C3 Glomerulonephritis Triggered by Toxocariasis

Introduction: C3 glomerulonephritis (C3GN) is a rare disease, triggered by a monoclonal gammopathy or auto-immunity or an infection resulting from the overactivation of the alternative pathway of the complement (APC), with a poor prognosis. We report a case of C3GN triggered by Toxocara cani (T. cani), a parasitic infection. Case Description: An 83 year-old man was admitted for fever, rash, pruritus, eosinophilia 1600/mm3 and a serum creatinine of 122 μmol/L. He had repaired a septic tank which required excavation of contaminated soil, 2 weeks prior. He was discharged with no diagnosis and readmitted 4 months later for a recurrent rash, fever, dyspnea, a nephrotic syndrome (NS), hematuria, a peak creatinine of 355 μmol//L, low C3 (0.2 UI/L) and a peak eosinophilia of 2400/mm3. A Staphylococcus aureus bacteremia was treated with IV cefazolin for 14 days. An extensive NS and eosinophilia work-up including ANCA, ANA, electrophoresis, free light chains, viral serologies, bone marrow biopsy, genetic mutations and autoantibodies against the APC regulators was negative, except for a repeatedly highly positive Toxocara sp serology. The kidney biopsy showed a severe diffuse endocapillary glomerulonephritis with C3 deposits. On the basis of the strong positivity of the T.cani serology, the marked eosinophilia, a diagnosis of C3GN associated with an active visceral toxocariasis was made. After 3 pulses of Solumedrol 1 g IV followed by predisone 1 mg/kg/day slowly tapered and albendazole 400 mg twice a day for 28 days, the T. cani infection abated. He required dialysis. Within 6 months, a second kidney biopsy showed an important decrease of the inflammation and of the C3 deposits with a lot of scarring tissue and fibrosis confirming end-stage renal disease. Discussion: Toxocariasis, a highly prevalent helminthic zoonosis worldwide, has been reported as a rare cause of NS and eosinophilia both in adults and children. Here, an active infection-related C3GN was probably triggered by a visceral toxocariasis, after exposure to a contaminated soil, suggesting the role of an uncontrolled activation of the APC. The treatment goals were : 1/ eradication of T.cani, 2/ control of the glomerular inflammation and prevention of flairs after the destruction of the larvae with slowly tapered steroids, 3/ supportive. We suggest to consider toxocariasis as a differential diagnosis for NS and eosinophilia.

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