The composition of the gut microbiome changes with age. Microbial populations that produce beneficial metabolites needed for optimal tissue function decline in number, while microbial populations that provoke the immune system into chronic inflammatory signaling increase in number. In recent years, researchers have demonstrated a range of specific consequences of gut microbiome aging, relationships with age-related loss of function and disease. This body of literature adds weight to the development of more precise means to produce lasting rejuvenation of the composition of the gut microbiome, an outcome that can be achieved via fecal microbiota transplantation or flagellin immunization, but with relatively little control over the exact outcome.
The gut microbiota is essential for immune function, nutrient absorption, digestion, and pathophysiological processes. However, aging influences alterations in the composition and diversity of gut microbiota. This age-related imbalance in the gut microbial community, characterized by reduced microbial diversity, loss of beneficial bacteria such as butyrate producers, and an increase in pathogenic species, results in gut dysbiosis. Dysbiosis is associated with impaired intestinal barrier integrity, weakened immune function, and elevated systemic inflammation, creating a vicious cycle that accelerates cellular senescence, tissue aging, and age-related kidney diseases.
Renal dysfunction further exacerbates this process by reducing toxin clearance and promoting the accumulation of uremic metabolites, which disrupt gut microbial balance. In turn, gut dysbiosis impairs kidney function, creating a self-perpetuating cycle of microbial imbalance and renal damage. Hence, breaking this vicious cycle of dysbiosis and kidney damage is important. This review sheds light on the bidirectional relationship between gut microbiota and kidney aging. It also highlights the potential of microbiota-targeted interventions to restore microbial balance and delay the onset of age-related issues.
Link: https://doi.org/10.1186/s12986-025-01032-w
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