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.
The coexistence of immune-mediated injury from IgA Nephropathy (IgAN) and metabolic damage from Diabetic Kidney Disease (DKD) presents a significant therapeutic challenge. Conventional therapies, particularly corticosteroids, often create a dilemma by compromising glycemic control while attempting to manage autoimmunity. Telitacicept, a novel dual inhibitor of B-lymphocyte stimulator (BLyS) and a proliferation-inducing ligand (APRIL), offers a promising steroid-sparing solution. This case report illustrates the efficacy and safety of telitacicept in the management of this complex dual pathology.
We report the case of a 59-year-old male patient who presented with a chief complaint of foamy urine for two weeks, against a background of an 8-year history of type 2 diabetes. Initial assessment revealed heavy proteinuria (24-hour urinary protein [24h-UP]: 4.39 g) and borderline impaired renal function (serum creatinine [SCr]: 108 μmol/L; estimated glomerular filtration rate [eGFR]: 65.54 ml/min/1.73 m²).
A renal biopsy confirmed the dual pathology: mild mesangial proliferative IgA Nephropathy (Lee class II; Oxford classification M1E0S1T0C0) coexisting with early-stage Diabetic Kidney Disease (Segmental and homogeneous thickening of the glomerular basement membrane (GBM) with arteriolar hyalinosis). Following standard-of-care treatment for diabetes, hypertension, and hyperlipidemia, a critical juncture in his management was a brief trial of targeted-release budesonide, which was promptly discontinued due to intolerable hyperglycemia. This event catalyzed a shift in the treatment strategy.
Subsequently, treatment with telitacicept was initiated, employing a dynamic dose-adjustment strategy based on clinical response:
Initial Phase (Jan-May 2024): 160 mg/week
Intensification Phase (May-Oct 2024): Dose increased to 240 mg/week to achieve deeper remission.
Maintenance Phase (Oct 2024-Present): Dose reduced to 160 mg/week after proteinuria target was met.
Throughout the treatment course, 24h-UP, SCr, and eGFR were closely monitored to assess efficacy and safety.
The introduction of telitacicept resulted in rapid, significant, and sustained clinical benefits.
Proteinuria Remission: The patient's 24h-UP demonstrated a dramatic reduction from a baseline of 4.39 g to a stable level below 0.5 g, representing a greater than 88% decrease and achieving a deep partial clinical remission.
Renal Function Stability: Throughout the follow-up period, his serum creatinine level remained stable around the baseline of 108 μmol/L, with no clinically significant decline in eGFR, indicating excellent preservation of renal function.
Safety and Tolerability: The patient tolerated all dose levels of telitacicept well, with no serious adverse events (SAEs) or drug-related infections reported.
This case suggests that for patients with concurrent IgAN and DKD, precisely targeting the B-cell pathogenic axis with telitacicept may be a superior approach to broad-spectrum immunosuppression. It provides a potent and safe therapeutic option devoid of adverse glycemic effects. This approach has the potential to shift the prognosis for these complex patients from merely delaying progression to actively achieving remission, heralding the emergence of a new, non-corticosteroid treatment paradigm.
