[Relation between bone matrix proteins and monocyte chemoattractant protein-1 in renal small artery in diabetic nephropathy rats].

OBJECTIVE: To observe the expressions of bone matrix proteins and monocyte chemoattractant protein-1 ((MCP-1) in the renal arteriole of diabetic nephropathy (DN) rats and analyze their correlations and roles in diabetic nephropathy. METHODS: Adult Sprague-Dawley male rats were used to establish the animal model of diabetic nephropathy induced by peritoneal injection of 55 mg/kg of streptozocin. Calcium deposit around the renal arteriole was observed by alizarin red staining. The protein and mRNA levels of core-bind factor alpha 1 (cbfalpha1), bone morphogenetic protein 2 (BMP-2) and matrix Gla protein (MGP) in renal arteriole of DN rats were detected by immunohistochemistry, in-situ hybridization and real-time PCR. The biochemical indices were detected by routine test. RESULTS: 1. Blood glucose and Urine protein of 24 h were significantly increased in the renal arteriole of DN rats versus the control rats (P < 0.05), serum creatinine (SCr) and phosphorus were significantly increased from 12 weeks. 2. Little deposit of calcium salt was observed in the renal arteriole of DN rats at the 4th week and a large amount of deposit was observed at 24th week, but no calcium deposit was observed in control rats. 3. Cbfalpha1 and BMP-2 expressions were significantly increased in the renal arteriole of DN rats from 4 to 24 weeks vs. the control rats. MGP mRNA expression in the renal arteriole of DN rats was significantly decreased from 4 to 24 weeks. MCP-1 expression was obviously upregulated in the renal arteriole of DN rats at 24th week versus that at 4th and 12th week. No MCP-1 expression was observed in the renal arterioles of control rats. MCP-1 were positively correlated with the expression of cbfalpha1 and BMP-2. CONCLUSION: Bone matrix proteins has already expressed in renal arteriole before the formation of vascular calcification. MCP-1 can affect the expression of cbfalpha1, BMP-2; cbfalpha1, BMP-2, MGP and MCP-1 may be involved in the formation of vascular lesions of DN.

[Comparison of the effects of alpha-keto/ amino acid supplemented low protein diet and diabetes diet in patients with diabetic nephropathy].

OBJECTIVE: To investigate if a-keto/amino acid supplemented low protein diet can slow down the progression of diabetic nephrophathy in comparison with non-supplemented diabetes diet. METHODS: A prospective, randomized, controlled clinical study was conducted. Twenty three cases of type 2 diabetic nephropathy in IV stage were randomly divided into alpha-keto/amino acid supplemented diet group (trial group) and conventional diabetes diet group (control group), The treatment duration was 52 weeks. 24 h urine protein was measured at 0, 12, 20, 36 and 52 weeks. Before and after the 52 weeks treatment, all the patients received the measurement of glomerular filtration rate (GFR), blood glucose, blood lipids, inflammatory markers, as well as nutritional status. RESULTS: After the treatment for 20, 36, 52 weeks, mean 24 h urine protein decreased significantly in trial groups (P < 0.05), and 24 h urine protein in trial group were significantly decreased (P < 0.05) compared with control group in 20 weeks after treatment. Either in trial group or in control group, GFR remained relatively stable during the observation period. Nutrition status, inflammatory markers, and serum calcium, phosphorus levels between the two groups were no significantly difference. The adverse events experienced by the patients in trial group were similar and consistent with the patients underlying renal diseases. CONCLUSION: Alpha-keto/amino acid can reduce proteinuria more effectively, while improve renal function and nutritional status in diabetic nephropathy patients with well-toleration.

[Influence of high glucose and mannose binding lectin complement pathway activation to IL-6 and TNF-alpha's expression by human renal glomerular endothelial cells].

