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Circulating immune complexes and C1 activation in patients with rapidly progressive glomerulonephritis, before and
Insights
Circulating immune complexes (CIC) are frequently detected in rapidly progressive glomerulonephritis, often indicating systemic disease. Levels decrease after treatment, but remain detectable.
Area of Science:
- Nephrology
- Immunology
- Clinical Chemistry
Background:
- Rapidly progressive glomerulonephritis (RPGN) is a severe kidney disease.
- Circulating immune complexes (CIC) are implicated in various glomerulonephritides.
- Assessing CIC levels aids in understanding disease activity and systemic involvement.
Purpose of the Study:
- To evaluate the prevalence and significance of CIC in patients with RPGN.
- To compare CIC detection across multiple established assays.
- To assess changes in CIC levels following plasma exchange treatment.
Main Methods:
- Utilized C1q binding assay, C1q deviation test, solid-phase C1q binding assay, solid-phase conglutinin binding assay, and platelet aggregation test.
- Analyzed serum samples from 30 RPGN patients.
- Re-evaluated 15 patients after plasma exchange and immunosuppressive therapy.
Main Results:
- CIC were detected in 89% of patients by at least one assay.
- C1q binding and/or conglutinin binding assays showed positivity in 81% of patients.
- Higher CIC levels and detection by multiple assays correlated with systemic disease involvement.
- CIC remained detectable post-treatment, albeit at lower levels.
Conclusions:
- CIC are common in RPGN and associated with systemic disease.
- Established assays effectively detect CIC in RPGN.
- Plasma exchange reduces CIC levels, but they persist during immunosuppression.
Abstract:
Well-known assays for detection of circulating immune complexes (CIC) (C1 q binding assay, C1q deviation test, solid-phase C1 q binding assay, solid-phase conglutinin binding assay, and the platelet aggregation test) were used in 30 patients with different kinds of rapidly progressive glomerulonephritis. In 89% of the patients evidence of CIC was found in at least one of the assays. 81% of the patients were positive in the C1q binding assay and/or the conglutinin binding assay with addition of complement. CIC were more often detected by several assays, and with higher values in patients with systemic disease than in patients with renal involvement alone. CIC were found in 2 patients with Goodpasture's syndrome. 15 patients were reexamined after treatment with plasma exchange, when the disease was clinically inactive. The patients were still on immunosuppressive treatment. In most of these, CIC were detectable, but with lower values than at the start of treatment. Before treatment, high levels of C1r-C1s-C1 inactivator complexes suggested increased C1 activation in 93% of the patients. C-reactive protein was raised, and the concentrations of C1 q, C1s, C4, C3 and factor B were normal or high in most of the patients. Pronounced hypocomplementemia was found only in 2 patients with systemic lupus erythematosus (SLE). After treatment, the levels of C-reactive protein, C1 q, C1s, C3 and factor B had decreased in the non-SLE patients, while the average levels of C4 and C1r-C1s-C1 inactivator complexes were essentially unchanged.