SUN-371 C4D STAINING IN INFECTION RELATED GLOMERULONEPHRITIS: A RETROSPECTIVE STUDY

Abstract

C4d is a byproduct of activation of the classic and lectin pathways. It is widely used as marker of antibody-mediated rejection. However, recent studies shown that C4d can be positive in immune complex glomerulonephritis. There is paucity in literature regarding utility C4d staining in suspected cases of infection related glomerulonephritis (IRGN) to demonstrate lack of activation of alternate complement pathway. In this retrospective observational study we included all biopsy proven IRGN from December 2016 to December 2017. Demographic data, initial lab values biopsy findings and treatment details were documented. C4d was done with IHC. Patients were followed up through a period of one year. Outcome variables were defined as persistence of proteinuria/ hematuria at one year, dialysis dependency and death. Of 90 patients with biopsy proven IRGN, C4d staining was done in 53 patients out of which 29 (55%) were C4d positive and 24 patients (45%) were negative. Out of the patients negative for C4d, 62% were C3 dominant and co-dominance was seen in 38%. The mean age of presentation was 41.89±14.58 years, with 51% Males. We observed that C4d IHC showed intense, diffuse >2+ glomerular capillary wall staining. In C4d +ve group mean creatinine at presentation was 2.9±1.8 g/dl and mean 24 hour urine protein was 2.84±1.5. Nephrotic range proteinuria was seen in 5 patients. Immunosuppression (IS) was started in 7 patients, HD was given to 6 patients and PLEX done in 2. At 1 year, 4 patients progressed to CKD, 4 patients were dialysis Dependent and 3 died. In C4d neg, C3 dominant group the mean creatinine at presentation was 4.1±2.6 g/dl and mean 24 hour urine protein was 3.1±1.3. Nephrotic range proteinuria was seen in 5 patients. IS & HD was started in 2 & 5 patients each. At 1 year 5 patients progressed to CKD, 1 patient became dialysis dependent and one died. In C4d neg, C3 co - dominant group the mean serum creatinine at presentation was 3.3±2.5g/dl and mean protenuria was 2.3±1.4gm and nephrotic range proteinuria seen in 1 patient. At 1 year 2 patients progressed to CKD, 1 patient became dialysis dependent. Our study demonstrates that C4d staining helps to differentiate IC GN from complement mediated GN. There was significant difference between the clinical presentation, and follow up between C4d positive, c4d negative - c3 dominant and Codominant IRGN. But the true differentiation of glomerulonephritis with c3 dominance (infection related) and C3 glomerulonephritis is not well established.