Serum hepcidin level and its clinical significance in maintenance hemodialysis patients.

Hepcidin is a key protein of iron metabolism, which may play an important role in the prognosis of patients with chronic renal failure on maintenance hemodialysis. The purpose of this study was to investigate the relationship between the prognosis of maintenance hemodialysis patients and serum hepcidin level. We enrolled 60 patients on maintenance hemodialysis and 30 healthy controls from March 2012 to December 2012 in our hospital. Peripheral blood samples were collected to determine hepcidin by an ELISA method. Hepcidin levels of hemodialysis patients were significantly higher than those of the healthy control group. Hepcidin level was positively correlated with the degree of anemia in the dialysis group. Therefore, we conclude that hepcidin level is significantly increased in patients with chronic renal failure on maintenance hemodialysis and that increased hepcidin seriously affects the prognosis of chronic renal failure.

Correlation between hepcidin level and renal anemia.

Anemia in patients with chronic renal insufficiency (CRI) is related to the chronic inflammatory state, low iron absorption rate, and low utilization rate. As a key protein for iron metabolism, hepcidin plays an important role in CRI anemia. The study aimed to determine the correlation between hepcidin level and renal anemia. Ninety CRI anemia patients treated in our hospital from February 2012 to December 2012 were enrolled in the study to compare with a healthy control group of 40 cases by measuring the hepcidin level and analyzing the correlation between hepcidin level and CRI anemia. The hepcidin level was significantly higher in the CRI anemia group than the control group; there was a positive correlation between hepcidin level and serum ferritin as well as IL-6 level. Hepcidin level was significantly related to degree of anemia, indicating that an increase in hepcidin level will result in anemia.

Mesenteric lymph reperfusion exacerbates spleen injury caused by superior mesenteric artery occlusion shock

The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.

Mesenteric lymph reperfusion exacerbates spleen injury caused by superior mesenteric artery occlusion shock.

The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.