Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by episodes of intravascular hemolysis and thromboembolic complications. However, renal abnormalities are rare and acute kidney injury (AKI) requiring hemodialysis is the exception. This case report describes a patient who was admitted to a hospital for emergency dialysis as the first manifestation of PNH.
A 20-year-old female patient, previously healthy, with no previous history of thrombosis, was admitted to the hospital in January 2025 complaining of fatigue and tiredness. She was lucid and denied recent use of nephrotoxic or illicit drugs or tobacco. Physical examination was unremarkable. Upon admission, the following tests were performed: creatinine: 22.7 mg/dL, urea nitrogen: 367 mg/dL, hyperkalemia: 6.3 mmol/L, and acidosis: BIC: 17.5 mmol/L, associated with anemia without bleeding (Hb: 4.6 g/dL), no thrombocytopenia, and normal bilirubin levels. Hemodialysis was initiated, and extensive diagnostic workup was performed to further elucidate the etiology of the anemia and renal dysfunction.
The tests showed: elevated LDH (LDH > 2000 U/l), reduced haptoglobin, negative direct Coombs, serologies for HIV, hepatitis B and C and syphilis, all non-reactive; FAN, anti-DNA, ANCA, rheumatoid factor, Anti-RO and LA, anti-RNP: all absent, without complement consumption; B-HCG: negative; urinalysis revealed proteinuria, hemoglobinuria and hematuria, absent erythrocyte dysmorphism; 24h proteinuria: 418.6 mg in a urinary volume of 2600ml; serum albumin 2.87, no dyslipidemia (total cholesterol: 182 mg/dl triglycerides: 43.6 mg/dl LDL: 100 mg/dl), normal thyroid function (TSH 2.94 uU/ml) and positive urine culture for multisensitive Escherichia coli 100,000 CFU, patient without urinary complaints. The anemia study showed ferritin: 304 ng/ml, iron 18 ug/dl, transferrin saturation index: 7%, vitamin B12 536 pg/ml, folic acid 17.4 ng/ml and blood count without schistocytes. A renal biopsy was not performed because there was no material available at the hospital. The patient underwent 4 hemodialysis sessions and received pulse therapy with methylprednisolone 1g IV for 3 days followed by prednisone with a gradual reduction until discontinuation in August 2025. Three months after the onset of the clinical picture, the patient showed full recovery of renal function (Creatinine: 0.62 mg/dL in March/2025), but persisted with increased LDH, reduced haptoglobin, anemia, hemoglobinuria, and non-glomerular hematuria. Given the persistent hemolysis, the possibility of paroxysmal nocturnal hemoglobinuria was considered and flow cytometry for PNH was performed, which confirmed the diagnosis. The patient was referred to a hematologist and a complement blocker was started in August 2025.
The diagnosis of PNH as an AKI phenotype is challenging and this case reinforces that it is always important to identify the mechanism of acute kidney injury, as it allows for earlier and more assertive treatment.
