b8272d6cd5ef6d502c6b9fa9fe5c08ce 308591.pdf a7e8428d8a5c276c1fdbef838612db70bb912cc7 308591.pdf 3a22c7a73f11ee73025b07c8cf5d04dde98e3c6967ff434bd2a72bb2bdbe485e 308591.pdf Title: Gut Dysbiosis and Its Role in the Anemia of Chronic Kidney Disease Subject: 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: gut dysbiosis; uremic toxins; anemia; ESA resistance; inflammation; chronic kidney disease Author: Elisabet Coll, Secundino Cigarran, Jose Portolés and Aleix Cases Creator: LaTeX with hyperref Producer: pdfTeX-1.40.25 CreationDate: Tue Nov 26 09:09:25 2024 CET ModDate: Tue Nov 26 09:11:56 2024 CET Custom Metadata: no Metadata Stream: no Tagged: no UserProperties: no Suspects: no Form: none JavaScript: no Pages: 23 Encrypted: no Page size: 595.276 x 841.89 pts (A4) Page rot: 0 File size: 1429235 bytes Optimized: no PDF version: 1.7 name type encoding emb sub uni object ID ------------------------------------ ----------------- ---------------- --- --- --- --------- BTFGED+VnURWPalladioL-Bold Type 1 Custom yes yes yes 10 0 BZFQZQ+URWPalladioL-Bold Type 1 Custom yes yes yes 16 0 WSPXTU+URWPalladioL-Roma Type 1 Custom yes yes yes 22 0 SNEXPR+URWPalladioL-Ital Type 1 Custom yes yes yes 27 0 UEMIXH+VnURWPalladioL Type 1 Custom yes yes yes 32 0 HGNLEF+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 71 0 HGNLEH+PalatinoLinotype TrueType WinAnsi yes yes no 74 0 HGNLEJ+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 77 0 HGNLEF+PalatinoLinotype,Bold TrueType WinAnsi yes yes no 85 0 HGNLEH+PalatinoLinotype TrueType WinAnsi yes yes no 88 0 HGNLEJ+PalatinoLinotype,Italic TrueType WinAnsi yes yes no 91 0 LHCXDL+EURM10 Type 1 Builtin yes yes yes 99 0 LGTZLE+CMSY10 Type 1 Builtin yes yes yes 132 0 CRUZTT+VnURWPalladioL-Italic Type 1 Custom yes yes yes 140 0 Jhove (Rel. 1.28.0, 2023-05-18) Date: 2025-03-01 02:49:36 CET RepresentationInformation: 308591.pdf ReportingModule: PDF-hul, Rel. 1.12.4 (2023-03-16) LastModified: 2025-02-28 12:52:54 CET Size: 1429235 Format: PDF Version: 1.7 Status: Well-Formed and valid SignatureMatches: PDF-hul MIMEtype: application/pdf PDFMetadata: Objects: 700 FreeObjects: 1 IncrementalUpdates: 0 DocumentCatalog: PageLayout: SinglePage PageMode: UseNone Outlines: Item: Title: Introduction Destination: section.1 Item: Title: Gut-Derived Uremic Toxins and Anemia in CKD Destination: section.2 Item: Title: Inflammation, Gut Microbiota, Uremic Toxins, and Anemia Destination: section.3 Item: Title: Gut Microbiota and ESA Responsiveness in CKD Patients Destination: section.4 Item: Title: Iron and Its Connection with Gut Microbiota and Host Destination: section.5 Item: Title: Iron Supplementation and Gut Microbiota Destination: section.6 Item: Title: Dietary Patterns, Gut Microbiota, and Anemia in CKD Patients Destination: section.7 Item: Title: Prebiotics, Probiotics, Symbiotics, Gut Microbiota, and Renal Anemia Destination: section.8 Item: Title: Fecal Microbiota Transplantation and Anemia of Chronic Disease Destination: section.9 Item: Title: Roxadustat and Gut Microbiota Destination: section.10 Item: Title: SGLT2i and Anemia: Possible Role of Gut Microbiota Destination: section.11 Item: Title: AST-120 Destination: section.12 Item: Title: Conclusions Destination: section.13 Item: Title: References Destination: section.14 Info: Title: Gut Dysbiosis and Its Role in the Anemia of Chronic Kidney Disease Author: Elisabet Coll, Secundino Cigarran, Jose Portolés and Aleix Cases Subject: 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. 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