Acute Kidney Injury and Gut Dysbiosis: A Narrative Review Focus on Pathophysiology and Treatment

Abstract

Acute kidney injury (AKI) and gut dysbiosis affect each other bidirectionally. AKI induces microbiota alteration in the gastrointestinal (GI) system, while gut dysbiosis also aggravates AKI. The interplay between AKI and gut dysbiosis is not yet well clarified but worthy of further investigation. The current review focuses on the pathophysiology of this bidirectional interplay and AKI treatment in this base. Both macrophages and neutrophils of the innate immunity and the T helper type 17 cell from the adaptive immunity are the critical players of AKI-induced gut dysbiosis. Conversely, dysbiosis-induced overproduction of gut-derived uremic toxins and insufficient generation of short-chain fatty acids are the main factors deteriorating AKI. Many novel treatments are proposed to deter AKI progression by reforming the GI microbiome and breaking this vicious cycle. Data support the benefits of probiotic treatment in AKI patients, while the results of postbiotics are mainly limited to animals. Prebiotics and synbiotics are primarily discussed in chronic kidney disease patients rather than AKI patients. The effect of adsorbent treatment seems promising, but more studies are required before the treatment can be applied to patients. Immune therapy and some repurposed drugs such as allopurinol are prospects of future treatments and are worth more discussion and survey.

Keywords: acute kidney injury; dysbiosis; immunity; prebiotics; probiotics; short-chain fatty acids; synbiotics.

Figure 1

The bidirectional interplay between AKI and gut dysbiosis. Note: AKI prompts innate and adaptive immunity, disrupting the epithelial barrier and causing the gut microbiome imbalance. Dysbiosis can also cause breaking of immune and hormonal equilibrium that further worsens kidney function. Abbreviation: IL = interleukin; Mφ = macrophages, MLCK = myosin light chain kinase; Th17 = T helper type 17.