RECOGNISING THE SUBTLE CLINCOPATHOLOGICAL FEATURES OF C3GN COMPARED TO OTHER COMPLEMENT MEDIATED GLOMERULOPATHY IN AN AUSTRALIAN TERTIARY INSTITUTION

P PURI1, M. FADIA1, T NEEMAN4, G.WALTERS1,3,  K. GIBSON1, S. JIANG1,2,3
1The Canberra Hospital , Canberra City., Australia, 2Department of Immunology and Infectious Disease, John Curtin School of Medical Research, Canberra City , Australia , 3Centre for Personalised Immunology, NHMRC Centre for Research Excellence, Canberra City ,  Australia, 4Statistical Consulting Unit The Australian National University , Canberra city,  Australia

C3 glomerulonephritis (C3GN) a recently described entity with heterogeneous histopathological features. Morphologically similar to dense deposit disease (DDD) and post-infectious glomerulonephritis (PIGN), C3GN maybe distinguished by electron microscopy (EM) and clinical history. This study was conducted to reclassify patients displaying predominant C3 staining on renal biopsies and C3GN, plus examine response to therapy.
Methods:We undertook a retrospective analysis of 883 renal biopsies collected at The Canberra Hospital. Samples with predominant C3 (> 2 orders of magnitude higher than other immunoreactants) were re-reviewed by a renal histopathologist. Of 30 biopsies with predominant C3 staining, 9/30 (30%) fulfilled histological criteria for C3GN. Clinical histories were examined by 2 nephrologists to exclude alternative causes of C3-mediated GN.
Results:Histological reclassification revealed 11% were originally diagnosed with PIGN and another 22% as C3 deposition disease, with the remainder being Mesangiocapillary glomerulonephritis (MCGN). EM demonstrated 33% of C3GN cases had C3 deposition in all 3 glomerular sites.
Presentation demographics were similar between C3GN and non-C3GN individuals, with the exception of elevated creatinine in patients with C3GN (136.81mmol/L vs 245.55mmol/L p= 0.006). C3GN patients trended to lower serum C3 levels (0.865g/L vs 1.085g/L, p= 0.2). Of the patients diagnosed with C3GN 33% received immunosuppression, achieving remission in 66%. 33% of C3GN cases were lost to follow up. Patients requiring long-term dialysis was 11% in the C3GN vs. 14% in others. All-cause mortality was higher in C3GN patients 66% vs 14%.
Conclusion: Recognising C3GN’s distinguishing features remains challenging however, it is noted that C3GN exists as a separate entity with differing progression when compared with other complement mediated GNs. Our series suggests C3GN cases are associated with worse all-cause mortality.


Biography:
I am a first year Renal trainee at the Canberra hospital. I have an interest in renal immunology and transplantation. I hope to undertake more research in these fields over the course of my training both in a lab and clinical setting

 

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