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Diabetes-related kidney disease is one of the most common causes of chronic kidney disease and kidney failure worldwide. It leads to structural and functional changes in the kidneys that eventually lead to kidney failure. The research team identified a signalling mechanism involving FXII and showed that this coagulation protein is increasingly produced when blood sugar is elevated. Irrespective of its role in blood coagulation, FXII has a protective effect on kidney cells: It activates a protein complex via a receptor mechanism that stimulates the formation of free oxygen radicals (oxidative stress). This mechanism remains permanently active, which leads to continuous damage to the DNA and, in the long term, to functional impairment of the kidneys.
Prof. Dr Berend Isermann, first author of the study, explained that the detection of FXII in the urine of diabetes patients offers a new possibility for early diagnosis. The marker could also provide information about the chances of successful treatment. The researchers investigated the mechanism using clinical values, kidney biopsies and urine samples from several human cohorts, including data from the LIFE Adult study at Leipzig University and the HEIST-DiC cohort at Heidelberg University.
Source: Press release University of Leipzig from 10 October 2024
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