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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.
Potassium (K+) is an essential ion that helps the cells/organs function properly. Systemic K+ deficiency occasionally leads to kidney dysfunction, inflammation, and injury, known as hypokalemic nephropathy (HN). A low-K+ microenvironment in the kidney triggers excessive immune activation, resulting in HN progression. To resolve this malnourished microenvironment, HN is commonly treated with K+ supplementation; however, the long-term prognosis of HN and the role of inflammation have not been thoroughly explored.
Five human kidney biopsy samples of clinically diagnosed HN, sourced from the kidney biopsy database at Jichi Medical University Hospital from 1997 to 2022, were immunostained. Clinical data were followed in the medical records.
Six-week-old C57BL6/J male mice were fed a low-K+ diet or standard chow for 6 weeks, followed by a recovery diet (standard chow) for 6 months. Blood and kidney samples were analyzed.
Five HN kidney biopsy samples of anorexia nervosa, Crohn’s disease, laxative abuse, Sjögren’s syndrome, and licorice overuse were immunostained. Macrophages (CD68) and T lymphocytes (CD3ε) were infiltrated in all samples. T lymphocyte aggregates were observed in HN kidneys with laxative abuse, Sjögren’s syndrome, and licorice overuse. Four in 5 HN patients were followed for a mean duration of 8.4±3.4 years. The change in eGFR was 1.3±2.7 mL/min/1.73m2/year, and no one progressed to end-stage kidney disease.
In mouse experiments, K+ depletion induced by a six-week treatment of a low-K+ diet was sufficient to cause kidney dysfunction, tubular necrosis, inflammation, and fibrosis. A six-month recovery diet following a low-K+ diet effectively restored serum K+ and kidney function. However, histological analysis displayed persistent tubular injury and fibrosis 6 months after recovery. Interstitial aggregates composed of T and B cells developed in the kidney 6 months after recovery from HN, suggesting tertiary lymphoid structure (TLS) de novo formation, which was not observed in age-matched controls or HN kidneys before K+ repletion.
Long-term prognosis of HN of various etiologies showed favorable kidney function. We identified TLS-like lymphocyte aggregates in human HN kidneys. TLSs developed in experimental post-HN kidneys of mice. This study suggests that TLSs may expand during or after the development of HN and serve as a perpetuating inflammatory microenvironment in the HN kidney.