OBJECTIVE: To investigate the effect of high glucose and mannose binding lectin (MBL) complement pathway activation's effect on expression of Interleukin-6 (IL-6) and Tumor necrosis factor-alpha (TNF-alpha) from human renal glomerular endothelial cells (HRGEC), to explore unknown pathogenesy of diabetic nephropathy. METHODS: Normal HRGEC was divided randomly into normal glucose group(5 mmol/L D-glucose), manicol group (5 mmol/L D-glucose+25 mmol/L manicol) and high glucose group (30 mmol/L D-glucose). Real-time PCR was used to detect IL-6 and TNF-alpha mRNA expression in each group, Euzymelinked Immunosorbent Assay (ELISA) was performed to examine the protein expression of IL-6 and TNF-alpha in supernatant after 24 hours' culture. HRGEC was then randomly divided into two groups: single high glucose group and high glucose + MBL group. After 24 hours' culture with 30 mmol/L D-glucose, 30% MBL deficiency human serum was added into two groups, 1 microg/mL MBL was only added into high glucose + MBL group, continued the culturation for another 4 hours. Flow cytometry and immunofluorescence technique were applied to evaluate MBL, C3 and membrane attacks complex (MAC) deposition on cell surface respectively. Real-time PCR and ELISA were performed to examine mRNA and protein expression of both IL-6 and TNF-alpha in each group. RESULTS: Compared with normal glucose group and manicol group, the mRNA and protein expression of IL-6 and TNF-alpha in high glucose group were increased (P < 0.05). Flow cytometry confirmed obvious MBL and C3 co-deposition and Immunofluorescence confirmed obvious MAC deposition on cell surface in high glucose+ MBL group. Compared with single high glucose group, the mRNA and protein expression of IL-6 and TNF-alpha in high glucose+ MBL group were significantly higher (P < 0.05). CONCLUSION: High glucose can bring inflammatory factors' overexpression from cultured HRGEC; high glucose together with MBL can bring MBL complement pathway activation and inflammatory factors' overexpression, this indicates that the activation of MBL complement pathway may be a potential unknown pathogenesy of diabetic nephropathy and its proinflammatory status.

[Relationship between activation of mannan-binding lectin complement and NF-kappaB in diabetic nephropathy].

OBJECTIVE: To study the activation of mannose-binding lectin (MBL) complement in STZ-induced diabetic nephropathy (DN) rats and its relationship with NF-kappaB. METHODS: Sprague-Dawley (SD) rats were randomly divided into two groups: normal control and diabetic nephropathy. Diabetes was induced by intraperitoneal injection of STZ. Five rats were sacrificed at the end of week 1, 2, 4, 8 respectively. Blood glucose, 24 h urine, 24 h urinary albumin, serum creatinine (Scr), body mass and kidney mass were examined at the same time points respectively. Creatinine clearance and renal hypertrophy index were calculated. The renal expression of MBL, membrane attack complex (MAC) and NF-kappaB were determined by immunohistochemistry. RESULT: MBL, MAC and NF-kappaB expression were significantly increased in glomerulus of diabetic nephropathy rats compared to the controls. The expression of MBL was positively correlated with NF-kappaB expression. CONCLUSION: The activation of mannose-binding lectin complement participates in the onset and development of DN.

[Influence of mannose binding lectin to expression of TGF-beta1 and NF-kappaB in high concentration of glucose cultured human renal glomerular endothelial cells].

OBJECTIVE: To investigate the effect of mannose binding lectin (MBL) complement pathway on expression of transforming growth factor-beta1 (TGF-beta1) and NF-kappaB in cultured human renal glomerular endothelial cells (HRGECs) stimulated by high concentration of glucose. METHODS: Human glomerular endothelial cells in culture were randomly divided into 5 groups according to different managements: normal concentration of glucose as controlled group, MBL + normal concentration of glucose group, high concentration of glucose, MBL + high glucose and MBL + high glucose + MBL blocker respectively. Flow cytometry was used to detect the depositions of MBL and C3 on the surfaces of HRGECs. Real-time PCR method was used to detect the mRNA levels of TGF-beta1. Human TGF-beta1 ELISA kit was used to detect the concentration of TGF-beta1 in supernatant fluid. ESMA was used to detect the activity of NF-kappaB in HRGECs. RESULTS: Compared with the normal glucose group and high glucose group, the depositions of MBL, C3 were apparently increased in MBL + high glucose group (P < 0.05). Expression of TGF-beta1 were significantly higher (P < 0.05) in MBL + high concentration of glucose groups than the normal glucose group and the high concentration of glucose group. Compared with the high glucose group, the activity of NF-kappaB in HRGECs was apparently increased in MBL + high glucose group, which could be significantly downregulated by MBL blocking antibody. CONCLUSION: High concentration of glucose can increase the expression of TGF-beta1 of cultured human glomerular endothelial cells. At the same time, high glucose together with MBL can up regulate the expression of TGF-beta1 and the activity of NF-kappaB in HRGECs.

