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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.
Chronic kidney disease (CKD) is a global health burden, often culminating in kidney fibrosis, a pathological process marked by excessive extracellular matrix (ECM) deposition and progressive loss of renal function. Fibrosis primarily affects the tubulointerstitium, disrupting homeostasis between tubules, capillaries, and surrounding tissue. Current in vivo and 2D in vitro models fail to recapitulate the complexity of human kidney fibrosis, limiting therapeutic development. There is a pressing need for physiologically relevant humanized 3D models that align with the 3Rs principles and enable disease progression studies and drug screening.
We developed a perfusable 3D bioprinted model of the renal tubulointerstitium using primary human renal proximal tubule epithelial and fibroblast cells encapsulated in a hydrogel composed of decellularized and partially digested extracellular matrix (ddECM) derived from porcine kidney tissue. The mechanical properties of the hydrogel were modulated via vitamin B2 crosslinking. Fibrosis was induced using transforming growth factor-β1 (TGF-β1), and the anti-fibrotic effects of pirfenidone (PFD), a drug approved for pulmonary fibrosis, were evaluated. Gene expression analysis and immunostaining were performed to assess ECM remodeling, cellular differentiation, and drug response.
The bioprinted model successfully mimicked the renal tubulointerstitium and demonstrated progressive fibrotic changes, including increased Young’s modulus, upregulation of fibrotic markers (FN1, VIM2, ACTA2, COL1A1, COL3A1, COL4A1), and collagen I, III, IV deposition. Morphological comparison with human fibrotic tissue confirmed structural resemblance. PFD treatment resulted in downregulation of LOX, SMAD1, and VIM2, along with reduced ECM protein accumulation. However, no significant impact on epithelial-mesenchymal transition or myofibroblast differentiation was observed via α-SMA staining.
This humanized 3D bioprinted model offers a physiologically relevant platform for studying kidney fibrosis and evaluating anti-fibrotic therapies. It overcomes limitations of conventional models, enabling mechanistic insights and high-throughput drug screening for future CKD treatment strategies.
