Emerging evidence suggests that intestinal dysbiosis and chronic low-grade inflammation play a critical role in the development and progression of diabetic kidney disease (DKD), particularly in the elderly. Reduced microbial diversity, loss of beneficial genera and over-representation of pathogenic bacteria are closely associated with declining kidney function. There is a possible causal relationship between specific gut microbiota profiles and DKD. Experimental models also show that gut-derived metabolites and altered intestinal permeability can promote renal inflammation, fibrosis and metabolic dysfunction. This editorial discusses the implications of these findings for future research and clinical practice, emphasizing the growing potential of microbiota-targeted therapies. Understanding the gut-kidney axis could ultimately open up new avenues for precision nephrology and metabolic care.

Unveiling the gut-kidney dialogue in diabetic kidney disease

Guido Gembillo
Primo
;
Luca Soraci;Luca Visconti
2025-01-01

Abstract

Emerging evidence suggests that intestinal dysbiosis and chronic low-grade inflammation play a critical role in the development and progression of diabetic kidney disease (DKD), particularly in the elderly. Reduced microbial diversity, loss of beneficial genera and over-representation of pathogenic bacteria are closely associated with declining kidney function. There is a possible causal relationship between specific gut microbiota profiles and DKD. Experimental models also show that gut-derived metabolites and altered intestinal permeability can promote renal inflammation, fibrosis and metabolic dysfunction. This editorial discusses the implications of these findings for future research and clinical practice, emphasizing the growing potential of microbiota-targeted therapies. Understanding the gut-kidney axis could ultimately open up new avenues for precision nephrology and metabolic care.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3358548
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