[Effect of high concentration of glucose on thickness of glycocalyx and expression of syndecan-1 and glypican-1 in cultured human renal glomerular endothelial cells].

OBJECTIVE: To investigate the influence of high concentration of glucose on the thickness of Glycocalyx and expression of core protein Sydecan-1 and Glypican-1 in cultured human renal glomerular endothelial cells (HRGECs). METHODS: HRGECs in culture were randomly divided into 3 groups, high concentration of glucose (30 mmol/L D-glucose, high glucose group), normal concentration of glucose as controlled group (5 mmol/L D-glucose+25 mmol/L mannitol, normal control group), and mannitol group (30 mmol/L mannitol) respectively. After 72 hours, confocal laser scanning microscopy (CLSM) was used to observe and characterize the fully hydrated glycoalyx of HRGECs. Real time quantitative PCR and Western blot were applied to detect the mRNA levels and protein expression of Syndecan-1 and Glypican-1, and the fluorescence microscope were used to observe the immunofluorescence change of Syndecan-1 and Glypican-1. RESULTS: Compared with normal control group, the thickness of Glycocalyx on the surface of HRGECs in high glucose group decreased to 36.8% (P < 0.05). Immunofluorescence shows the depositions of Syndecan-1 and Glypican-1 were weakened in high glucose group. The mRNA and protein expression of Syndecan-1 and Glypican-1 were significantly decreased (P < 0.05) compared with normal control group and mannitol group. CONCLUSION: High concentration of glucose can reduce thickness of Glycocalyx on the surface of human glomerular endothelial cell. At the same time, high glucose can decrease the expression of core protein Sydecan-1 and Glypican-1 of HRGECs.

[Effects of high glucose on expression of core binding factor alpha1 and osteocalcin in vascular smooth muscle cells].

OBJECTIVE: To investigate the effects of high glucose on expression of core binding factor alpha1 (cbfalpha-1) and osteocalcin (OC) in vascular smooth muscle cells (VSMCs), and discuss the mechanism of small vessels calcification induced by high glucose (GS) in vitro. METHODS: The primary cultured VSMCs from rats' aortic segments were divided into three groups, including normal control group (5 mmol/L D-glucose), high glucose group (25 mmol/L D-glucose) and mannitol group (5 mmol/L D-glucose plus 25 mmol/L mannitol). We measured quantitatively the calcium deposition in VSMCs and investigated the calcium extent of VSMCs by alizarin red stain in each group. The mRNA levels of cbfalpha-1 and OC were measured by real-time PCR, and the protein expression levels of cbfalpha-1 and OC were examined by Western blot. The activity of alkaline phosphatase was measured by alkaline phosphatase activity testing kit, and the protein level of alpha-smooth muscle actin (a-SMA) was detected by immunohistochemistry. RESULTS: When compared with the normal group and mannitol group, the high glucose group showed that the calcium deposition and calcium extent of VSMCs increased obviously, the mRNA and protein levels of cbfalpha-1 and OC also increased significantly (P < 0.05), while the protein level of alpha-SMA decreased (P < 0.05), which were in a dose-dependent manner. The level of alkaline phosphatase activity of VSMCs was approximately doubled in high glucose group. CONCLUSION: The mechanism of high glucose induced calcification in VSMCs may be due to the increased expression of cbfalpha-1 and OC. High glucose decrease the expression of alpha-SMA in VSMCs, which could induce the transdifferentiation from RVSMCs to osteoblast-like cells.

