51 research outputs found
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Ferric Citrate Attenuates Cardiac Hypertrophy and Fibrosis in a Rat Model of Chronic Kidney Disease.
IntroductionChronic kidney disease (CKD) promotes hypertrophy and fibrosis in heart, and increases the risk of cardiovascular mortality. Ferric citrate is a dietary phosphate binder used to control hyperphosphatemia in CKD patients. It has been shown to raise iron stores, improve anemia and secondary hyperparathyroidism, and decrease vascular calcification in CKD patients. The present study was done to explore the effects and mechanism of actions of ferric citrate on cardiac hypertrophy and fibrosis.Materials and methodsMale SD rats were randomized to CKD (5/6 nephrectomized) and sham-operated control groups. CKD rats were fed regular diet or a diet containing 4% ferric citrate. After 8 weeks, hemoglobin, renal function and cardiovascular endpoints including blood pressure, heart/body weight ratio, serum N-terminal prohormone of brain natriuretic peptide (NT-proBNP), cardiac histology and markers of hypertrophy, fibrosis and inflammation were assessed.ResultsCompared to the controls, untreated CKD group exhibited hypertension, elevated serum urea, creatinine, phosphate, and NT-proBNP concentrations, anemia, cardiomegaly ,cardiac hypertrophy and fibrosis. Treatment with ferric citrate significantly increased hemoglobin and serum iron concentrations, reduced serum phosphate and NT-proBNP levels and ameliorated hypertension, heart/body weight ratio, cardiac hypertrophy, fibrosis and inflammation. In addition, ferric citrate administration reduced the size of cardiomyocytes and expressions of myocardin, transforming growth factor-β, interleukin-6 and monocyte chemotactic protein 1.ConclusionsTreatment with ferric citrate attenuated renal failure and cardiovascular abnormalities including myocardial hypertrophy and fibrosis in CKD rats
Risk of Postoperative Venous Thromboembolism Among Pregnant Women
Venous thromboembolism (VTE) is a critical complication after surgery. Although pregnancy is a known risk factor of VTE, available data on the risk of postoperative VTE are scarce. Using the American College of Surgeons National Surgical Quality Improvement Program database between 2006 and 2012, we matched 2,582 pregnant women to 103,640 nonpregnant women based on age, race, body mass index, and modified Rogers score. Pregnant women, compared with matched nonpregnant women, experienced higher incidence of VTE (0.5% vs 0.3%; odds ratio 1.93, 95% confidence interval 1.1 to 3.37, p = 0.02). Pregnant women also showed higher risk of pneumonia, ventilator dependence ≥48 hours, bleeding, and sepsis than did the counterparts. In conclusion, pregnancy was associated with higher risk of VTE after surgery as well as other postoperative complications. The absolute risk difference was small, and careful evaluation against the potential risk and benefit should be given when surgical treatment is considered among pregnant women
Serum CETP Activity and Risk of Mortality in Patients With End Stage Renal Disease (ESRD) on Maintenance Hemodialysis
Serum Paraoxonase Activity is a Better Predictor of Mortality than Serum HDL Cholesterol Level in Patients on Maintenance Hemodialysis
Serum Aclorein-Modified Apolipoprotein A-I is Significantly Increased in Patients With End Stage Renal Disease on Maintenance Hemodialysis
Association of Serum Paraoxonase/Arylesterase Activity With All-Cause Mortality in Maintenance Hemodialysis Patients.
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[Uremic toxins and gut micro biome].
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
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