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Clinical presentation of human C1q deficiency: How much of a lupus?
Mihaela Stegert1, Merete Bock1, Marten Trendelenburg2
1Division of Internal Medicine, University Hospital Basel, Basel, Switzerland.
Insights
Hereditary C1q deficiency increases lupus susceptibility. Patients often show discoid rash and oral ulcers more than sporadic lupus, but less arthritis and anti-ds-DNA antibodies.
Area of Science:
- Immunology
- Rheumatology
- Genetics
Background:
- Hereditary C1q deficiency is linked to high susceptibility for systemic lupus erythematosus (SLE).
- Limited data exists on the specific diagnosis and clinical features of SLE in C1q-deficient individuals.
- This review analyzes published reports on C1q deficiency and associated lupus phenotypes.
Purpose of the Study:
- To comprehensively review and analyze clinical manifestations of SLE in patients with C1q deficiency.
- To compare the features of C1q deficiency-associated SLE with sporadic SLE.
- To understand the diagnostic criteria and disease course in this patient subgroup.
Main Methods:
- Comprehensive search of electronic databases up to November 2014.
- Identification and analysis of published reports on 71 C1q-deficient patients from 45 families.
- Comparison of clinical manifestations between C1q deficiency-associated SLE/SLE-like disease and sporadic SLE.
Main Results:
- 55% of C1q-deficient patients met American College of Rheumatology (ACR) criteria for SLE; 22.5% had SLE-like syndrome.
- Discoid rash (56% vs 10%) and oral ulcers (49% vs 24%) were more frequent in C1q deficiency-associated SLE.
- Arthritis (38% vs 84%) and anti-ds-DNA antibodies (18% vs 78%) were less frequent compared to sporadic SLE.
Conclusions:
- C1q deficiency is strongly associated with SLE, presenting distinct clinical features.
- Discoid rash and oral ulcers are characteristic of C1q deficiency-related lupus.
- Severe disease courses are often linked to infections rather than aggressive lupus manifestations.
Abstract:
Hereditary human C1q deficiency has been well described to be associated with high susceptibility for the development of systemic lupus erythematosus (SLE). The majority of subjects present a clinical syndrome closely related to SLE. However, limited information is available about the primary diagnosis and particular clinical manifestations of SLE in this specific subgroup of patients. In this review, we performed a comprehensive search of electronic databases up to November 2014 to identify and analyze reports on patients with C1q deficiency. We identified 71 C1q-deficient patients descending from 45 families that had been published. According to the American College of Rheumatology (ACR) diagnostic criteria for SLE 39/71 (55%) subjects could be classified as having SLE. Another 16/71 (22.5%) presented a SLE-like syndrome (defined as 3 positive ACR criteria) whereas in 16/71 (22.5%) no SLE could be diagnosed at time of publication. Symptoms began at a median age of 5 years, male and females being equally affected. Discoid rash (56% versus 10%, p<0.001) and oral ulcers (49% versus 24%, p<0.001) occurred significantly more frequent in C1q deficiency-associated SLE/SLE-like disease than in sporadic SLE, whereas arthritis (38% versus 84%, p<001) and anti-ds-DNA (18% versus 78%, p<0.001) occurred less frequently. Renal and neurological manifestations were found to occur similarly frequent. The severe course of disease in some patients seemed to be mostly due to severe infections at early ages and not in particular due to more aggressive SLE manifestations.
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