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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.
Sjögren’s syndrome (SS) is an autoimmune disorder primarily affecting exocrine glands, but renal involvement such as tubulointerstitial nephritis and, less commonly, glomerular lesions can occur. SS is also associated with autoimmune thyroid disease, and approximately 15–30% of patients develop thyroid dysfunction, most often hypothyroidism. However, hyperthyroidism in SS is rare, and its renal impact remains unclear. We report a case of chronic kidney disease (CKD) in a patient with SS complicated by hyperthyroidism, in which both diseases may have contributed to renal injury.
A 70-year-old woman with a history of SS diagnosed 17 years earlier presented with progressive anorexia and a 10 kg weight loss over six months. Laboratory tests revealed renal dysfunction (eGFR[Cr] 30.4 mL/min/1.73 m²; eGFR[CysC] 13 mL/min/1.73 m²), hematuria (3+), and mild proteinuria. Hyperthyroidism was newly diagnosed, and methimazole therapy was initiated. Despite treatment, proteinuria increased (U-P/Cr 1.13 → 6.16 g/gCr), prompting a kidney biopsy.
Histopathology showed tubulointerstitial fibrosis with lymphocytic and plasma cell infiltration, consistent with SS-associated tubulointerstitial nephritis. No immune complex deposition was observed by immunofluorescence. Electron microscopy revealed subendothelial edema without electron-dense deposits, suggesting endothelial injury rather than immune complex–mediated glomerulonephritis. After prednisolone therapy was initiated, renal function improved (eGFR[Cr] 45.3 mL/min/1.73 m²; eGFR[CysC] 43 mL/min/1.73 m²), and urinary abnormalities resolved. Moreover, the initial discrepancy between creatinine- and cystatin C–based eGFR values normalized after treatment, indicating recovery of hemodynamic stability and thyroid function. The patient has remained stable without recurrence.
This case suggests that renal injury in SS can be exacerbated by hyperthyroidism through hemodynamic and endothelial alterations rather than immune complex deposition. The observed discrepancy—and subsequent normalization—between creatinine- and cystatin C–based eGFR values highlights that thyroid dysfunction can significantly influence renal function estimation. Comprehensive evaluation of kidney function using multiple biomarkers is essential in patients with SS complicated by thyroid abnormalities.
