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Background: Idiopathic intracranial hypertension (IIH), also known as benign intracranial hypertension or pseudotumor cerebri, is characterized by elevated intracranial pressure in the absence of an intracranial mass or hydrocephalus. It typically occurs in young, obese women (Al Riyami et al., 2024). Corticosteroids have a paradoxical relationship with IIH: although high doses are sometimes used to manage severe IIH, steroid therapy particularly abrupt withdrawal has been implicated in precipitating the condition (Lorrot et al., 1999). Idiopathic nephrotic syndrome (INS) often necessitates prolonged corticosteroid therapy, predisposing patients to this rare complication.
Case Presentation: We report the case of a 19-year-old non-obese woman with idiopathic nephrotic syndrome (focal segmental glomerulosclerosis identified on renal biopsy) diagnosed in June 2024 and treated with prednisone at 1 mg/kg/day. Her nephrotic syndrome entered remission, and corticosteroids were gradually tapered over several months to 10 mg/day. A few weeks after beginning this taper, she developed progressively worsening, intense, intermittent frontal headaches without radiation, vertigo, tinnitus, or visual disturbances. The headaches were not relieved by vomiting and persisted for one week. She also experienced postprandial vomiting twice daily, preceded by nausea, lasting four days without associated diarrhea or constipation. Fundoscopic examination revealed bilateral papilledema. Computed tomography demonstrated non-communicating triventricular hydrocephalus with suspected aqueductal stenosis. Laboratory investigations showed marked leucocytosis (23,930/mm³) and elevated C-reactive protein (>192 mg/L), although no identifiable clinical source of infection was detected. The peripheral smear was negative for malaria, and there were no signs of meningitis.
Lumbar puncture, magnetic resonance imaging, and venography were not performed.
In view of the clinical findings, fundoscopy, brain CT scan results and biology, the diagnosis of idiopathic intracranial hypertension induced by corticosteroid tapering was suggested.
Acetazolamide (500 mg twice daily) was initiated and corticosteroid taper was gradually reduced over the next two weeks, her headaches and vomiting resolved and the papilledema regressed. No surgery was required and her vision acuity remained preserved.
Discussion: Idiopathic intracranial hypertension is a rare but recognized complication of corticosteroid therapy in idiopathic nephrotic syndrome (INS). Similar cases have been reported in children and young adults receiving high dose or undergoing corticosteroid tapering (Lorrot et al., 1999).
The mechanisms found include transient suppression of the adrenal axis resulting in decreased CSF absorption ( Pseudotumor Cerebri Associated With Prolonged Corticosteroid Therapy: Reports of Four Cases | JAMA | JAMA Network , n.d.) and steroid-induced hypercoagulability causing disruption of cerebral venous outflow (Sakamaki, n.d.)
INS itself predisposes to cerebral venous thrombosis (CVT) due to hypercoagulability, which should be excluded in any patient with NS presenting with hypertension intracranial (Piccini et al., 2023) .
Management of IIH in this setting consists of administering standard therapy (acetazolamide, therapeutic lumbar punctures) alongside correction the underlying triggering factor.
Careful tapering corticosteroid and early ophthalmologic evaluation are essential in patients with INS, even those in remission, who develop headache or visual symptoms during corticosteroid dose reduction . (Lorrot et al., 1999) .
Early recognition and treatment of IIH are essential to prevent permanent vision loss. In the remainder of the report, we will also review the literature on steroid-tapering-induced IIH in INS, the differential diagnosis (especially compared to CVT or true hydrocephalus), and outline therapeutic approaches.
Conclusion: Steroid taper-induced IIH is a rare but potential complication in the management of idiopathic nephrotic syndrome. In patients on corticosteroids who present with headache, vomiting, or papilledema, particularly during dose reduction, prompt evaluation for possible IIH is warranted.
This case highlights the need for vigilance and a multidisciplinary approach to differentiate IIH from other causes of intracranial hypertension and to initiate timely treatment, thereby preventing vision-threatening complications.
