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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Hypertension is common among patients with systemic lupus erythematosus (SLE), particularly those with lupus nephritis (LN), with a prevalence reaching up to 74% in some cohorts. A cohort study by Liu JL (2021) reported a high prevalence of uncontrolled hypertension, 39.8% based on Canadian guideline and 66.7% based on ACC/AHA guidelines. Beyond nephropathy, other factors such as inflammation, medications (corticosteroids), and metabolic changes also contribute to the development of hypertension in lupus.
An 18-year-old male was admitted to the emergency ward with severe vomiting, persistent severe headache which was unresponsive to analgesics. Two days prior to this admission, he had been hospitalized for seven days with a diagnosis of severe active SLE with LN, suspected neuropsychiatric SLE (NPSLE), hypertension, optic neuritis and retinal vasculitis. At that time, his blood pressure 130/80 mmHg. He was treated with azathioprine (Imuran) 50 mg once daily, amlodipine 10 mg once daily, irbesartan 300 mg once daily, intravenous (IV) methylprednisolone 250 mg every 6 hours for three days, then tapered to 62.5 mg every 12 hours, followed by oral prednisone 55 mg once daily for seven days. The current admission presenting with a blood pressure of 200/110 mmHg. Intravenous nicardipine was initiated at a rate of 5 mg/hour. Blood pressure remains high even after receiving IV nicardipin for 10 days. Blood pressure began to decrease gradually following the tapering of prednisone and becomes normal when the prednison dose is 20 mg. Normal blood pressure is achieved with single anti hypertension ramipril 2,5 mg.
The prevalence of hypertension in SLE ranges from 14% to 75%. Multiple factors contribute including age, sex, metabolic changes, ethnicity, renal disease, systemic inflammation, immune dysregulation, endothelial dysfunction, and medication side effects (corticosteroids). Corticosteroids promotes endothelial dysfunction, sodium retention, and volume expansion, resulting in elevated blood pressure. Directly, glucocorticoids reduce vasodilator production, suppress nitric oxide synthesis, upregulate angiotensin II type I receptors, increase renal sodium reabsorption, expand plasma volume, elevate total peripheral resistance, and contribute to metabolic syndrome. Indirectly, corticosteroids affect fluid and electrolyte balance via mineralocorticoid activity. The incidence of hypertension increases with cumulative glucocorticoid exposure. This effect can appear within days of therapy initiation. In this case, the patient developed hypertension 4 days after administration of high-dose corticosteroid and it normalized after dose reduction.
Understanding and addressing factors contributing to suboptimal blood pressure control are essential to prevent cardiovascular and renal complications in SLE patient. In this case, hypertension was primarily induced by corticosteroid therapy. Preventing hypertension in SLE requires close monitoring of corticosteroid-related adverse effects and appropriate management of lupus nephritis.