[Effects of valsartan on the renal vascular endothelial growth factor and its receptor flk-1 of diabetic rats].

OBJECTIVE: To explore effects of valsartan on expression changes of vascular endothelial growth factor (VEGF) and its receptor Flk-1 in diabetic rat kidney. METHODS: To establish the diabetic nephropathy (DN) rat models and divide the experiment rats into three groups--the DN group, the valsartan group and the control group, and use the reverse transcriptase polymerase chain reaction (RT-PCR), Western Blotting and immunohistochemical techniques to detect the expression of VEGF and Flk-1, and detect the urine protein and glomerular area and volume, then analyze the relationship of the data. RESULTS: The mRNA and protein expression of VEGF and Flk-1, the urine protein and glomerular area and volume in the DN were higher than those in the control group and valsartan group (P < 0.05). VEGF and Flk-1 were positively correlated with the urine protein and glomerular area and volume (P < 0.05). CONCLUSION: VEGF and Flk-1 play an important role in the pathogenesis of DN, of which over-expression may lead to the damage of kidney. The angiotensin II receptor antagonist--valsartan can protect kidney through the non-hemodynamic mechanism of inhibiting the abnormal expression of VEGF and Flk-1.

[Expression of VEGF in kidney of diabetic rats].

OBJECTIVE: To investigate the expression of vascular endothelial growth factor (VEGF) in the kidney of diabetic rats and probe its relationship with the development of diabetic nephropathy (DN). METHODS: Diabetes mellitus was induced in SD rats by Streptozotocin. The renal tissues of rats were taken out at 2, 4, 8, 12, 16, 20 and 24 weeks after operation. The expression of VEGF was assessed by immunohistochemistry methods. VEGF mRNA in kidney was detected by RT-PCR at the same time points. The levels of VEGF mRNA and immunostaining were quantified by computer image analysis. The relationships of VEGF with the indices of renal damage, including renal/body weight, urinary protein excretion, glomerular volume and glomerular area, were analyzed. RESULTS: The expression of VEGF mRNA in diabetic kidney was significantly up-regulated after operation from 2 weeks to 24 weeks with the peak level at 20 weeks, when compared with control at the same time-points. The positive results of VEGF staining in diabetic glomeruli was increasingly observed after operation from 2 weeks to 24 weeks, with the peak at 20 weeks. The positive results of VEGF staining in diabetic tubuli was increasingly seen from 2 weeks to 24 weeks, with the peak at 8 weeks. CONCLUSION: VEGF level is increased continuously in the diabetic kidney of rat. The increased expression of VEGF is mainly located in the glomeruli at the early and middle stages, and is in the tubuli at the middle and late stages. VEGF expression in the diabetic kidney of rat is related to the development of renal changes.

[Effects of losartan on expressions of plasminogen activator and plasminogen activator inhibitor-1 of rat proximal tubular epithelial cells cultured with high glucose].

OBJECTIVE: To investigate the effects of high glucose on expressions of plasminogen activator (PA) and plasminogen activator inhibitor-1 (PAI-1) of rat proximal tubular epithelial cells, and the role of angiotensin II receptor antagonist Losartan. METHODS: The cultured NRK-52E cells (a renal proximal tubular epithelial cell line of rat origin) were divided into five groups: control group, mannitol group (5 mmol/L D-glucose plus 25 mmol/L mannitol), high glucose group (30 mmol/L D-glucose), losartan group (10(-3) mmol/L losartan), high glucose plus losartan group (30 mmol/L D-glucose plus 10(-3) mmol/L losartan). Semi-quantity RT-PCR was used to detect the expression of PA/PAI-1 mRNA. RESULTS: Compared with control group, the high glucose group decreased the expressions of tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA) mRNAs (P < 0.01) and increased PAI-1 mRNA expression (P < 0.01) in cultured NRK-52E cells. Losartan could reverse partly the expression of PA/PAI-1 mRNA. Compared to high glucose group, the PA mRNA expression was significantly increased (P < 0.01) and the PAI-1 mRNA expression was decreased greatly (P < 0.01) to high glucose plus losartan group. CONCLUSION: The abnormal expression of PA/PAI-1 mRNA may play an important role in the accumulation of extracellular matrix (ECM) of diabetic nephropathy (DN). Losartan may keep the balance of PA/PAI-1 and have a protective effect on DN.

