Infection is a common, serious and costly complication in patients with chronic renal failure (CRF) and has been the major cause of high mortality in these patients. Increased evidences suggest that prophylaxis can significantly decrease the prevalence of infections in CRF patients, such as tuberculosis, S. aureus infection and hepatitis virus induced liver diseases. It remains an important issue for clinical nephrologists to investigate and to provide strategies for prevention and treatment of various infections in CRF patients.

Animals ; Bone Marrow Cells ; cytology ; Cell Differentiation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Humans ; Mesenchymal Stromal Cells ; cytology ; Myocytes, Cardiac ; cytology

Objective: Enhanced expression of adhesion molecules on synovial tissu e has been demonstrated in patients with dialysis-related amyloidosis (DRA). T he study was conducted to elucidate the mechanisms by which the expression of adh esion molecules on synovial cells was up-regulated.Methods: Human type-B synov ial cells were cultured in vitro with β2-microglobulin modified with adva nced glycation end products (AGE-β2m) , native β2-microglobulin (β2 m) , tumor necrosis factor-α（TNF-α）and interleukin -1β（ IL-1β）. The expression of intercellular adhesion molecule-1(ICAM-1), vasc ular cell adhesion molecule-1(VCAM-1), and E-selectin was examined by immunofluor esc enct staining and flow cytometer analysis. Results:ICAM-1 and VCAM-1, but not E -selectin, were constitutively expressed on human type-B synovial cells. TNF -α a nd IL-1β enhanced the expression of ICAM-1 and VCAM-1 in a dose- and time - depen dent manner. Neither of these cytokines appeared to induce the expression of E - selectin. Both β2m and AGE-β2m had no direct effect on the expression of the a dhesion molecules.Conclusion: Elevated level of IL-1β and TNF-α in the synov ial tissue may up-regulate the expression of adhesion molecules on synovial cel ls and therefore promote local monocytes infiltration.

The rats were fed on low salt diet for seven days,and then were randomly divided into five groups: control (n=7), CsA treated (n=7), CsA+Verapamil (n=7), CsA+Enalapril (n=7) and CsA+Losartan (n=7).CsA was given by subcutaneous injection (15mg?kg -1?d -1) for four weeks. The apoptosis of tubular and interstitial cells was detected by TUNEL assay. The proliferating cell nuclear antigen and Fas antigen expression were examined by immunohistochemical staining. Apoptosis of tubular and interstitial cells increased in CsA treated rats. CsA+Losartan and CsA+Enalapril treated rats had a statistically significant decrease in apoptosis when compared to CsA treated rats (7.3?1.1 and 6.6?0.8 vs 13.9?1.2 respectively, P

To elucidate the role of reactive carbonyl compounds in the pathogenesis of vascular complication in patients with chronic renal failure or diabetes. Vascular endothelial cells (VECs) were isolated from human umbilical vein and cultured with 3-deoxyglucosone (3-DG) or methylglyoxal(MGO) in vitro. Expression of ICAM-1 and VCAM-1 on the surface of VECs was detected by flow cytometer. The results showed that up-regulation of expression of ICAM-1 and VCAM-1 was observed when either 3-DG or MGO was added into the cultures, which was inhibited by a carbonyl compounds scavanger, aminoguanidine. These data suggested that accumulation of reactive carbonyl compounds in patients with chronic renal failure or diabetes might be involved in the mechanism of arteriosclerosis.

Radioactive ligand receptor binding assay was used to study the binding effect of heparin and low molecular weight heparin (LMWH) on the receptor of advanced glycation end products (AGE) on monocyte surface in normal individual and chronic renal failure (CRF) patients undergoing hemodialysis. The results showed that heparin caused a dose dependent inhibition of receptor binding to AGE, however LMWH did not have such inhibitory effects. The results suggest that heparin could interrupt AGE clearance and degradation, and LMWH had not these effects.

The study was performed to detect the binding proteins for advanced glycation end products (AGEs) on human joint synovial cells (HSCs). Normal human synovial cells (type A and type B cells) were isolated and cultured in vitro. Binding assay was performed with radiolabeled human serum albumin modified by AGE (AGE HSA). Specific binding was defined as total binding minus binding in the presence of excess unlabeled AGE HSA. The result showed that: specific dose dependent binding of 125 I AGE HSA to immobilized HSCs was observed with R=4.90 0.75 10 4 /cell , Kd = 1.27 0.19 10 -6 M in type A HSCs , and R= 3.48 0.32 10 5 /cell, Kd= 1.38?0.16 10 -7 M in type B HSCs. TNF ?,IL 1? and AGE HSA upregulated the expression of AGE binding proteins on HSCs. Normal HSCs express specific AGE binding proteins. TNF ?, IL 1? and AGE HSA upregulate the expression of these proteins, suggesting that joint resident cells may be involved in the pathogenesis of dialysis related amyloidosis.

Objective To investigate hyperhomocysteinemia in chronic renal failure (CRF), its prevalence, etiology and potential relationship to arteriosclerotic events. Methods Plasma total homocysteine (tHcy) was measured in 160 patients with CRF, 31 patients with coronary artery disease and 45 healthy controls by using fluorescence polarization immunoassay. Results Eighty-two percent of CRF patients had hyperhomocysteinemia compared to 22% in patients with coronary artery disease. Mean plasma tHcy level in heomodialysis (HD) patients [(24. 13 ?12. 68) ?mol/L] was significantly higher than that in continuous ambulatory peritoneal dialysis (CAPD) patients [(16. 43?5. 58) ?mol/L] and that in normal controls [(7. 97 ?2. 65)?mol/L] . Plasma tHcy level in dialysis patients with cardiovascular diseases [(27. 12 ?15. 94)?mol/L, n=30] was higher than that in those without clinical manifestation of these complications [(20. 17?8. 71) ?mol/L, n = 62] . The levels of tHcy correlated inversely with Ccr (r = -0. 374, P

To elucidate the effects of pro inflammatory mediators on mRNA expression of AGE receptors in type B synovial cells, type B synovial cells from normal subjects were isolated and cultured in vitro with human serum albumin modified with advanced glycation end products (AGE HSA), tumor necrosis factor ?(TNF ?)and interleukin 1?(IL 1?). The expression of RAGE mRNA and AGE R3 mRNA was examined by RT PCR techniques. TNF ?, AGE HSA and IL 1? up regulated the expression of AGE R3 mRNA in type B synovial cells in a dose and time dependent manner. In contrast, TNF ? and AGE HSA down regulated the expression of RAGE mRNA in a dose and time dependent manner. IL 1? had no effect on RAGE mRNA expression. The regulatory responses induced by AGE HSA were blocked by a neutralizing polyclonal anti human TNF ? antibody, suggesting that the effects of AGE HSA were mediated by TNF ?. The proinflammatory mediators may regulate the gene expression of AGE receptors in type B synovial cells, and the regulatory role of these receptors is different in response to the proinflammatory mediators.

To investigate the clinical characteristics of patients with post traumatic acute renal failure (ARF)effect of early renal replacement therapy on their propnosis, a case control study was carried out in 71 cases of post traumatic ARF and 40 cases of post operative ARF. The effect of early renal replacement therapy on prognosis was evaluated. The incidence of post traumatic ARF in traumatic patients was 1 06%, and 16 21% in ARF. Rhabomyolysis and hypovolemia were the most common causes of ARF. Respiratory failure and coma were the predisposing factors of ARF. The incidence of multiple organ failure was 85 9% and the mortality was 70 4%. Early renal replacement therapy might improve the prognosis. The mortality of patients with Post traumatic ARF remains high, renal replacement therapy should be given as early as possible.