Chronic Kidney Disease Elicits an Intestinal Inflammation Resulting in Intestinal Dysmotility Associated with the Activation of Inducible Nitric Oxide Synthesis in Rat

Chen, Yu; Tan, Shanjun; Wang, Zhen; Deng, Bing; Jin, Li; Wang, Qiang; Zhou, Chunyu; Kang, Xin; Yu, Zhen; Zhuang, Songlin

doi:10.1159/000481618

Cited by 10 publications

(6 citation statements)

References 41 publications

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“…Another pathogenic factor that potentially links CKDrelated gut dysbiosis to constipation may be intestinal inflammation. Yu et al showed that intestinal motility in CKD rats underwent 5/6 nephrectomy was significantly HD hemodialysis, PD peritoneal dialysis decreased compared with that in the control rats [17]. The expression levels of interleukin-6, tumor necrosis factor-α, and inducible nitric oxide synthesis were increased in the gut of uremic rats.…”

Section: Gut Dysbiosismentioning

confidence: 99%

“…Wu et al reported that the colonic transit time of patients treated with hemodialysis (HD) or peritoneal dialysis (PD) was significantly longer than that of age and sex-matched healthy subjects [15]. Delayed intestinal transit was also observed in CKD animal models [16][17][18]. Thus, constipation in CKD may primarily be classified as the slow transit type.…”

Section: Prevalence Of Constipation In Ckdmentioning

confidence: 99%

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Constipation in chronic kidney disease: it is time to reconsider

Ikee

Yano

Tsuru³

2019

Ren Replace Ther

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Constipation is highly prevalent in patients with chronic kidney disease (CKD) and is primarily characterized by decreased intestinal motility. This chronic disorder affects the quality of life of patients. However, nephrologist and dialysis clinicians have long had a disproportionately limited understanding of constipation. Accumulating evidence has revealed a relationship between constipation and cardiovascular disease and CKD. The pathogenesis of constipation in CKD patients is multifactorial: decreased physical activity, comorbidities affecting bowel movement, such as diabetes mellitus, cerebrovascular disease, and hyperparathyroidism, a restricted dietary intake of plantbased fiber-rich foods, and multiple medications, including phosphate binders and potassium-binding resins, have all been implicated. CKD is associated with alterations in the composition and function of the gut microbiota, socalled gut dysbiosis. Recent studies showed that CKD-related gut dysbiosis decreased intestinal motility via intestinal inflammation or the increased generation of gut-derived uremic toxins, such as indoxyl sulfate and pcresyl sulfate. Furthermore, the gastrointestinal secretion of mucin was found to be decreased in CKD animal models, which may delay colonic transit by diminished lubrication in the alimentary tract. Thus, CKD-related gut dysbiosis may play a role in constipation, but limited information is currently available. Since constipation is often intractable, particularly in CKD patients, every available means needs to be employed in its treatment. The effects of probiotics, prebiotics, and synbiotics on the composition of the gut microbiota and gut-derived uremic toxins have been increasingly reported. However, their effects on stool consistency or frequency in CKD patients remain unclear. Some laxatives may be beneficial for improving not only bowel habits but also gut dysbiosis. Further studies are required to elucidate the CKD-specific pathogenesis of constipation and develop novel effective treatment options.

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Section: Gut Dysbiosismentioning

confidence: 99%

Section: Prevalence Of Constipation In Ckdmentioning

confidence: 99%

Constipation in chronic kidney disease: it is time to reconsider

Ikee

Yano

Tsuru³

2019

Ren Replace Ther

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“…The colonic transit time increased from 24 ± 12 h in healthy subjects to 33 ± 14 h in continuous ambulatory peritoneal dialysis patients and 43 ± 22 h in hemodialysis patients [46]. Elongated intestinal transit was observed in the SNx rat model [17][18][19] and the mouse model induced by an adenine-enriched diet [20]. In contrast, oro-anal transit and colonic transit times were decreased in SNx dogs [16].…”

Section: Motility Dysfunction and Gut Barriermentioning

confidence: 99%

Gut–Kidney Axis Investigations in Animal Models of Chronic Kidney Disease

Bartochowski

Gayrard

Bornes

et al. 2022

Toxins

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Chronic kidney disease (CKD) is an incurable disease in which renal function gradually declines, resulting in no noticeable symptoms during the early stages and a life-threatening disorder in the latest stage. The changes that accompany renal failure are likely to influence the gut microbiota, or the ecosystem of micro-organisms resident in the intestine. Altered gut microbiota can display metabolic changes and become harmful to the host. To study the gut–kidney axis in vivo, animal models should ideally reproduce the disorders affecting both the host and the gut microbiota. Murine models of CKD, but not dog, manifest slowed gut transit, similarly to patient. Animal models of CKD also reproduce altered intestinal barrier function, as well as the resulting leaky gut syndrome and bacterial translocation. CKD animal models replicate metabolic but not compositional changes in the gut microbiota. Researchers investigating the gut–kidney axis should pay attention to the selection of the animal model (disease induction method, species) and the setting of the experimental design (control group, sterilization method, individually ventilated cages) that have been shown to influence gut microbiota.

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“…As optimal intestinal motility is critical to nutrition and several biological functions, the loss of normal gut function compromises nutrition and results in prolonged hospital stay 2,5 . GIT dysmotility can be the result of several disease processes, including but not limited to inflammatory bowel disease, 6,7 chronic kidney disease, 8,9 peritonitis, 10,11 hemodynamic instabilities, 12–14 neurodegenerative disorders, 15–17 and spinal cord injury 18 . The pathophysiological mechanisms of GIT dysmotility are multifactorial.…”

Section: Introductionmentioning

confidence: 99%

Erythropoietin promotes functional recovery in a mouse model of postoperative ileus

Elfar

Gurjar

Talukder

et al. 2020

Neurogastroenterology Motil

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Background Dysmotility and postoperative ileus (POI) are major clinical problems after surgical trauma and it is associated with increased intestinal inflammation and oxidative stress. Despite the high occurrence of POI following intra‐abdominal surgeries, no effective treatment is currently available. Erythropoietin (EPO) is a multifunctional tissue‐protective cytokine with potent anti‐inflammatory and anti‐oxidative properties, and it is an FDA approved medicine for clinical use. While both EPO and EPO receptors (EPOR) are widely expressed in the gut, the role of EPO in POI is largely unknown. This study was designed to explore the possible beneficial effect of EPO in a mouse model of POI. Methods Mice were subjected to intestinal manipulation to induce standard POI and intestinal transit time was determined at 24‐h post‐injury with or without EPO treatment (5000 units/kg, once, IP, immediately after intestinal trauma). Intestinal samples were harvested for histological and immunohistochemical analysis. Results Systemic EPO significantly improved intestinal transit time compared with control group and it was associated with significantly increased levels of tissue macrophages and reduced levels of oxidative stress. Conclusions and Inferences This is the first pre‐clinical study to document novel beneficial effects of EPO in gut dysmotility and our findings suggest that the beneficial effects of EPO in POI is predominantly mediated by its anti‐oxidative and immunomodulatory properties.

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Chronic Kidney Disease Elicits an Intestinal Inflammation Resulting in Intestinal Dysmotility Associated with the Activation of Inducible Nitric Oxide Synthesis in Rat

Cited by 10 publications

References 41 publications

Constipation in chronic kidney disease: it is time to reconsider

Constipation in chronic kidney disease: it is time to reconsider

Gut–Kidney Axis Investigations in Animal Models of Chronic Kidney Disease

Erythropoietin promotes functional recovery in a mouse model of postoperative ileus

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