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All relevant data are within the paper. Introduction {#sec001} ============ Systemic lupus erythematosus (SLE) is the archetype of a systemic autoimmune disease taking a relapsing and remitting course. Immune dysregulation leads to the production of autoantibodies, immune complexes, complement activation and tissue inflammation, which together cause a clinical syndrome with multiorgan involvement and unpredictable courses \[[@pone.0123572.ref001]\]. Lupus nephritis, that occurs in about 50% of all SLE patients \[[@pone.0123572.ref002]\], is a common and severe complication, and considered to be a major cause of morbidity and mortality in SLE patients \[[@pone.0123572.ref003]\]. The large number of different autoantibodies observed in SLE mostly target nuclear as well as cell surface antigens, but also serum molecules such as complement components. Among these complement C1q is the most prominent target \[[@pone.0123572.ref004]\]. Complement C1q is the starter molecule of the classical pathway of complement activation and plays an important role in the clearance of immune complexes and apoptotic cell debris \[[@pone.0123572.ref005],[@pone.0123572.ref006]\]. Interestingly, hereditary homozygous deficiency of C1q has been described to be the strongest risk factor for developing SLE \[[@pone.0123572.ref007]--[@pone.0123572.ref009]\]. Whereas most SLE patients do not suffer from hereditary C1q deficiency they often show very low levels of C1q, in particular during disease flares. Low levels of C1q are typically associated with the occurrence of autoantibodies against C1q \[[@pone.0123572.ref010]--[@pone.0123572.ref012]\] that are found in about 20--50% of unselected SLE patients and in up to 100% of SLE patients with active proliferative lupus nephritis \[[@pone.0123572.ref013], [@pone.0123572.ref014]\]. This strong association has also been described in pediatric-onset SLE patients \[[@pone.0123572.ref015], [@pone.0123572.ref016]\]. As a consequence, anti-C1q antibodies not only have a high negative predictive value for the occurrence of severe lupus nephritis but seem to be necessary (but not sufficient in themselves) for the development of proliferative lupus nephritis. However, although it is likely that they alter the physiological role of C1q, e.g. the uptake of immune complexes and apoptotic debris \[[@pone.0123572.ref017]\], the pathogenic role of anti-C1q still needs to be elucidated. Independently anti-C1q might serve as a biomarker of active lupus nephritis. This view is based on a number of cross-sectional studies on anti-C1q in which the antibody was found to have a significant association with renal involvement and general disease activity \[[@pone.0123572.ref018]--[@pone.0123572.ref022]\]. However, studies investigating the value of anti-C1q during clinical follow-up are scarce. In a large study, Moroni and colleagues followed patients with lupus nephritis during a period of 6 years measuring anti-dsDNA antibodies, C3, C4 and anti-C1q as markers of renal disease activity \[[@pone.0123572.ref023]\]. Anti-C1q levels were found to better correlate with renal flares in patients with proliferative lupus nephritis than the other markers, but not all patients with renal flares had increased levels of anti-C1q. In another study Akhter et al. followed patients with SLE and changes in renal disease activity showing an association between anti-C1q and changes in urine protein concentrations and a renal activity score as well as a modified SLEDAI \[[@pone.0123572.ref024]\]. In addition, it was reported that levels of anti-C1q antibodies decreased after successful treatment of lupus nephritis \[[@pone.0123572.ref025]\]. However, these findings are in