[The expression and significance of the angiopoietin-1 in the kidney of diabetic rats].

OBJECTIVE: To explore the expression and significance of angiopoietin-1 (Ang-1) in the renal tissue of diabetic rats. METHODS: The SD rats were divided into the diabetic and control groups. The diabetic group was treated by streptozotocin. The expression of Ang-1 in renal tissue was detected by RT-PCR and immunohisochemistry at 2, 4, 8, 12, 16, 20 and 24 weeks. The level of Ang-1 was quantified by computer image analysis. The relationship between Ang-1 and the index of renal damage including renal/body weight, urinary protein excretion, glomerular volume, and glomerular area was analyzed. RESULTS: Ang-1 mRNA in diabetic renal tissue was significantly upregulated at 4 and 8 weeks, compared with diabetic group at other time points or control group at the same time points, and then downregulated gradually after 12 weeks. The level of Ang-1 mRNA decreased significantly as compared with control group at 24 week. Ang-1 was outstandingly expressed in glomeruli. From 4-week to 24-week, the number of Ang-1 staining in diabetic glomeruli increased significantly as compared with control group, being maximal at 4 and 8 weeks, and subsequently decreased after 12 week. Ang-1 level was correlated with renal/body weight, glomerular volume, glomerular area, and urine protein excretion, respectively. CONCLUSION: The change of Ang-1, which is early upregulation and late downregulation, exists in diabetic renal tissue. The unusual expression of Ang-1 is partly connected with the renal changes of diabetic rats.

[Effect of rosiglitazone on integrin beta1 expression and apoptosis of proximal tubular cell exposed to high glucose].

OBJECTIVE: To evaluate the effect of rosiglitazone (ROS) on integrin beta1 expression and apoptosis of proximal tubular cell exposed to high glucose. METHODS: The proximal tubular cells of rats were cultured in vitro and divided into 6 groups: control group, normal glucose (5 mmol/L) group, high glucose (30 mmol/L) group, only ROS (10 micromol/L) group, glucose (30 mmol/L)+ROS (5 micromol/L) group, and glucose (30 mmol/L) +ROS (10 micromol/L) group. The cells were cultured for 48 hrs and the integrin beta1 expressions were detected by Western blot and RT-PCR; The apoptosis was evaluated by flow cytometry after the cells were cultured for 24, 48, 72 hrs. RESULTS: The expressions of integrin beta1 protein and mRNA of high glucose (30 mmol/L) group were significantly increased as compared with control group and normal glucose (5 mmol/L) group. The integrin beta1 of glucose (30 mmol/L)+ROS (5 or 10 micromol/L) group was decreased as compared with high glucose group (P < 0.05). Flow cytometry demonstrated the decreased apoptosis to be with time-dependence. CONCLUSION: ROS can strikingly inhibit the expression of integrin beta1 in proximal tubular cells exposed to high glucose, with a marked dose-dependent manner. The effect of ROS on cell apoptosis may be relevant to integrin beta1.

[Effects of rosiglitazone on the expression of beta1, integrin and ICAM-1 in high glucose-induced rat glomerular mesangial cells].

