Nihon Jinzo Gakkai shi最新文献

A man in his fifties with diabetes had a past history of myocardial infarction and ventricular septal perforation. He underwent hemodialysis about a year ago and was taking amiodarone. He presented with sores and purpura on the lower limbs.-Skin biopsy showed immunofluorescence-negative leukocytoclastic vasculitis. Skin lesions were treated with ointments, which ameliorated the symptoms to some extent, but ulceration relapsed and deteriorated in both number and size. Calciphylaxis was suspected, and a second skin biopsy was performed. No calcium detection,on the arteries was observed, but leukocytoclastic vasculitis was seen. Antineutrophil cytoplasmic antibody-related vasculitis, cryoglobulin vasculitis, or anti-phospholipid syndrome were ruled out by negative findings for autoantibodies. Although he was treated with 30 mg prednisolone, his systemic condition deteriorated, and he died of disseminated intravascular coagulation. Autopsy findings showed no vasculitis in the lung, kidney or intestine, and perimyocardial patch infection was observed.Although calciphylaxis was clinically suspected, his condition was diagnosed finally as cutaneous small-vessel vasculitis.

In the past, little attention had been paid to the intestine and its microbial flora as a potential source of systemic inflammation in chronic kidney disease(CKD). Systemic inflammation plays a central role in progression of CKD and its cardiovascular and various other complications. The gastrointestinal tract houses a large community of microbes that have a symbiotic relationship with the host. The normal microbial flora protects the host against pathogenic microorganisms. It also contributes to the energy metabolism, micronutrient homeostasis and nitrogen bal- ance. Recent studies have revealed significant changes in the composition and function of the microbial flora in CKD patients and animals. These changes are driven by altered intestinal bio- chemical environment caused by: I-heavy influx of urea and uric acid from body fluids into the gastrointestinal tract, II- restrictions of potassium-rich food including fruits and vegetables which as the main source of indigestible complex carbohydrates are the essential nutrients for the guts' symbiotic microbial com- munity, and III- various medications such as phosphate binders, antibiotics etc. Together the changes in intestinal milieu and the resultant microbial dysbiosis play a major role in systemic inflammation and uremic toxicity by several mechanisms : I-generation of several microbial derived uremic toxins such as indoxyl sulfate, p-cresol sulfate and trimethylamine-N-oxide etc. II-reduction of microbial derived micronutrients such a short chain fatty acids (SCFA) which are the main source of nutrients for colonocytes. This is caused by diminished substrates (indigestible complex carbohydrates) which leads to depletion of SCFA-making bacteria. In addition, III-Disruption of the intestinal epithelial barrier by ammonia and ammonium hydroxide generated from hydrolysis of urea by urease-possessing microbial species which are common complications of CKD, and bowel ischemia caused by excessive use of diuretics (in CKD patients) and aggressive ultrafiltration by hemodialysis (in ESRD patients) can impair gastrointestinal epithelial barrier. The resulting breakdown of the gut epithelial barrier (tight junction complex) leads to influx of endotoxin, microbial fragments, and other noxious luminal products in the sub-epithelial tissue and systemic circulation leading to local and systemic inflammation and oxidative stress which are the major cause of morbidity and mortality in CKD population. This review is intended to provide an overview of the effects of CKD on the gut microbiome and intestinal epithelial barrier structure and the potential interventions aimed at mitigating these abnormalities.