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World J Nephrol. Mar 25, 2026; 15(1): 115357
Published online Mar 25, 2026. doi: 10.5527/wjn.v15.i1.115357
Gut-kidney axis: Dysbiosis and renal disease
Maurizio Salvadori, Giuseppina Rosso
Maurizio Salvadori, Department of Renal Transplantation, Careggi University Hospital, Florence 50139, Tuscany, Italy
Giuseppina Rosso, Department of Nephrology, San Giovanni di Dio Hospital, Florence 50143, Toscana, Italy
Co-first authors: Maurizio Salvadori and Giuseppina Rosso.
Author contributions: Salvadori M and Rosso G equally contributed to generating the manuscript; both authors wrote, controlled and approved the final version of the manuscript.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
Corresponding author: Maurizio Salvadori, MD, Professor, Department of Renal Transplantation, Careggi University Hospital, Viale Pieraccini 18, Florence 50139, Tuscany, Italy. maurizio.salvadori1@gmail.com
Received: October 21, 2025
Revised: November 25, 2025
Accepted: January 14, 2026
Published online: March 25, 2026
Processing time: 144 Days and 10.3 Hours
Abstract

According United States renal data system the morbidity rate for chronic kidney disease (CKD) is 2.5 times than patients not affected by CKD and the mortality rate is 144.9 per 1000 persons-years. The gut microbiota is involved in uremic toxins (UTs) production. This fact was demonstrated by experiments in rats, which revealed better survival in CKD rats that were deprived of the gut microbiota. In men, UT levels are low in CKD patients without a colon. Diet may affect the gut microbiota through food additives such as prebiotics, probiotics and post biotics. Conservation processes and food processing may also affect the gut microbiota. Other factors are food quantity and composition. The gut microbiota may be the cause of UTs production and accumulation in the blood. Additionally, there is interplay among different organs such as liver, kidney and gut. Several theories have been formulated to justify the interplay between the metabolic dysfunctions. In particular, the increase of species such as Eggerthelia lenta, Fusobacterium nucleatum and Alistipes shahii leads to an increase of the aromatic amino acids degradation, and secondary bile acids and trimethyamine oxide biosynthesis in the intestine. This fact determines an increase of the levels of UT precursors such as indole, p-cresol, phenol, phenylacetaleyde, benzoic acid and trimethylamine. Recent studies document the following. The human microbiome project revealed that the gut microbiota may play an important role in both human health and diseases, including kidney disease. Recently, several studies have shown a strict correlation between the gut microbiota and CKD. Probiotics, prebiotics and synbiotics are possible therapies. Probiotics are living microorganisms that, consumed in adequate quantities, are beneficial for the patient, and act on the intestinal microbiome equilibrium. Lactobacilli and Bifidobacteria are common examples of probiotics. Prebiotics are generally fibers not absorbed by the gut, representing a selective nutrient for the microbiome already present in the gut, which favors their growth and activity. Inulin, fructo-oligosaccharides and other fibers are examples of prebiotics. The association and synergism between probiotics and prebiotics is symbiotic.

Keywords: Gut-kidney axis; Chronic kidney disease; Gut microbiota; Dysbiosis; Uremic toxins; Prebiotics; Synbiotics

Core Tip: It has been recently established an axis among gut, liver and kidney. In conditions of gut microbiota modifications, otherwise called dysbiosis, this alteration can favor uremic toxins (UTs) in blood circulation and the progression of chronic kidney disease (CKD). The principal questions are which exactly is the cross talk between gut, liver and kidney, whether a specific microbiota is linked to CKD and in generating UTs, whether gut dysbiosis favors the progression of CKD. Finally, which are the possible therapeutical measures for such condition.