Authors
Filipa Fonte Rodrigues, Diogo Borges, Rita Manso, Sara Barreto
Published in
BMJ case reports. Volume 19. Issue 8. Aug 20, 2026. Epub Aug 20, 2026.
Abstract
Zebra bodies-electron-dense lamellar lysosomal inclusions-are the renal hallmark of Fabry disease, caused by deficient α-galactosidase A (GLA) activity. However, several pharmacological agents with cationic amphiphilic properties produce morphologically indistinguishable deposits, resulting in drug-induced phospholipidosis. We describe a woman in her 50s referred to nephrology with non-nephrotic proteinuria and non-visible haematuria following an ischaemic stroke treated with prednisolone and methotrexate for concomitant medium-vessel vasculitis. Aetiological workup-including autoimmunity, anti-phospholipase A2 receptor and GLA gene sequencing-was negative. Renal biopsy revealed lamellated myelin bodies in podocyte cytoplasm on electron microscopy, alongside thin basement membrane disease. Given negative Fabry testing and chronic sertraline exposure-a selective serotonin reuptake inhibitor with known cationic amphiphilic properties-the drug was discontinued. Proteinuria fell from 2.8 g/24 hours to 0.13 g/24 hours at 6 months, with complete resolution of non-visible haematuria. This case underscores the importance of pharmacological review in Zebra body nephropathy.
PMID:
42624633
Bibliographic data and abstract were imported from PubMed on 21 Aug 2026.
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