OBJECTIVE: To observe the effects of PPARgamma activators thiazolidinediones (Rosiglitazone) on the expression of intercellular adhesion molecule-1 (ICAM-1) and beta1 integrin in high glucose-induced rat glomerular mesangial cells (GMC) in order to elucidate the relationship between PPARgamma and adhesion molecules. METHODS: Rat HBZY-1 GMCs were cultured in vitro and divided into 9 groups: Normal Glucose group (N), High Glucose group (H), Mannitiol group (M), Normal and High Glucose plus 1, 5, 10 micromol/L Rosiglitazone. Every group was treated for 24 hours. The expression of ICAM-1 was measured by immunohistochemistry, the expression of beta1 integrin by indirect immunofluorescence staining and flow cytometry. RESULTS: It was found that high glucose can significantly increase the expression of ICAM-1 and beta1 integrin in GMCs, which is independent of the osmotic pressure. Rosiglitazone can inhibit the expression of ICAM-1 and beta1 integrin in normal and high glucose treated GMCs, and the inhibition is stronger in high glucose treated-group, which is in a dose-dependent manner. The expression of beta1 integrin is positively correlated with ICAM-1. CONCLUSION: Adhesion molecules involves in the pathogenesis of diabetic nephropathy (DN). PPARgamma activators-Rosiglitazone may exert effect on mesangial expansion and glomerulosclerosis in DN through the inhibition of expressions of adhesion molecules induced by high glucose.

[Effects of N-linked oligosaccharide chains on expression of integrin beta1 and apoptosis in glomerular mesangial cells].

OBJECTIVE: The effects of N-linked oligosaccharide chains (TM), an inhibitor of N-glycosylation of proteins, on the expression of beta1 integrin and the apoptosis of glomerular mesangial cells (GMC) were observed for exploring the role of inhibitors of N-linked oligosaccharide chains in cell apoptosis, proliferation, and expression of beta1 integrin and cyclin D1, and hence finding a new approach to the synteresis of proliferative nephropathy. METHODS: Cultured rat mesangial cells were divided into 4 groups: control group, and 0.5, 1.0 and 2.0 microg/mL TM-treatment groups. The expression of beta1 integrin and apoptosis rate were measured by flow cytometry; the expression of cyclin D, was measured by immunohistochemistry, and proliferation of GMCs was measured by MTT. RESULTS: The expression of beta1 integrin and cyclin D1 were decreased notably by inhibitors of N-linked oligosaccharide chains-TM. TM increased apoptosis and decreased the proliferative abilitiy of cells, and all the effects of TM were dose-dependent. CONCLUSION: Through repressed glycosylation of glycoprotein, TM can suppress the expression of beta1, integrin, affect the adhesion of cells, and increase the apoptosis rate; at the same time, the expression of cyclin D1 and the proliferative ability of cells were decreased, and all these were dose-dependent.

[Expression level of cubilin in the rat model of diabetic nephropathy].

OBJECTIVE: To observe the expression level of Cubilin in the renal tubules of rats with STZ-induced diabetic nephropathy, to assess its correlation with 24 hours' albuminuria, and to investigate the mechanisms of tubular dysfunction at the early stage of diabetic nephropathy. METHODS: Diabetic nephropathy was induced in Sprague-Dalwley rats by intraperitoneal injection of STZ, while the rats of normal group were injected with normal saline. Biochemical indices of blood and urine specimens were observed in both groups at weeks 2, 4 and 6 respectively. The renal expression levels of Cubilin in the two groups were determined by immunohistochemistry and RT-PCR. RESULTS: The expression level of Cubilin in the diabetic nephropathy group was significantly decreased at week 2 after operation (P < 0.05), and it continued to decrease from week 2 to week 6. Also there was significant difference between each two time-points (P < 0.05), and the Cubilin expression level was negatively correlated with albuminuria (P < 0.01). CONCLUSION: The decreased expression level of Cubilin in early-stage diabetic nephropathy rats may partly contribute to the development of microalbuminuria. Cubilin can be regarded as one of the early markers when tubular dysfunction develops in the case of diabetic nephropathy.

[Epidemiology of cardiovascular risk in Chinese chronic kidney disease patients].

