Gut microbiota dysbiosis in AKI to CKD transition

Background and aim: The symptoms of acute kidney injury (AKI) include a sudden drop-in glomerular filtration rate (GFR), a rise in serum creatinine (sCr), blood urea nitrogen (BUN), and electrolytes, which leads to a rapid loss of kidney function. Chronic kidney disease progresses when AKI symptoms persist for over three months or 90 days. Numerous prevalent secondary risk factors, including diabetes, hypertension, obesity, and heart illness, are directly or indirectly linked to the development of AKI and the switch from AKI to CKD. Recently, the change of intestinal bacteria known as "gut dysbiosis" has been linked to distant organ dysfunction, including the heart, lungs, kidneys, and brain. Indirectly or directly, gut dysbiosis contributes to the progression of CKD and AKI. However, the effects of gut dysbiosis and the mechanism of action in the progression from AKI to CKD are unknown or need further investigation. The mechanism by which gut dysbiosis initiates AKI's progression to CKD should be explicitly concerned. The review primarily focuses on the action of gut dysbiosis in kidney disease, the effects of dysbiosis, the characterisation of dysbiosis and its pathogenic products, the various pathogenic routes and mechanism involved in expediting the transition from AKI to CKD. Conclusion: We identified and briefly reviewed the impacts of dysbiosis in various situations such as hypoxia, mitochondrial induced reactive oxygen species (mtROS), aryl hydrocarbon receptor (AhR) activation and microbiota derived uremic toxemic substances profoundly to push AKI to CKD conditions.