Kidney Week

Abstract: SA-PO673

C3 Glomerulonephritis Triggered by Toxocariasis

Session Information

• Glomerular Diseases: IgA and Complement-Mediated GN
  November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1302 Glomerular Diseases: Immunology and Inflammation

Authors

• Ben m'rad, Mona, Hopital du Haut-Richelieu, Saint-Jean-sur-Richelieu, Quebec, Canada

Mona Ben m'rad,

• Beaulac, Alexandre, Centre integre universitaire de sante et de services sociaux de l'Estrie Centre hospitalier universitaire de Sherbrooke du Quebec, Sherbrooke, Quebec, Canada

Alexandre Beaulac,

• Palanchuck, Steven, Hopital du Haut-Richelieu, Saint-Jean-sur-Richelieu, Quebec, Canada

Steven Palanchuck,

• Beaunoyer, Veronique, Hopital du Haut-Richelieu, Saint-Jean-sur-Richelieu, Quebec, Canada

Veronique Beaunoyer,

• Luong, Me Linh, Centre Hospitalier de l'Universite de Montreal, Montreal, Quebec, Canada

Me Linh Luong,

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.