus nephritis biomarker investigation and articulates a perspective of how future efforts should be focused.

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Predictive value of IgG autoantibodies against C1q for nephritis in systemic lupus erythematosus.

Abstract: Objectives-Antibodies against Clq (CIqAb)

Cited by 127 publications

References 26 publications

Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

An in vitro assay for detection of glomerular binding IgG autoantibodies in patients with systemic lupus erythematosus.

Biomarkers for Lupus Nephritis

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