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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.
Low birth weight (LBW) is associated with reduced nephron endowment, predisposing adults to hypertension and chronic kidney disease (CKD). Here, we present the case of hypertensive emergency and focal segmental glomerulosclerosis (FSGS) in a patient who had a history of LBW.
A 40-something old man, born prematurely at 32 weeks (birth weight 1300 g), had a history of frontal lobe injury in adolescence but no prior antihypertensive therapy. The patient was emergently admitted to our hospital with elevated blood pressure (233/142 mmHg) and acute kidney injury (serum creatinine 8.47 mg/dL). Laboratory tests revealed microangiopathic hemolytic anemia (platelets 76 × 10³/µL, LDH 816 U/L, undetectable haptoglobin) with elevated plasma renin (102 ng/mL/h) and aldosterone (179 pg/mL). Urinalysis showed proteinuria (> 1 g/day) and glomerular hematuria. Brain MRI demonstrated posterior reversible encephalopathy syndrome (PRES), and funduscopic examination revealed hypertensive choroidopathy. Intravenous nicardipine was administered, followed by oral nifedipine, amlodipine, and methyldopa. Hemodialysis was initiated on day 3 and discontinued on day 15. A kidney biopsy was performed on day 38 after lowering blood pressure. It demonstrated FSGS (NOS variant) with endothelial injury, suggesting that compensatory hyperfiltration likely due to LBW-associated nephron deficiency contributed to the development of adaptive FSGS and hypertension. Indicators of renal function, neurological function, and endothelial damage were improved after successful management of blood pressure. The patient was discharged to a rehabilitation facility on day 49 in stable condition.
Our case reinforces LBW as a critical risk factor of hypertension and kidney disease.
