Pancreatic Pathology in Chronic Dialysis Patients – an Autopsy Study of 78 Cases

Vaziri, N.D.; Dure-Smith, B; Miller, R C; Mirahmadi, Mahdi

doi:10.1159/000184387

Cited by 118 publications

(112 citation statements)

References 5 publications

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“…2), confirming previous findings in CKD rats [5] and ESRD patients [4]. Colon wall inflammation was significantly reduced in the dh404-treated CKD rats.…”

Section: Histological Findingssupporting

confidence: 88%

“…Almost 30 years ago, Vaziri et al [4] showed the presence of inflammation throughout the gastrointestinal tract (including gastritis, enteritis, and colitis) in a postmortem analysis of 78 hemodialysis patients. Recent studies by our group have demonstrated disruption of the epithelial tight junction throughout the gastrointestinal tract and its association with endotoxemia, local and systemic inflammation, and oxidative stress in animal models of CKD [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

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Role of Nrf2 Dysfunction in Uremia-Associated Intestinal Inflammation and Epithelial Barrier Disruption

et al. 2014

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Background Gut inflammation is prevalent in chronic kidney disease (CKD) and likely contributes to systemic inflammation via disruption of the epithelial tight junction with subsequent endotoxin and bacterial translocation. Aims To study the expression profile of inflammatory and tight junction proteins in the colon from CKD rats compared to healthy controls, and demonstrate the role of Nrf2 (transcription factor nuclear factor erythroid 2-related factor 2) using a potent Nrf2 activator. Methods CKD was induced via 5/6 nephrectomy in Sprague-Dawley rats, and dh404 (2 mg/kg/day) was used to study the effects of systemic Nrf2 activation. The experimental groups included sham, CKD and CKD? dh404 rats. Blood and colon tissues were analyzed after a 10-week study period. Results Colon from CKD rats showed histological evidence of colitis, depletion of epithelial tight junction proteins, significant reduction of Nrf2 and its measured target gene products (NQO1, catalase, and CuZn SOD), activation of NFkB, and upregulation of pro-inflammatory molecules (COX-2, MCP-1, iNOS, and gp91 phox ). Treatment with dh404 attenuated colonic inflammation, restored Nrf2 activity and levels of NQO1, catalase and CuZn SOD, decreased NFkB and lowered expression of COX-2, MCP-1, iNOS, and gp91 phox . This was associated with restoration of colonic epithelial tight junction proteins (occludin and claudin-1). Conclusions CKD rats exhibited colitis, disruption of colonic epithelial tight junction, activation of inflammatory mediators, and impairment of Nrf2 pathway. Treatment with an Nrf2 activator restored Nrf2 activity, attenuated colonic inflammation, and restored epithelial tight junction proteins.

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“…2), confirming previous findings in CKD rats [5] and ESRD patients [4]. Colon wall inflammation was significantly reduced in the dh404-treated CKD rats.…”

Section: Histological Findingssupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Role of Nrf2 Dysfunction in Uremia-Associated Intestinal Inflammation and Epithelial Barrier Disruption

et al. 2014

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“…The high concentration of urea in intracellular and extracellular compartments, due to reduced renal function, generates high influx of this compound into the gastrointestinal tract where microbial ureases catalyze the hydrolysis of urea and generate large amounts of ammonia. Ammonium hydroxide, a by-product of ammonia, increases the intestinal pH, which leads to mucosal irritation and interferes with the growth of commensal bacteria, favoring the establishment of intestinal dysbiosis [78,79]. The negative impact of urea conversion by microbial urease over intestinal epithelial cells was demonstrated in an in vitro study when colonocytes were incubated with urea plus urease.…”

Section: Gut Microbiota In Ckdmentioning

confidence: 99%

The cross-talk between the kidney and the gut: implications for chronic kidney disease

Andrade

Ramos

Cuppari

2017

Nutrire

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In recent decades, special attention has been given to the potential association between the gut ecosystem and chronic diseases. Several features and complications of chronic kidney disease (CKD) may induce an unbalanced gut environment, leading to unfavorable consequences for a patient's health. The first section of this review is dedicated to a description of some aspects of gut microbiota and intestinal barrier physiology. The following section explores the impact of CKD on the gut ecosystem and intestinal barrier, particularly the association with uremic toxins, inflammation, and immunodeficiency. Finally, the review describes the state of the art of potential therapies with prebiotics, probiotics, and synbiotics employed to modulate the gut environment and to reduce the generation of colon-derived uremic toxins in CKD.

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“…Although the underlying mechanism for the relationship between ESRD dialysis and NODM are not fully understood, the factors associated with ESRD dialysis, including being older 2 , having histological abnormalities and dysfunction in the pancreas [4][5][6] , having CVD 2 , including stroke and heart failure, and in a state of chronic inflammation 7 , can induce insulin resistance and the development of type 2 DM.…”

Section: Risk Factors and Possible Mechanismsmentioning

confidence: 99%

“…ESRD patients on dialysis are always older and have multiple comorbidities, including cardiovascular disease (CVD), stroke and heart failure 2 . In addition, many of them have histological abnormalities and dysfunction of the pancreas [4][5][6] . They have also been found to be in a state of chronic inflammation associated with the development of insulin resistance and DM 7 .…”

Section: Introductionmentioning

confidence: 99%

Epidemiology of new-onset diabetes mellitus after dialysis

Chien¹,

Kan²,

Ym³

et al. 2013

OA Nephrology

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IntroductionDiabetic nephropathy is the leading cause of end-stage renal disease in patients undergoing dialysis. Most studies evaluate the association between pre-existing diabetes mellitus, but very few focus on newonset diabetes mellitus after dialysis. Chronic dialysis patients are often older and have multiple comorbidities, including cardiovascular diseases and pancreatic disorder. In addition, these patients have been found to be in a state of chronic inflammation. These characteristics have been associated with the development of insulin resistance and diabetes. Herein, we critically review the epidemiology, risk factors and mortality of new-onset diabetes mellitus after dialysis. ConclusionThe dialysis population has a higher incidence of new-onset diabetes mellitus and a greater risk of mortality than the general population. In addition, the post-transplant incidence of diabetes mellitus, which always occurs the first year after transplant, is much higher than the pre-transplant incidence. However, dialysis modality does not appear to be associated with new-onset diabetes mellitus after dialysis and post-transplant. The independent predictors of newonset diabetes mellitus are old age, cardiovascular comorbidity and dyslipidemia. Other possible contributing factors are inflammation and use of some commonly prescribed drugs for cardiovascular disease, such as statin. Physicians may need to pay more attention to the possibility of new-onset diabetes mellitus when treating high-risk patients undergoing dialysis.

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Pancreatic Pathology in Chronic Dialysis Patients – an Autopsy Study of 78 Cases

Cited by 118 publications

References 5 publications

Role of Nrf2 Dysfunction in Uremia-Associated Intestinal Inflammation and Epithelial Barrier Disruption

Role of Nrf2 Dysfunction in Uremia-Associated Intestinal Inflammation and Epithelial Barrier Disruption

The cross-talk between the kidney and the gut: implications for chronic kidney disease

Epidemiology of new-onset diabetes mellitus after dialysis

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