An Interesting Case of Secondary IgAN

Introduction: Secondary IgA nephropathy (IgAN) can arise from systemic antigenic stimulation or chronic infections. As opposed to primary IgAN, the secondary type develops due to chronic pathogen exposure, immunological imbalance, or underlying comorbidities. Case Description: A 71-year-old man with uncontrolled Type 2 DM, hypertension and peripheral vascular disease presented with worsening bilateral foot burns and was found to have bacteremia with MRSA, ESBL-producing Enterobacter cloacae, positive serologies for syphilis and hepatitis C, as well as urinary tract infections caused by E. coli and candida glabrata. He developed an acute kidney injury with a significant rise in creatinine to 4.0 mg/dl, nephrotic-range proteinuria with urine protein/Cr (6700 mg/gm), microscopic hematuria and severe hypoalbuminemia (1.7 g/dL). Kidney biopsy showed mesangial and endocapillary hypercellularity with fibrocellular crescent formation and segmental sclerosis. MEST-C score: M1 E1 S1 T0 C1, IgA-dominant mesangial staining and C3 deposits confirmed by immunofluorescence (IF). No dense immune deposits were identified on electron microscopy. Discussion: Infections involving the skin, urinary tract, and bloodstream, along with systemic immune activation, can trigger an exaggerated IgA-mediated glomerular response in susceptible individuals. Despite broad-spectrum antibiotics and wound debridement, renal function continued to decline, prompting the initiation of corticosteroid therapy. This case emphasizes the importance of deciphering secondary IgAN in patients with coaxialIgA and C3 deposits on IF