Brain AKI

Kidney disease is usually complicated by multiple organ dysfunctions like cognitive impairment, and neuropathy. Dipeptidyl peptidase 4 (DPP-4) inhibitors decrease the degradation of glucagon-like peptide-1 (GLP-1) improving glycemic control. The study investigated the effect of acute kidney injury (AKI) on social interaction; and tried to explain the possible underlying role of inflammation, altered energetics, and the possible mode of action of the DPP-4 inhibitor on the brain in AKI. We evaluated the sociability and social novelty indices, platelets, and hippocampal content of mitochondrial enzyme complexes (I-V), serum urea, blood urea nitrogen (BUN), creatine phosphokinase, hippocampal ATP content, hippocampal expression of the glial fibrillary acidic protein (GFAP), activity-regulated cytoskeleton-associated protein (Arc), toll-like receptor 4 (TLR-4), and Nuclear Factor Kappa B (NF-κB). The DPP-4 inhibitor showed a promising role against AKI and its CNS-resulted hippocampal functions’ deterioration by improving inflammatory markers and platelets and hippocampal energetics.