Sertraline-induced renal phospholipidosis
Filipa Fonte Rodrigues, Diogo Borges, Rita Manso, Sara BarretoZebra 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.