OBJECTIVE: To identify the risk factors associated with cardiovascular disease (CVD) in Chinese chronic kidney disease (CKD) patients. METHODS: As part of a multicenter Chinese cohort study, the clinical data associated with CVD of 1239 patients with CKD (stage 2 - 5) hospitalized in 7 grade 3A hospitals distributed in 5 regions of China 2002 - 2003 were collected. Logistic regression model was used to analyze the association between CVD and the demographic variables, lifestyle, medical history, medication, physical examination, and laboratory variables. RESULTS: (1) Increase of serum C-reactive protein (CRP, cut off > 10 mg/L) was an independent risk factor for development of coronary artery disease (CAD) (OR 2.13; 95% confidence interval [CI], 1.32 - 3.43). 21.5% of the patients in this group showed a value of CRP > 10 mg/L. (2) Being female, anemia, and systolic hypertension were the major determinants of the development of left ventricular hypertrophy (OR 2.99, CI 2.09 - 4.26; OR 2.66, CI 1.19 - 3.57; and OR 1.02, CI 1.00 to -1.02). 54.2% of the patients in this group had their systolic pressure controlled under 140mmHg, and only 15% of the patients in this group had their hemoglobin remain at the level >or= 110 g/L. (3) There was a significant interaction between the calcium-phosphate product and congestive heart failure (CHF) (OR 1.023, CI 1.01 - 1.03). 25.9% of the patients in this cohort had their calcium-phosphate product >or= 55. (4) Hypoalbuminemia (OR 6.01, CI 1.25 - 28.96) and diastolic hypertension (OR 1.05, CI 1.00 - 1.09) played major role in determining cerebrovascular accidents (CVA). In these cohort the prevalence of hypoalbuminemia was 37.3%. (5) Diabetes was associated with CAD (OR 2.34), CHF (OR 1.97), and CVA (OR 4.40), although its prevalence was lower in Chinese CKD patients (20%). Age was the risk factors of CAD (OR 1.04) and CVA (OR 1.22). Hypertension was associated with LVH (OR 1.016), CHF (OR 1.02), and CVA (OR 1.04). CONCLUSION: CKD is associated with nontraditional risk factors for the development of CVD, including chronic inflammation, malnutrition and calcium-phosphate disorders. Particular care must be taken to give optimal treatment for the most important CVD risk factors active in Chinese CKD patients, e.g. anemia and hypertension.

[Cardiovascular disease in Chinese chronic renal insufficiency patients-epidemiology survey].

OBJECTIVE: Cardiovascular (CV) disease (CVD) is the single most important cause of death among Chinese dialysis patients, accounting for 51% of overall mortality. The study was performed to investigate the prevalence and the spectrum of CVD in Chinese chronic kidney disease (CKD) patients. METHODS: The multicenter Chinese cohort study examined 1239 CKD patients from 7 main medical centers (distributed in 5 regions of China) who were hospitalized between 2002 and 2003. RESULTS: (1) The most prevalent pathological form of CVD was left ventricular (LV) hypertrophy (LVH), accounting for 58.5% of total patients. The prevalence of coronary artery disease (CAD), congestive heart failure (CHF), and cerebrovascular accidents (CVA) was 16.5%, 27.7% and 5.6%, separately. (2) The cohort with minor renal dysfunction (stage 2-3) had higher prevalence of CAD (5.9%) and CVA (1.0%) compared with general population in the same regions. Up to 41.2% of minor CKD patients were complicated with LVH, and 13.8% of them had clinical evidence of CHF. The prevalence of CAD, LVH and CHF increased as glomerular filtration decline. (3) The prevalence of CAD (20.0%) was much lower and the prevalence of CVA (5.4%) was higher in Chinese dialysis patients than that in American dialysis population. There was significant geographical variations in CAD prevalence, but it was not different between genders. CONCLUSION: The CV risk is significantly increased in patients with CKD. Even minor CKD has a major impact on the CV risk. The prevalence of CAD in Chinese dialysis patients is markedly lower than that in American dialysis population.

[Effects of RGD tripeptide on the expression of FAK and HA in glomerular mesangial cells].

