PROPYLTHIOURACIL-INDUCED ANTI-MPO POSITIVE ANCA VASCULITIS WITH CONCURRENT IGA NEPHROPATHY: A CASE REPORT

PROPYLTHIOURACIL-INDUCED ANTI-MPO POSITIVE ANCA VASCULITIS WITH CONCURRENT IGA NEPHROPATHY: A CASE REPORT

Georgina Oakman1,2, Cindy Ong1

1Bendigo Health, Bendigo, Victoria, Australia
2Austin Health, Heidelberg, Victoria, Australia

Abstract

Background:
The anti-thyroid medication propylthiouracil (PTU) can induce antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Pauci-immune crescentic glomerulonephritis is the characteristic histological finding of this condition. We present a case of PTU-induced AAV with concurrent IgA nephropathy in a young female with treatment-resistant Graves’ disease.

Case report
A 26-year-old female presented with an acute kidney injury, macroscopic haematuria and proteinuria in the context of approximately 14 months of treatment with high-dose PTU for Graves’ disease. Microscopic haematuria was also present in a urine sample taken 9 months prior. Furthermore, she had established thyroid eye disease and a history of a severe adverse drug reaction to Carbimazole. Her autoantibodies were strongly positive for myeloperoxidase (MPO)-ANCA (199 U/mL). Renal biopsy demonstrated both necrotising crescentic glomerulonephritis and prominent mesangial deposition of IgA. She was treated with glucocorticoids and Rituximab with sustained improvement in her renal function but persisting mild proteinuria and microscopic haematuria. Her PTU was ceased following a dose of radioactive iodine (RAI). 12 months post RAI, her Graves’ orbitopathy remained stable and thyroid function was gradually normalising.

Conclusions
This case of drug-induced AAV was also associated with histological features of IgA nephropathy. We propose that this patient had pre-existing subclinical IgA nephropathy and then developed AAV secondary to PTU. The management of her coexistent renal and thyroid disease presented a dilemma requiring multi-disciplinary input given the PTU-induced AAV, previous reaction to Carbimazole, risks of a thyroidectomy on immunosuppression and concerns that RAI would worsen her eye disease. The steroids administered for AAV likely prevented RAI-associated progression of her orbitopathy. B-cell depletion with Rituximab may have also facilitated the return to a euthyroid state.

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