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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.
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Abstract titles should be brief and reflect the content of the abstract.
Chronic lymphocytic leukemia (CLL) is an uncommon cause of nephrotic syndrome (NS), most often linked to membranoproliferative glomerulonephritis; association with focal segmental glomerulosclerosis (FSGS) is rare. We report steroid-responsive FSGS (tip variant) occurring concomitantly with incident, low-stage CLL and discuss potential pathogenetic links.
Case report
A 78-year-old woman with no prior kidney disease presented with progressive leg edema and dyspnea. Laboratory evaluation revealed hypoalbuminemia (2.4 g/dL), elevated serum creatinine (1.96 mg/dL), microscopic hematuria (100 RBC/HPF), and nephrotic-range proteinuria (urine protein-to-creatinine ratio [UPCR] 22.7 g/gCr). Serological tests were negative for MPO-ANCA, PR3-ANCA, and anti-glomerular basement membrane antibodies, and the proteinuria selectivity index was 0.39. Renal biopsy demonstrated FSGS, tip variant, without crescents or interstitial inflammation. Immunofluorescence was negative for immunoglobulins, complement, fibrinogen, and light chains; electron microscopy showed diffuse podocyte foot-process effacement. On transfer to our hospital, leukocytosis was noted (WBC 18,800/µL; lymphocytes 9,600/µL) with atypical lymphoid cells on smear. Soluble Interleukin-2 receptor was mildly elevated (932 U/μL). Trunk CT and PET-CT showed no lymphadenopathy or abnormal uptake. A bone marrow biopsy revealed proliferation of small, atypical cells characterized by a high nuclear-to-cytoplasmic ratio. immunophenotyping was CD20+, CD5+, CD23+, LEF1+, CD3–, consistent with CLL (Rai 0, Binet A). A watch-and-wait strategy was chosen for CLL. Oliguria progressed to anuria, necessitating hemodialysis. Prednisolone (50 mg/day) was initiated, leading to a rapid reduction of proteinuria, recovery of urine output (1,000 mL/day), and discontinuation of dialysis. Prednisolone was tapered. After discharge, kidney function had improved (creatinine 0.99 mg/dL) with marked proteinuria reduction (UPCR 0.4 g/gCr) and normalization of lymphocyte count (2,600/µL).
This case highlights FSGS associated with incident, low-burden CLL in the absence of leukemic renal infiltration. The clinicopathologic pattern (podocytopathy with negative immunofluorescence, diffuse foot-process effacement, and a prompt response to corticosteroids) supports injury mediated by circulating permeability factors rather than immune-complex deposition. Among proposed mediators, soluble urokinase-type plasminogen activator receptor (suPAR) can activate β3-integrin signaling and induce podocyte dysfunction; suPAR is produced by bone-marrow–derived cells and has been reported to be elevated in several malignancies, including leukemias. Although a direct causal link between CLL and suPAR has not been established, our patient’s findings are compatible with a paraneoplastic, factor-mediated mechanism. This case adds to the limited literature on CLL-associated FSGS and underscores the need for further studies on factor-mediated podocyte injury in lymphoid malignancies.