OBJECTIVE: Observing the effects of Arg-Gly-Asp (RGD) peptides on the proliferation of glomerular mesangial cells (GMCs), and on the expression of focal adheshion kinase (FAK) and hyaluronic acid (HA) in GMCs. METHODS: GMCs of rats were induced with RGD peptide in vitro. The proliferation of GMCs was measured by MTT; the expression of FAK, by immunohistochemistry; and the quantity of HA, by radioimmunoassay. RESULTS: After being incubated with RGD peptides, some of the attached GMCs became round, detached, and floated. As compared with the control, the proliferation (A value) of the induced with RGD peptide GMCs was significantly lower. After the cultured GMCs had been induced with RGD (1 mmol/L) for 24 h, the expression of FAK decreased by 3.10%, and the secretion of HA decreased by 5.64%. After the cultured GMCs had been incubated with RGD (4 mmol/L) for 8 h and 24 h, the expression of FAK decreased by 6.50% and 15.95%, and the secretion of HA decreased by 6.37% and 18.43%, respectively. CONCLUSION: RGD peptides can inhibit the attachment of the cultured GMCs, reduce the proliferation of GMCs and decrease the secretion of the extracellular matrix.

[Effects of leukocyte depletion filter on canine kidney during cardiopulmonary bypass].

OBJECTIVE: To explore the effect of a reforming leukocyte depletion filter (LDF-1) on the functional and pathologic changes of canine kidney during cardiopulmonary bypass (CPB). METHODS: Twelve Mongolian dogs were randomly allocated into a control group (no LDF-1, n = 6) or a leukocyte-depleted filter group (LDF-1 placed in venous line, n = 6). CPB of the dogs anestheitized with sodium pentobarbitone at 25 mg/kg was set up. After 10 min of CPB, aorta was clamped and St. Thomas cardioplegic solution at 20 mg/kg was immediately injected into the root of aorta. The aortic cross-clamp was released and CPB was closed at 70 min. Dogs were observed for 2 h after weaning from CPB. LDF-1 was opened at 2 min and stoped at 7 min during initially running CPB in the LDF-1 group. Circulating leukocytes, plasma L-selectin, and plasma IL-8 were respectively counted before CPB, at 10 minutes, 40 min, and 75 min during CPB, the end of CPB, and 2 h after CPB. The urine analysis and renal pathology, which were obtained before CPB and 2 h after CPB, were observed. RESULTS: The number of leukocytes significantly decreased by 55% - 68% in the LDF-1 group compared with the baseline during CPB. The value at 10 min of CPB in the LDF-1 group was lower than that in the control group (P < 0.05). Plasma levels of L-selectin and IL-8 obviously increased in the 2 groups compared with the baseline during CPB, but both levels at 2 h after CPB in the LDF-1 group were lower than those in the control group (P <0. 05). No statistic difference was found in plasma levels of urea and creatinine, but hematuria was observed in the 2 groups at 2 hours after CPB. The pathologic changes of kidney, which was mainly renal tubule swelling accompanied partly with vacuolar degeneration, were similar under the light microscope in the 2 groups at 2 h after CPB. Obvious glomerular damage was not found. CONCLUSION: LDF-1 can effectively decrease leukocyte counts and the inflammatory reaction, but it can not bring about excellent protective effect on kidney during CPB when used alone. Attention to should be paid the renal protection in the postoperative CPB.

[Clinical and pathological analyses of lipoprotein glomerulopathy].

OBJECTIVE: To investigate the clinical and pathological characteristics of lipoprotein glomerulopathy. METHODS: We retrospectively analyzed 3 cases of lipoprotein glomerulopathy. RESULTS: The 3 patients, 1 male and 2 females, were young Hans. They were admitted to our hospital because of edema. Patient 1 had a positive family history. Her proteinuria ranged between 0.8-1.5 g/d, her serum albumin levels were below the normal lower limit, and she was afflicted with anemia. Patient 2 was found having slightly increased serum creatinine, hypertension, and increased total cholesterol and triglyceride level. The kidneys of patient 3 were enlarged. Increments of glomerular size and capillary lumen space were observed under microscope. Bioptic specimens of the patients' kidneys displayed extensive prominent lucent casts in the capillary lumen, which were stained as pale mesh-like substance and were not stained by silver impregnation. Immunofluorescence microscopy revealed faint immunoglobulin deposit. These casts were stained positive for apoE. CONCLUSION: Lipoprotein glomerulopathy is pathologically characterized by extensive glomerular capillary casts which are stained positive for apoE, and clinically it is characterized by edema, proteinuria, hypoalbuminaemia and anemia.