Investigations for Nephritic Syndrome • • • • • • • SLE: ANA, anti-dsDNA, hypocomplementaemia (C3, C4) ANCA-associated vasculitis: ANCA, MPO/PR3 Post-Streptococcal GN (PSGN): anti-strep antibodies, streptozyme Chronic bacterial infections: blood culture Anti-GBM disease: note that pulmonary haemorrhage is common Cryoglobulinaemia GN: cryoglobulins Hep B/C: positive serology doesn’t prove that HBV/HCV is the cause of the GN Complement Levels • Low in: o SLE (Lupus nephritis) o PSGN o Membranoproliferative GN (MPGN) o Mixed globulinaemia • • • Detected by measuring serum C3 and C4 Due to compliment activation at higher rates than complement production There is a lesser or slower rate of complement activation in IgA nephropathy, fibrillary GN and membranous nephropathy  High in: o Anti-GBM disease o Wegener’s (Granulomatosis with Polyangiitis, GPA) o Polyarteritis nodosa o Henoch-Schönlein Purpura (HSP) • Hypocomplementaemia in glomerular disease includes: o Hereditary/acquired deficiency of complement components or its regulators o Presence of factors that promote complement activation • Deficiencies of regulators of alternative complement pathway are associated with certain types of MPGN such as dense deposition disease and C3 GN Renal Biopsy • • Light microscopy (LM) shows gross changes Immunofluorescence (IF) o IgG, IgA, IgM o C3, C4 o κ, λ • Electron microscopy (EM) shows deposits, membranes