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Review
. 2024 Nov 17;16(11):495.
doi: 10.3390/toxins16110495.

Gut Dysbiosis and Its Role in the Anemia of Chronic Kidney Disease

Elisabet Coll  1   2 , Secundino Cigarran  3   4 , Jose Portolés  2   4   5   6 , Aleix Cases  2   7
Affiliations
Review

Gut Dysbiosis and Its Role in the Anemia of Chronic Kidney Disease

Elisabet Coll et al. Toxins (Basel). .

Abstract

The gut dysbiosis present in chronic kidney disease (CKD) has been associated with anemia. Factors such as the accumulation of gut-derived uremic toxins, increased gut barrier permeability-induced inflammation, and a reduced intestinal production of short-chain fatty acids (SCFAs), all associated with changes in the intestinal microbiota composition in CKD, may lead to the development or worsening of anemia in renal patients. Understanding and addressing these mechanisms related to gut dysbiosis in CKD patients can help to delay the development of anemia and improve its control in this population. One approach is to avoid or reduce the use of drugs linked to gut dysbiosis in CKD, such as phosphate binders, oral iron supplementation, antibiotics, and others, unless they are indispensable. Another approach involves introducing dietary changes that promote a healthier microbiota and/or using prebiotics, probiotics, or symbiotics to improve gut dysbiosis in this setting. These measures can increase the presence of SCFA-producing saccharolytic bacteria and reduce proteolytic bacteria, thereby lowering the production of gut-derived uremic toxins and inflammation. By ameliorating CKD-related gut dysbiosis, these strategies can also improve the control of renal anemia and enhance the response to erythropoiesis-stimulating agents (ESAs) in ESA-resistant patients. In this review, we have explored the relationship between gut dysbiosis in CKD and renal anemia and propose feasible solutions, both those already known and potential future treatments.

Keywords: ESA resistance; anemia; chronic kidney disease; gut dysbiosis; inflammation; uremic toxins.

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Conflict of interest statement

The authors declare: SC declare funding to conduct clinical trials from AstraZeneca, Bayer, Boehringer Ingelheim, and Novo Nordisk (all to the FIDES Research Institute). Consulting fees are from AstraZeneca, Bayer, Boehringer-Ingelheim, and Novo Nordisk; honoraria for lectures are from AstraZeneca, Novo Nordisk, Bayer, ChemoCentrix, Boehringer-Ingelheim, and Chiesi. These are all outside the scope of the work. AC: AC has received research grants from CSL Vifor; consultancy fees from Astellas, Astra Zeneca, Bayer, Boehringer Ingelheim, GSK, Lilly, Novo Nordisk, Otsuka, CSL Vifor, and lecture fees from Astellas, Astra Zeneca, Amgen, Bayer, Medscape, Novo Nordisk, Sanofi (Mexico), and CSL Vifor. These are all outside of the submitted work. EC and JP declare no conflicts of interest.

Figures

Figure 1
Figure 1
Causes and consequences of gut dysbiosis in CKD patients and its role in anemia.
Figure 2
Figure 2
Therapeutic approaches to prevent/correct renal anemia related to gut dysbiosis.
See this image and copyright information in PMC

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