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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.
Lithium salts are the first-line treatment for bipolar disorder, a common and severe psychiatric condition. However, long-term use can cause two renal side effects: nephrogenic diabetes insipidus (NDI) and chronic microcystic tubulointerstitial nephropathy. The latter involves collecting duct hyperplasia and remodeling, with expansion of type A intercalated cells (A-ICs). GDF15 (Growth Differentiation Factor 15) is induced by vasopressin (AVP) and promotes A-IC proliferation in acidosis. We hypothesized that GDF15 may link lithium-induced NDI and nephropathy.
Serum GDF15 levels were measured by ELISA in a cohort of 200 lithium-treated patients and correlated with clinical outcomes, including resistance to vasopressin (AVP), overt diabetes insipidus, and microcystic chronic kidney disease. In vitro, mIMCD3 cells were exposed to lithium, and proliferation rate as well as GDF15 expression were assessed in the presence or absence of AVP. In vivo, wild-type and GDF15⁻/⁻ mice were treated with lithium chloride for 28 days. Phenotypic analyses included metabolic cage assessment of diuresis and water intake, collecting duct remodeling evaluated by OMCD microdissection and machine learning–based image analysis, and transcriptomic profiling by bulk RNA sequencing and spatial transcriptomics (10X Genomics Visium HD, 8-μm pixel resolution). Finally, V2 receptor antagonism by tolvaptan was performed in wild-type mice under control or lithium-enriched diet, and GDF15 levels (ELISA, qPCR) as well as collecting duct remodeling were analyzed.
The urinary GDF15-to-creatinine ratio was increased in lithium-treated patients with partial vasopressin (AVP) resistance, and further elevated in those with overt diabetes insipidus, but remained unchanged in patients without renal involvement or with primary polydipsia. In lithium-treated mice, renal GDF15 expression was upregulated and localized predominantly to principal cells, particularly in the inner medulla and in the epithelium lining microcystic dilations. GDF15⁻/⁻ mice exhibited attenuated polyuria and a reduced proportion of type A intercalated cells, with no change in overall tubular hyperplasia. Loss of GDF15 restored AQP2 expression, and gene ontology enrichment analysis of RNA sequencing data revealed in GDF15⁻/⁻ mice a significant upregulation of biological processes related to distal nephron development and sodium and urea transport, together with downregulation of pathways associated with the cell cycle, fibroblast proliferation, and collagen synthesis.
These findings identify GDF15 as a key modulator of lithium-induced nephrogenic diabetes insipidus and collecting duct remodeling. Ongoing experiments involving V2R antagonism will help refine the mechanisms linking GDF15 expression to epithelial plasticity. The V2R–GDF15 signaling axis may define a novel adaptive pathway and represent both a biomarker and a potential therapeutic target to mitigate lithium-associated kidney injury.
