PO:01:004 Urine levels of complement proteins differentiate lupus nephritis from non-renal systemic lupus erythematosus

Objectives Complement activation plays a dual role in systemic lupus erythematosus (SLE) and lupus nephritis (LN) pathogenesis: protective through clearance of immune complexes and cellular waste, but damaging when uncontrolled activation promotes kidney injury. While complement dysregulation is recognized in SLE, mechanisms influencing LN activity remain poorly understood. We evaluated circulating and excreted complement activation and regulatory markers in relation to SLE and LN activity, and treatment response in active LN.Methods We analysed classical and alternative complement pathway activation and regulatory protein concentrations in matched serum and urine samples from 21 SLE patients with active biopsy-proven LN (19 from Saint-Luc University Hospital, Brussels; 2 from Karolinska University Hospital, Stockholm), 20 SLE patients without LN (10 active, 10 in remission), and 15 healthy controls from Karolinska University Hospital. LN samples were collected before immunosuppressive therapy (T0) and after one year (T1). Complement proteins Ba, Bb, C3a, C4a, C5a, sC5b-9, factor H, and factor I were assessed using Quidel MicroVue Multiplex Complement Array. Serum levels were normalised to the median HC concentration. Urine concentrations were normalized to urinary creatinine (ng protein/mg creatinine). The Mann-Whitney U test was used to compare protein levels between groups.Results Serum C4a and sC5b-9 were significantly higher in LN patients versus SLE without LN or HC (p