Stercoral ulceration results from impaction of hard fecal mass on the colonic wall and is a relatively unknown cause of lower gastrointestinal bleeding. In this report, we describe a case of lower gastrointestinal ble...Stercoral ulceration results from impaction of hard fecal mass on the colonic wall and is a relatively unknown cause of lower gastrointestinal bleeding. In this report, we describe a case of lower gastrointestinal bleeding due to stercoral ulceration resulting from Sevelamer, a drug which is commonly associated with constipation.展开更多
A catalyst system of Sevelamer, a phosphate-binding drug, has been prepared and used in the Knoevenagel reaction of aromatic aldehydes in water to produce substituted electrophilic alkenes. The products were obtained ...A catalyst system of Sevelamer, a phosphate-binding drug, has been prepared and used in the Knoevenagel reaction of aromatic aldehydes in water to produce substituted electrophilic alkenes. The products were obtained in excellent yields. Several novel, related catalytic systems showed promising catalytic properties for aromatic and heterocyclic aldehydes. The Sevelamer catalyst can be recovered using simple filtration and reused numerous times（up to 15 times） in the aqueous Knoevenagel reaction without any significant lowering of activity.展开更多
Back ground: There are no published clinical data in hemodialysis (HD) patients with mineral bone disorder (CKD-MBD) regarding the effect of sevelamer hydrochloride on the absorption of the oral calcitriol. Objectives...Back ground: There are no published clinical data in hemodialysis (HD) patients with mineral bone disorder (CKD-MBD) regarding the effect of sevelamer hydrochloride on the absorption of the oral calcitriol. Objectives: The aim of the present study was to determine the association of the sevelamer hydrochloride and serum 1-25(OH)2D concentration during oral calcitriol therapy. Methods: This was a before-and-after study in HD patients. Forty-six patients co-administered with phosphate-binder and calcitriol for CKD-MBD therapy took lanthanum carbonate (LC) and sevelamer hydrochloride (SH) for 4 weeks, respectively with calcitriol. The serum 1-25(OH)2D concentration was assessed after each period. Results: Serum 1-25(OH)2D concentration was significantly reduced with co-administration of SH compared to LH (mean, calcitriol with LC→SH: 19.9 pg/ml → 14.2 pg/ml, p 2D concentrations after oral calcitriol administration compared to LH in HD patients. When we use SH as a phosphate binder with calcitriol for HD patients with CKD-MBD, we should consider the inhibitory effect of SH on oral calcitriol absorption.展开更多
Chronic kidney disease （CKD） patients are endangered with the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the fatalities. Cardiovascular calcifcations af...Chronic kidney disease （CKD） patients are endangered with the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the fatalities. Cardiovascular calcifcations affect most of the CKD patients. Most of this calcification is related to disturbed renal phosphate handling. Fibroblast growth factor 23 and klotho defciency were incriminated in the pathogenesis of vascular calcification through different mechanisms including their effects on endothelium and arterial wall smooth muscle cells. In addition, deficient klotho gene expression, a constant feature of CKD, pro-motes vascular pathology and shares in progression of the CKD. The role of gut in the etio-pathogenesis of systemic infammation and vascular calcifcation is a newly discovered mechanism. This review will cover the medical history, prevalence, pathogenesis, clinical relevance, different tools used to diagnose, the ideal timing to prevent or to withhold the progression of vascular cal-cification and the different medications and medical procedures that can help to prolong the survival of CKD patients.展开更多
文摘Stercoral ulceration results from impaction of hard fecal mass on the colonic wall and is a relatively unknown cause of lower gastrointestinal bleeding. In this report, we describe a case of lower gastrointestinal bleeding due to stercoral ulceration resulting from Sevelamer, a drug which is commonly associated with constipation.
基金financial support by the National Natural Science Foundation of China (Nos. 21242004, 21302168)
文摘A catalyst system of Sevelamer, a phosphate-binding drug, has been prepared and used in the Knoevenagel reaction of aromatic aldehydes in water to produce substituted electrophilic alkenes. The products were obtained in excellent yields. Several novel, related catalytic systems showed promising catalytic properties for aromatic and heterocyclic aldehydes. The Sevelamer catalyst can be recovered using simple filtration and reused numerous times（up to 15 times） in the aqueous Knoevenagel reaction without any significant lowering of activity.
文摘Back ground: There are no published clinical data in hemodialysis (HD) patients with mineral bone disorder (CKD-MBD) regarding the effect of sevelamer hydrochloride on the absorption of the oral calcitriol. Objectives: The aim of the present study was to determine the association of the sevelamer hydrochloride and serum 1-25(OH)2D concentration during oral calcitriol therapy. Methods: This was a before-and-after study in HD patients. Forty-six patients co-administered with phosphate-binder and calcitriol for CKD-MBD therapy took lanthanum carbonate (LC) and sevelamer hydrochloride (SH) for 4 weeks, respectively with calcitriol. The serum 1-25(OH)2D concentration was assessed after each period. Results: Serum 1-25(OH)2D concentration was significantly reduced with co-administration of SH compared to LH (mean, calcitriol with LC→SH: 19.9 pg/ml → 14.2 pg/ml, p 2D concentrations after oral calcitriol administration compared to LH in HD patients. When we use SH as a phosphate binder with calcitriol for HD patients with CKD-MBD, we should consider the inhibitory effect of SH on oral calcitriol absorption.
文摘Chronic kidney disease （CKD） patients are endangered with the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the fatalities. Cardiovascular calcifcations affect most of the CKD patients. Most of this calcification is related to disturbed renal phosphate handling. Fibroblast growth factor 23 and klotho defciency were incriminated in the pathogenesis of vascular calcification through different mechanisms including their effects on endothelium and arterial wall smooth muscle cells. In addition, deficient klotho gene expression, a constant feature of CKD, pro-motes vascular pathology and shares in progression of the CKD. The role of gut in the etio-pathogenesis of systemic infammation and vascular calcifcation is a newly discovered mechanism. This review will cover the medical history, prevalence, pathogenesis, clinical relevance, different tools used to diagnose, the ideal timing to prevent or to withhold the progression of vascular cal-cification and the different medications and medical procedures that can help to prolong the survival of CKD patients.
