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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Around 50 % of cases of infection-associated glomerulonephritis in developed countries are caused by Streptococci and Staphylococci. The remainder relates to other bacteria, viruses, parasites, and fungi. A kidney biopsy is mandatory for diagnosis and typical changes of postinfectious glomerulonephritis are C3 deposits ± immunoglobulin deposits, but other less common diagnoses that need to be entertained in the background of infection include C3 glomerulopathy and ANCA-mediated pauci-immune glomerulonephritis. The mainstay of therapy in these patients is clearance of infection. There may be a role for immunosuppressive therapy in severe crescentic glomerulonephritis or if pauci-immune glomerulonephritis is a consideration.
A 55-year-old gentleman, known to have type 2 diabetes on oral medications, hypertension, dyslipidaemia, and chronic kidney disease stage III, with a creatinine of 128 micromole/L, came with right foot swelling and a wound on the plantar side, and fever. His labs showed persistent leucocytosis 35.3x10^9. He also had worsening renal function, creatinine increased to 324 micromole/L, started on piperacillin-tazobactam and linezolid. Urine analysis showed protein and RBCS. A US KUB ruled out obstruction. Complement C3 was low, 0.69g/L, and C4 was normal. Normal ANA, dsDNA antibodies, P and C-ANCA. anti-ASO titer was high 454 IU/ml(normal 0-200) and Extractable nuclear antibodies were positive for anti-Jo. All cultures however were negative. Protein creatinine ratio was 2 1g/g and urine analysis showed RBCs >100.
The biopsy shows diffuse endocapillary proliferation involving peripheral capillary loops of diabetic glomeruli with C3 dominant IF staining (3+) consistent with C3 dominant proliferative glomerulonephritis. The differential diagnosis may include infection-related proliferative glomerulonephritis and C3 glomerulonephritis. Both infection-related proliferative glomerulonephritis and C3 glomerulonephritis are due to activation of complement alternative pathway. The biopsy also shows foci of moderate to heavy interstitial inflammatory cells infiltration of sampled renal tissue consisting of lymphocytes mainly with frequent plasma cells, neutrophil polymorphs and eosinophils, with foci of acute tubular necrosis, consistent with Acute tubulointerstitial nephritis. The patient however went agianst medical advised immedietly after the biopsy and refused to come for follow up.
Treating the infection usually results in the resolution of IRGN, whereas no robust guidelines exist in the treatment of C3GN. However, we did not get a chance to entertain this option.
