Anti-C1q antibodies in systemic lupus erythematosus

Orbai, Ana‐Maria; Truedsson, Lennart; Sturfelt, Gunnar; Nived, Ola; Fang, Hong; Alarcón, Graciela S.; Gordon, Caroline; Merrill, Joan T.; Fortin, Paul R.; Bruce, Ian N.; Isenberg, David; Wallace, Daniel J.; Ramsey‐Goldman, Rosalind; Bae, Sang Cheol; Hanly, John G.; Sánchez‐Guerrero, Jorge; Clarke, Ann E.; Aranow, Cynthia; Manzi, Susan; Urowitz, Murray B.; Gladman, Dafna D.; Kalunian, Kenneth C.; Costner, Melissa; Werth, Victoria P.; Zoma, Asad; Bernatsky, Sasha; Ruiz‐Irastorza, Guillermo; Khamashta, Munther A.; Jacobsen, Søren; Buyon, Jill P.; Maddison, P. J.; Dooley, Mary Anne; Vollenhoven, R F van; Ginzler, Ellen M.; Stoll, Thomas; Peschken, Christine A.; Jorizzo, Joseph L.; Jp, Callen; Lim, S. Sam; Fessler, Barri J.; İnanç, Murat; Kamen, Diane L.; Rahman, Arifur; Steinsson, Kristján; Franks, Andrew G.; Sigler, Lisa; Hameed, Suhail; Pham, Ngoc Minh; Brey, Robin L.; Weisman, Michael H.; McGwin, Gerald; Magder, Laurence S.; Petri, Michelle

doi:10.1177/0961203314547791

Cited by 101 publications

(71 citation statements)

References 32 publications

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“…41 Serial determination of anti-C1q in SLE patients with renal flares might help to identify treatment responders and define patients remaining at risk for renal relapses. 5 The latest data from the SLICC international cohort 37 confirmed the association of anti-C1q with lupus nephritis with a prevalence of 45.5% in patients with SLE with American College of Rheumatology (ACR) renal involvement. Younger individuals with SLE were more likely to be antiC1q positive than older individuals.…”

Section: Clinical Significancementioning

confidence: 92%

“…They are detected in all patients with hypocomplementemic urticarial vasculitis, 33,34 although they do not seem to have a pathogenic role in this entity. Other conditions characterized by high anti-C1q antibody prevalence include SLE (28%-60%), 21,[35][36][37] scleroderma (26%), rheumatoid arthritis (19%), undifferentiated connective tissue disease (15%), and Sjo¨gren syndrome (14%). 37 Anti-C1q antibodies are also seen in 26% of hepatitis C patients and correlate with low complement C4 in this population.…”

Section: Clinical Significancementioning

confidence: 99%

“…Other conditions characterized by high anti-C1q antibody prevalence include SLE (28%-60%), 21,[35][36][37] scleroderma (26%), rheumatoid arthritis (19%), undifferentiated connective tissue disease (15%), and Sjo¨gren syndrome (14%). 37 Anti-C1q antibodies are also seen in 26% of hepatitis C patients and correlate with low complement C4 in this population. 38 The first study that showed an association between anti-C1q autoantibodies and lupus nephritis included 35 patients with biopsy-proven diffuse proliferative or membranous lupus nephritis that showed elevations of the C1q solid-phase assay for immune complexes in all the patients with diffuse proliferative nephritis and in 71.4% of the patients with membranous nephritis.…”

Section: Clinical Significancementioning

confidence: 99%

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Anti-C1q in systemic lupus erythematosus

Stojan

Petri

2016

Lupus

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C1q is the first component of the classical complement pathway. Both clinically validated inhouse ELISA assays as well as commercial ELISA kits are used for detection of anti-C1q antibodies. Anti-C1q autoantibodies can be detected in a wide range of autoimmune diseases and are highly sensitive for hypocomplementemic uticarial vasculitis. In SLE, anti-C1q are strongly associated with proliferative lupus nephritis, and their absence carries a negative predictive value for development of lupus nephritis of close to 100%. Anti-C1q in combination with anti-dsDNA and low complement has the strongest serological association with renal involvement. The anti-C1q titers correlate with global disease activity scores in patients with renal involvement, and higher titers seem to precede renal flares. After the successful treatment of a renal flare, anti-C1q has the tendency to decrease or even become undetectable. The main obstacle to the inclusion of anti-C1q in the classification criteria and clinical management of SLE is the lack of standardized laboratory assays. Lupus (2016) 25, 873-877.

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Section: Clinical Significancementioning

confidence: 92%

Section: Clinical Significancementioning

confidence: 99%

Section: Clinical Significancementioning

confidence: 99%

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Anti-C1q in systemic lupus erythematosus

Stojan

Petri

2016

Lupus

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“…There is an ample of evidence confirming kidney involvement in a very early stage of SLE (even in the absence of clinical symptoms), and the occurrence of low-level proteinuria and hematuria may be associated with significant renal disease [118][119][120]. Typically, LN is linked with the CP of complement activation by circulating immune complexes and autoimmunity directed to the components of the CP [112,118,119,121,122]. Growing evidence indicates that the AP takes part in the LN pathogenesis.…”

Section: Lupus Nephritismentioning

confidence: 99%

The role of the alternative pathway of complement activation in glomerular diseases

2018

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The complement system (CS) has recently been recognized as a bridge between innate and adaptive immunity that constitutes a very complex mechanism controlling the clearance of pathogens, cellular debris, and immune complexes. Out of three known pathways of complement activation, the alternative pathway (AP) plays a critical role in host defense by amplifying the complement response, independently of initiation pathway and continuously maintaining low-level activity in a process called 'thick-over.' A key molecule of the CS is C3, in which the AP is constantly activated. To prevent host cell destruction, a group of the AP regulators tightly controls this pathway of the CS activation. Acquired and genetic abnormalities of the CS may alter the delicate balance between enhancing and inhibiting the AP cascade. These can lead to the uncontrolled CS activation, inflammatory response, and subsequent tissue damage. Since complement components are locally produced and activated in the kidney, the abnormalities targeting the AP may cause glomerular injury. C3 glomerulopathy is a new entity, in which the AP dysregulation has been well established. However, recent studies indicate that the AP may also contribute to a wide range of kidney pathologies, including immune-complex-mediated glomerulonephritis (GN), pauci-immune GN, and primary membranous nephropathy (PMN). This article provides insight into current knowledge on the role of the AP in the pathogenesis of glomerular diseases, focusing mainly on various types of primary and secondary GN and PMN.

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“…Although anti-doublestranded DNA antibodies and complement levels have long been recognized as pathophysiologic contributors and predictors of disease activity, their ability to accurately predict flares or histopathology is limited. Anti-C1q antibodies have been associated with lupus nephritis, but the ability of this antibody to track disease or predict histopathology has not been shown (4). Other biomarkers, such as uMCP-1 and uIL-8, have also shown insufficient predictive ability (5).…”

mentioning

confidence: 99%