Background/Purpose:

Anti-C1q antibodies (C1Q Ab) are observed in 30-60% of patients with Systemic Lupus Erythematosus (SLE). A number of studies have shown that the presence of C1Q Ab correlates with disease activity. In particular C1Q Ab is reported to strongly correlate with active renal disease with some studies reporting antibody absence having a negative predictive value of close to 100% for active lupus nephritis (LN) (1). However specificity for active lupus remains controversial and variations may be due to timing of samples, assay used, cut off values and population studied.

Here we undertook a point-in-time measurement of C1Q Ab in a multi ethnic cohort of SLE patients and investigated correlations between this and clinical and serologic parameters of SLE.

Methods:

SLE patients attending an inner city Lupus Clinic were involved in the study. Disease activity was calculated using the SLE Disease Activity Index (SLEDAI 2K); erythrocyte sedimentation rate (ESR), dsDNA Ab, complement levels (C3, C4), and urine protein creatinine ratio (uPCR) were measured. For patients with biopsy proven LN renal inactivity was defined as a PCR < 50 mg/mmol. C1Q Ab was quantified by ELISA (Orgentec Diagnostika GmbH). A positive test defined by the manufacturer is a level above 10 U/ml. Correlation of C1Q Ab levels with disease activity markers was measured using Pearson’s correlation.

Results:

116 patients were included in the study. All fulfilled the 2012 SLICC criteria for SLE. 103 (89%) were female. There were 38 (32.8%) South Asians (SA), 48 (41.3%) Afro Caribbean (AC) and 25 (21.6%) White Caucasians (WC). C1Q Ab positivity was present in 29% SA patients, 13% AC patients and 28% WC patients (p=0.06).

There was a positive correlation between C1Q Ab levels and dsDNA levels (r=0.358, p<0.01); whilst a negative correlation was observed with C3 levels (r=-0.406, p<0.01). No correlation was found with SLEDAI scores(r=0.18, p=0.053), uPCR (r=0.13, p=0.16) and ESR (r=0.045, p=0.63). Positive C1Q Ab was more common in patients with a history of biopsy proven LN (32.7%); of these patients, 43% (n=12/28) had inactive LN at the time of sampling with a positive C1q Ab. In addition, C1Q Ab was present in 15.5% (n=9) of patients with minimally active disease (SLEDAI≤ 4).

Conclusion:

The overall prevalence of C1Q Ab was 23.3% in our lupus cohort, and was present in all ethnic groups. Its presence was correlated with dsDNA but not with SLEDAI score, ESR and PCR. There was a negative correlation with C3 level. C1Q Ab was found more commonly in renal than in non-renal patients. Importantly a positive C1Q Ab level was found in 15.5% of patients with inactive disease defined as SLEDAI≤ 4 and in 43% of LN patients with inactive renal disease (defined as PCR<50). We would therefore caution against use of C1Q Ab as a stand-alone biomarker for active lupus.

References

1. Fremeaux-Bacchi V, Noel LH, Schifferli JA. No lupus nephritis in the absence of antiC1q autoantibodies? Nephrol Dial Transplant 2002; 17:2041–2043.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/anti-c1q-antibodies-and-disease-activity-in-a-multi-ethnic-lupus-cohort/