Short Chain Fatty Acids and InflammationAKI is associated with inflammation, both locally in the kidney and systemically. Edema and ischemia of the intestinal wall complicating kidney diseases lead to increased intestinal permeability (leaky gut), which further activates the immune system and can lead to systemic inflammation.
HypertensionRecent studies have focused on the connection between the microbiome and hypertension, a frequent finding in AKI. In a study with mice, eight weeks of high-salt-feeding resulted in hypertension and renal damage. Fecal transplantation from these mice into normal mice resulted in leaky gut and hypertensive renal damage.
SepsisSepsis—life-threatening organ dysfunction caused by a dysregulated host response to infection—is the leading cause of AKI in the intensive care unit.
Amino AcidsAbundant in kidneys of animal models, D-amino acids are metabolites of gut microbiota with distinct functions. One such amino acid, D-serine from intestinal bacteria, showed protective effects in a murine AKI model.
Uremic SubstancesThe gut microbiota generates toxins that are absorbed into the blood and cleared by the kidneys. Dysbiosis can lead to excessive secretion, which can lead to uremia—a buildup of toxins in the blood—which may damage the kidneys.
ProbioticsProbiotics may be useful in AKI in several ways: by altering the gut microbiota composition, restoring mucosal barrier function, and affecting the inflammatory response. A few small studies explored their effect in AKI.
PrebioticsThe role of various prebiotics in CKD has been studied with promising results but a role in AKI is not reported. However, anaerobic fermentation of prebiotics results in the production of short chain fatty acids. Many studies in mice have shown that administration of SCFAs (especially acetate and butyrate) improves outcomes of AKI.
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