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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.
IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Obesity and resistant hypertension accelerate CKD progression through glomerular hyperfiltration and podocyte injury. The FLOW trial demonstrated that semaglutide reduced kidney disease events by 24% in diabetic CKD. However, evidence for GLP-1 receptor agonists in non-diabetic glomerular diseases remains unexplored. We present a case of non-diabetic IgAN with resistant hypertension showing remarkable benefits from tirzepatide
A 29-year-old male (BMI 39.1 kg/m²) with biopsy-proven IgAN (2019, Oxford M0E0S1T1C0, 26-50% fibrosis) presented with CKD stage 3b (creatinine 1.8 mg/dL, eGFR 46 mL/min/1.73m²), resistant hypertension (BP 200/100 mmHg on six medications with confirmed compliance for >1 year), baseline proteinuria (UPCR 1.1 g/g), and non-diabetic status (HbA1c 5.5%). SGLT2 inhibitors and spironolactone were previously discontinued due to recurrent balanoposthitis and hyperkalemia. Given advanced fibrosis limiting immunosuppression benefit and patient's priority for weight loss, tirzepatide 2.5 mg weekly was initiated in July 2025 alongside continued RAAS blockade.
Over 10 weeks, weight decreased 6% (112.0→105.75 kg). BP normalized dramatically (200/100→118/70 mmHg, 82/30 mmHg reduction), achieving KDIGO targets and enabling 50% medication reduction (6→3 drugs: discontinued minoxidil, prazosin, clonidine; continued telmisartan, chlorthalidone, cilnidipine). Proteinuria decreased 56% (UPCR 1.1→0.48 g/g), approaching complete remission. Renal function remained stable (eGFR 46 mL/min/1.73m²). HbA1c remained 5.5%. One reversible AKI episode occurred at week 3 (creatinine 1.8→2.1 mg/dL) during intercurrent febrile illness, managed with temporary antihypertensive hold and volume replacement without tirzepatide discontinuation. Creatinine normalized within 3 weeks.
This case demonstrates tirzepatide's remarkable efficacy in non-diabetic IgAN with resistant hypertension, achieving dramatic BP normalization (82/30 mmHg reduction), significant proteinuria reduction (56%), modest weight loss (6%), and 50% medication reduction while maintaining stable renal function. Benefits likely stem from synergistic mechanisms including natriuresis, sympathetic modulation, vasodilation, podocyte protection, and anti-inflammatory effects. The starting dose efficacy suggests potential for further benefit with dose escalation. This represents a paradigm shift toward metabolic intervention in proteinuric non-diabetic CKD with obesity and resistant hypertension. GLP-1 receptor agonists merit investigation as cornerstone therapies alongside RAAS inhibitors and SGLT2 inhibitors, particularly in advanced fibrosis where immunosuppression risks may outweigh benefits.
