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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.
The disorders between kidneys and heart are closely related, and this pathophysiological connection is known as the cardiorenal syndrome. Renal congestion caused by elevated central and renal venous pressures contributes to the progression of kidney injury. Neprilysin (MME; membrane metallo-endopeptidase) is a membrane-bound enzyme that degrades various vasoactive peptides, including natriuretic peptides, adrenomedullin, and angiotensins. Human atrial natriuretic peptide (hANP) is clinically used to treat acute heart failure. However, the role of MME in renal injury induced by renal congestion remains unclear. This study aimed to elucidate the effects of MME deficiency on renal injury in a rat model of renal congestion using Mme knockout (KO) rats generated by genome editing.
The Mme gene was disrupted in Sprague-Dawley rats using the rat Genome-editing via Oviductal Nucleic Acids Delivery (rGONAD) technique, an in vivo clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-based genome editing method. Renal congestion was induced in the left kidney by ligating the inferior vena cava between the right and left renal veins in male Mme KO and wild-type (WT) rats. Three days after surgery, blood pressure was measured using the tail-cuff method. Both the congested left and control right kidneys were harvested and weighed. Gene and protein expression were analyzed by quantitative polymerase chain reaction (qPCR), Western blotting, and immunohistochemistry. Plasma ANP levels were measured by enzyme-linked immunosorbent assay (ELISA).
In WT rats, MME immunostaining was localized to the proximal tubules, whereas it was completely absent in Mme KO rats. Blood pressure and plasma ANP levels were significantly lower in Mme KO rats than in WT rats. The weight of the congested kidney increased in both genotypes but this weight gain was significantly lower in Mme KO rats. qPCR and Western blot analyses showed upregulation of tubular injury markers (KIM1, OPN), fibrosis markers (ACTA2, FN1), and inflammatory markers (CD68) in congested kidneys of both genotypes, with these increases suppressed in Mme KO rats. Immunohistochemistry also confirmed reduced staining of ACTA2, KIM1, and CD68 in the congested kidneys of Mme KO rats compared with WT rats.
MME deficiency attenuated renal interstitial fibrosis, inflammation, and tubular injury induced by renal venous congestion in rats. These findings are consistent with the renoprotective effects of natriuretic peptides and suggest that MME inhibition may provide therapeutic potential against renal injury associated with venous congestion and cardiorenal syndrome.
