Complement and immunoglobulin profiles in ANCA-associated vasculitis with renal involvement: a serotype-stratified analysis of disease activity and renal outcomes.

C3 and C4 were within the reference interval in nearly all patients, so frank complement consumption was uncommon.

• C3 was within the reference interval in 97.3% of patients and C4 in 86.3%.
• The cohort comprised 73 AAV patients (PR3-ANCA n = 39; MPO-ANCA n = 34) with complete complement and immunoglobulin data at admission and at least 6 months of follow-up.
• Samples were taken at baseline before immunosuppressive treatment, and none after plasma exchange had begun.

Neither C3 nor C4 showed a gradient across CKD severity groups, unlike the inflammatory indices.

• C3 across CKD groups: p = 0.453; C4: p = 0.550.
• The inflammatory indices C-NLR and PLR did differ across the CKD severity groups.
• The authors state this contrasts with lupus nephritis, where complement consumption tracks renal injury severity.

IgA was nominally higher in MPO-ANCA than PR3-ANCA patients, but the difference did not survive FDR correction and all values were within the reference range.

• IgA median [IQR] 2.60 [1.92-2.88] g/L in MPO-ANCA vs 2.11 [1.78-2.30] g/L in PR3-ANCA, nominal p = 0.011.
• After FDR adjustment across the five immune parameters, q = 0.055.
• No treatment-adjusted IgA model was retained because induction-regimen coding was sparse and heterogeneous.

IgG correlated positively with ESR and with 6-month change in eGFR.

• IgG vs ESR: ρ = +0.40, p < 0.001.
• IgG vs ΔeGFR at 6 months: ρ = +0.26, p = 0.037.

Serum C4 was nominally higher in the eight patients who did not achieve clinical remission, but the association was not robust.

• C4 0.35 [0.28-0.44] vs 0.28 [0.20-0.33] g/L, nominal p = 0.037; FDR q = 0.184.
• AUC 0.729, 95% bootstrap CI 0.473-0.953, an interval that includes 0.5.
• The direction (higher C4 in non-remission) ran opposite to a complement-consumption interpretation and rested on only eight events.

C3 correlated inversely with neutrophil-to-lymphocyte ratio.

• NLR vs C3: ρ = -0.24, p = 0.043.

The authors interpret the findings as compatible with prior cohorts linking relatively lower C3 to adverse renal outcomes, with prognostic signal lying within the reference interval rather than in consumption proportional to glomerular injury.

• The data are described as not conflicting with published cohorts in which relatively lower C3 predicted adverse renal outcomes.
• Findings are consistent with pauci-immune pathogenesis, in contrast to immune-complex-mediated glomerulopathies such as lupus nephritis.
• The serotype IgA difference and C4–remission association are labeled exploratory and require confirmation in larger prospective cohorts.