
This study explores the pathophysiological role of D-Alanine (Ala) in AKI. We analyzed the transcripts of the N-methyl-D-aspartate (NMDA) receptor, a receptor for D-Ala, in tubular epithelial cells (TECs). Then, the therapeutic effect of D-Ala was assessed in vivo and in vitro. Lastly, the plasma level of D-Ala was evaluated in AKI patients. D-Ala protected TECs from hypoxia-related cell injury and induced proliferation after hypoxia. The ratio of D-Ala/L-Ala was increased in faeces, plasma, and urine after the induction of I/R. Moreover, enterobacteriaceae, such as Escherichia coli, Klebsiella oxytoca produced D-Ala. The oral administration of D-Ala ameliorated kidney injury after I/R induction in mice. D-Ala has protective effects on I/R-induced kidney injury. Moreover, the plasma level of D-Ala reflects the eGFR in AKI patients. D-Ala could be a promising therapeutic target and potential biomarker for AKI.
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