Changes in antibodies to C1q predict renal relapses in systemic lupus erythematosus

Coremans, I.; Spronk, Peter E.; Bootsma, Hendrika; Daha, Mohamed R.; Voort, E. A. M. Van Der; Kater, L.; Breedveld, Ferdinand C.; Kallenberg, Cornelis

doi:10.1016/0272-6386(95)90595-2

Cited by 158 publications

(99 citation statements)

References 23 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: 51%

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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

103

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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: 51%

“…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

103

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“…As suggested by Clancy et al (21), the antigens on apoptotic cells bound by autoantibodies may themselves be involved in the normal engulfment of apoptotic cells. SLE IgG might block molecules on the apoptotic cells that are necessary for recognition and facilitation of their uptake by macrophages, such as phosphatidylserine (PS) or C1q (22)(23)(24)(25). Otherwise, we showed in our study that preincubation with a peptide that blocks the IgG Fc region or blockade of Fc␥ receptors on the macrophage abrogated the inhibitory effect of the SLE autoantibodies.…”

Section: Discussionmentioning

confidence: 57%

Opsonization of late apoptotic cells by systemic lupus erythematosus autoantibodies inhibits their uptake via an Fcγ receptor–dependent mechanism

Reefman¹,

Horst²,

Nijk³

et al. 2007

Arthritis & Rheumatism

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Objective. Decreased clearance of apoptotic cells is suggested to be a major pathogenic factor in systemic lupus erythematosus (SLE). The aim of this study was to investigate whether the binding of SLE autoantibodies to apoptotic cells influences the phagocytosis of these cells by macrophages. Conclusion. Autoantibodies from SLE patients are able to opsonize apoptotic cells and inhibit their uptake by macrophages via an Fc␥R-dependent mechanism. Methods. Apoptosis was induced in a human

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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: 85%

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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Changes in antibodies to C1q predict renal relapses in systemic lupus erythematosus

Cited by 158 publications

References 23 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

Opsonization of late apoptotic cells by systemic lupus erythematosus autoantibodies inhibits their uptake via an Fcγ receptor–dependent mechanism

Biomarkers for Lupus Nephritis

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