Association between gut dysbiosis and chronic kidney disease: a narrative review of the literature

Feng, Zhe; Wang, Ting; Dong, Sheng; Jiang, Hongli; Zhang, Jianzhong; Raza, Hafiz Khuram; Lei, Genping

doi:10.1177/03000605211053276

Cited by 34 publications

(37 citation statements)

References 64 publications

(74 reference statements)

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“…Dysbiosis is associated with an increased pro-inflammatory immune response, due to an abnormal proliferation of immune cells and increases the production of pro-inflammatory compounds, such as lipopolysaccharides. 49 Gut dysbiosis furthermore impairs the energy supply to the colonic epithelium and increases epithelial permeability, leading to a “leaky gut.” 50 , 51 In this respect, lyso-Gb 3 increases the biofilm-forming capacity of several individual bacteria, including Bacteroides fragilis . 45 In detail, lyso-Gb 3 also modifies the bacterial composition of the human colon microbiota suspension, increasing bacterial counts of B. fragilis , and modified the formation of short-chain fatty acids, leading to a striking decrease in butyrate concentration.…”

Section: Pathophysiology and Potential Mechanismsmentioning

confidence: 99%

Fabry disease – a multisystemic disease with gastrointestinal manifestations

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2022

Gut Microbes

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Nonspecific gastrointestinal (GI) symptoms, such as postprandial cramping pain, diarrhea, nausea and vomiting are typical symptoms for irritable bowel syndrome or inflammatory bowel disease, but may also be the first symptoms of Fabry disease (FD). This review focus on GI manifestations in FD, by providing an overview of symptoms, a proper diagnosis, an appropriate management by FD-specific and concomitant medications and lifestyle interventions. We provide comprehensive literature-based data combined with personal experience in the management of FD patients. Since FD is rare and the clinical phenotype is heterogeneous, affected patients are often misdiagnosed. Consequently, physicians should consider FD as a possible differential diagnosis when assessing unspecific GI symptoms. Improved diagnostic tools, such as a modified GI symptom assessment scale can facilitate the diagnosis of FD in patients with GI symptoms of unknown cause and thus enable the timely initiation of a disease-specific therapy. Expansive intravenous enzyme replacement therapy with α-galactosidase A or oral chaperone therapy for patients with amenable mutations improve the disease burden including GI symptoms, but a timely start of therapy is crucial for the prognosis. A special diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) or pro- and prebiotics might improve FD-typical GI symptoms. Furthermore, preliminary success was reported with the oral administration of α-galactosidase A. In addition to a timely initiation of FD-specific therapy, affected patients with GI symptoms might benefit from a FODMAP-low diet, pro- and prebiotics and/or low-cost oral substitution with AGAL to support digestion and reduce dysbiosis.

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Section: Pathophysiology and Potential Mechanismsmentioning

confidence: 99%

Fabry disease – a multisystemic disease with gastrointestinal manifestations

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2022

Gut Microbes

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“…A hallmark of CKD is OS which is present in the initial stages of the disease. CKD is strongly associated with age, hypertension, insulin resistance, dyslipidemia, nicotine use, OSA, vitamin D deficiency, air pollution, gut dysbiosis, neuropsychiatric disorders, poor lifestyle, obesity, autoimmune disease, periodontal disease, chronic infection, and hyperuricemia (96,(165)(166)(167)(168)(169)(170)(171)(172)(173)(174)(175)(176). It seems reasonable that one or more of these conditions that increase OS may initiate the onset of CKD.…”

Section: Chronic Kidney Diseasementioning

confidence: 99%

The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress

Bale

Doneen

Leimgruber

et al. 2022

Front. Cardiovasc. Med.

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The formation of an atheroma begins when lipoproteins become trapped in the intima. Entrapped lipoproteins become oxidized and activate the innate immune system. This immunity represents the primary association between lipids and inflammation. When the trapping continues, the link between lipids and inflammation becomes chronic and detrimental, resulting in atherosclerosis. When entrapment ceases, the association between lipids and inflammation is temporary and healthy, and the atherogenic process halts. Therefore, the link between lipids and inflammation depends upon lipoprotein retention in the intima. The entrapment is due to electrostatic forces uniting apolipoprotein B to polysaccharide chains on intimal proteoglycans. The genetic transformation of contractile smooth muscle cells in the media into migratory secretory smooth muscle cells produces the intimal proteoglycans. The protein, platelet-derived growth factor produced by activated platelets, is the primary stimulus for this genetic change. Oxidative stress is the main stimulus to activate platelets. Therefore, minimizing oxidative stress would significantly reduce the retention of lipoproteins. Less entrapment decreases the association between lipids and inflammation. More importantly, it would halt atherogenesis. This review will analyze oxidative stress as the critical link between lipids, inflammation, and the pathogenesis of atherosclerosis. Through this perspective, we will discuss stopping oxidative stress to disrupt a harmful association between lipids and inflammation. Numerous therapeutic options will be discussed to mitigate oxidative stress. This paper will add a new meaning to the Morse code distress signal SOS-stopping oxidative stress.

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“…The association between kidney-gut axis and gut microbiome is bidirectional. The changes in gut environment cause gut dysbiosis [ 39 ]. The interaction between them is a bidirectional relationship, as CKD leads to a shift of healthy intestinal microbiome to a condition of imbalance between healthy and pathogenic bacteria called gut dysbiosis.…”

Section: Microbiome In Chronic Kidney Diseasementioning

confidence: 99%

Microbiome in Chronic Kidney Disease

Tourountzis

Λιούλιος

Fylaktou

et al. 2022

Life

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The gut microbiome is a complex collection of microorganisms with discrete characteristics and activities. Its important role is not restricted to food digestion and metabolism, but extends to the evolution, activation and function of the immune system. Several factors, such as mode of birth, diet, medication, ageing and chronic inflammation, can modify the intestinal microbiota. Chronic kidney disease (CKD) seems to have a direct and unique effect, as increased urea levels result in alteration of the gut microbiome, leading to overproduction of its metabolites. Therefore, potentially noxious microbial uremic toxins, which have predominantly renal clearance, including p-cresyl sulfate, indoxyl sulfate and N-oxide of trimethylamine [Trimethylamine-N-Oxide (TMAO)], accumulate in human’s body, and are responsible not only for the clinical implications of CKD, but also for the progression of renal failure itself. Certain changes in gut microbiome are observed in patients with end stage renal disease (ESRD), either when undergoing hemodialysis or after kidney transplantation. The purpose of this review is to summarize the changes of gut microbiome and the protein bound uremic toxins which are observed in CKD and in different kidney replacement strategies. In addition, we attempt to review the connection between microbiome, clinical implications and immune response in CKD.

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Association between gut dysbiosis and chronic kidney disease: a narrative review of the literature

Cited by 34 publications

References 64 publications

Fabry disease – a multisystemic disease with gastrointestinal manifestations

Fabry disease – a multisystemic disease with gastrointestinal manifestations

The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress

Microbiome in Chronic Kidney Disease

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