Effects of Chronic Renal Failure on Gastrointestinal Motility: A Study on the Changes of Gastric Emptying, Small Intestinal Transit, Interdigestive Myoelectric Complex, and Fecal Water Content

Fu, Rongguo; Wang, Yan; Yuan, Haozheng; Zhou, Jianping; Wang, Li; Liu, Xiaodan; Feng, Mang; Jun, Zhang

doi:10.3109/0886022x.2011.581404

Cited by 19 publications

(28 citation statements)

References 23 publications

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“…In the present study, we therefore chose this model, and used the charcoal transport assay to objectively assess the effect of CKD on intestinal motility. The results showed that CKD induced a progressive decrease in the intestinal transit at all investigated time points, reaching statistical significance level on postoperative weeks 8 and 10, indicating that CKD could indeed decrease intestinal motility, which were consistent with the results reported by others [4,31].…”

Section: Discussionsupporting

confidence: 81%

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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

et al. 2018

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This study was conducted to investigate whether chronic kidney disease (CKD) affects intestinal inflammation and intestinal motility and the underlying mechanisms. Rats were randomized into control group and uremic group. Uremia rats were induced by the 5/6 kidney resection, while the control went through the same procedures but without any kidney resection. Intestinal motility was assessed by charcoal transport assay; intestinal inflammation was assessed by analyses of levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 in the ileum tissue. The inducible nitric oxide synthesis (iNOS) activity was assessed in the ileum tissue. The results showed that the intestinal motility in uremic group was significantly decreased compared with that in the control group on postoperative weeks 8 and 10. Meanwhile, the uremic group presented significantly higher concentrations of TNF-α, IL-6, and IL-10 than control group on postoperative weeks 8 and/or 10, and higher gene expression on postoperative weeks 6, 8, and 10. Furthermore, the intestinal iNOS activity in the uremic group was significantly increased compared with that in control group on postoperative weeks 8 and 10. These results suggest that CKD could induce intestinal inflammation and lead to intestinal dysmotility, which may be associated with iNOS activation in the intestine.

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Section: Discussionsupporting

confidence: 81%

“…In the CKD progression, the intestine and CKD influence each other [1], and intestinal dysmotility often occurs [2][3][4]. In clinical practice, patients with in- testinal dysmotility could present some main symptoms including abdominal bloating and distension and a mix of nausea and vomiting [5].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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“…In humans, CRF is mainly caused by hypertension, glomerulonephritis, and diabetes mellitus 3, 4 . This condition is made worse by a deterioration in nutrition level caused by accumulation of uremic toxins and reduced food intake, which could be attributed to many factors, such as gastrointestinal congestion, loss of appetite, and reduced glomerular filtration rate 4–6 . Compared to patients with other chronic diseases, patients with CRF tend to require longer and more frequent hospitalizations which are associated with higher morbidity and mortality 7 .…”

Section: Introductionmentioning

confidence: 99%

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Luo

Wang

et al. 2017

Sci Rep

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Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H2S) plays important roles in renal physiological and pathophysiological processes. However, whether H2S could protect against CRF in rats remains unclear. In this study, we found that H2S alleviated gentamicin-induced nephrotoxicity by reducing reactive oxygen species (ROS)-mediated apoptosis in normal rat kidney-52E cells. We demonstrated that H2S significantly improved the kidney structure and function of CRF rats. We found that H2S decreased the protein levels of Bax, Caspase-3, and Cleaved-caspase-3, but increased the expression of Bcl-2. Treatment with H2S reduced the levels of malondialdehyde and ROS and increased the activities of superoxide dismutase and glutathione peroxidase. H2S significantly abolished the phosphorylation of extracellular signal-regulated protein kinase 1/2, c-Jun N-terminal kinase, and p38 in the kidney of CRF rats. Furthermore, H2S decreased the expression levels of tumor necrosis factor-α, interleukin (IL)-6, IL-10, and monocyte chemoattractant protein-1, as well as the protein levels of p50, p65, and p-p65 in the kidney of CRF rats. In conclusion, H2S could ameliorate adenine-induced CRF in rats by inhibiting apoptosis and inflammation through ROS/mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways.

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“…Several investigations suggested that there was impaired small intestinal motility [36], impaired intestinal barrier function [37], lower number of crypts, and reduction in epithelial cell in patients with chronic renal insufficiency [3]. In addition, patients with diabetic nephropathy might have more-serious diabetic neuropathy and microangiopathy, which are linked to serious mucosal injuries.…”

Section: Discussionmentioning

confidence: 99%

Type 2 Diabetes Mellitus Is Associated with More Serious Small Intestinal Mucosal Injuries

et al. 2016

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BackgroundClinical and experimental research has revealed that diabetes mellitus (DM) is characterized by intestinal hypomotility, gut microbial dysbiosis, increased gut permeability, microcirculation disorders, circulatory changes, and dysfunction of intestinal stem cells, which may be linked to inflammation of intestinal mucosa. However, the relationship between type 2 DM (T2DM) and macroscopic small intestinal mucosal injuries is still unclear. Therefore, we retrospectively studied capsule endoscopy data to determine the relationship between T2DM and small intestinal mucosal injuries.Materials and MethodsWe compared the records of 38 T2DM patients with those of 152 non-DM patients for small intestinal mucosal injuries. Different types of mucosal injuries and Lewis scores were compared between T2DM and non-DM patients. The relationships between patients with or without different types of diabetic complications and the Lewis score was assessed. Moreover, the relationships between insulin resistance and Lewis score, between HbA1c and Lewis score, were also both assessed.ResultsThe prevalence of a villous edema in subjects with T2DM was significantly higher than in those without DM (P < 0.001), but incidence of ulcers was not different (P = 1.000). With T2DM, the Lewis score was also significantly higher (P = 0.002). In addition, subjects with diabetic nephropathy showed significantly higher Lewis scores than patients without diabetic nephropathy (P = 0.033). In Pearson’s correlation tests, the homeostasis model assessment of insulin resistance (HOMA-IR) value was correlated positively with the Lewis score (γ = 0.175, P = 0.015), but no statistical correlation was found between HbA1c level and Lewis score (γ = 0.039, P = 0.697).ConclusionsSubjects with T2DM, especially those with diabetic nephropathy, have higher Lewis scores and more serious small intestinal mucosal lesions.

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Effects of Chronic Renal Failure on Gastrointestinal Motility: A Study on the Changes of Gastric Emptying, Small Intestinal Transit, Interdigestive Myoelectric Complex, and Fecal Water Content

Abstract: The GI motility of the CRF rats is obviously impaired. This finding may indicate that the effects of CRF on GI motility might be relatively prevalent.

Cited by 19 publications

References 23 publications

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

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

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Type 2 Diabetes Mellitus Is Associated with More Serious Small Intestinal Mucosal Injuries

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