Assessment of Renal Function and Risk Factors for Chronic Kidney Disease in Patients With Peripheral Arterial Disease.

Chronic kidney disease (CKD) and peripheral arterial disease (PAD) share common risk factors. We assessed renal function and the prevalence of CKD in patients with PAD and investigated the characteristics of the risk factors for CKD in this population. Renal function of 421 patients with PAD was evaluated. Among the participants, 194 (46.1%) patients had decreased estimated glomerular filtration rate (eGFR). The prevalence of CKD was much higher among patients with PAD. Hypertension (odds ratios [ORs] 2.156, 95% confidence interval [CI] 1.413-3.289, P < .001), serum uric acid (OR 3.794, 95% CI 2.220-6.450, P < .001), and dyslipidemia (OR 1.755, 95% CI 1.123-2.745, P = .014) were significantly associated with CKD and the independent risk factors for CKD in patients with PAD. CKD is common and has a high prevalence in a population with PAD. Patients with PAD may be considered as a high-risk population for CKD. Recognition and modification of risk factors for CKD might beneficially decrease CKD incidence and improve prognosis in patients with PAD.

Characterization of Lipoprotein-associated Phospholipase A2 in Serum in Patients With Stage 3-5 Chronic Kidney Disease.

BACKGROUND: This study aims to test the lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity in patients with chronic kidney disease (CKD) and to analyze their connection of Lp-PLA2 with the development of disease and with the occurrence of atherosclerosis in this population. MATERIALS AND METHODS: In total, 59 patients older than 18 years and with a diagnosis of CKD were recruited. Kidney function was evaluated by serum creatinine, serum urea and estimated glomerular filtration rate according to Chronic Kidney Disease Epidemiology Collaboration formula and clinical data were collected. A total of 24 healthy volunteers served as healthy controls. Lp-PLA2 mass is measured by enzyme-linked immunosorbent assay. Lp-PLA2 activity is determined by an enzymatic platelet-activating factor acetylhydrolase assay. RESULTS: Serum mass and activity of Lp-PLA2 were higher in patients with CKD compared with healthy controls (P < 0.001 and P = 0.031). There was a positive linear relationship betweenLp-PLA2 mass and activity in the patients with CKD (r = 0.586, P < 0.001). The similar result was observed in the healthy controls (r = 0.585, P = 0.003). However, the ratio of Lp-PLA2 mass to activity in the patients with CKD was significantly higher than those of healthy controls (P < 0.001). Lp-PLA2 mass and activity were correlated with low-density lipoprotein (r = 0.366 and r = 0.303, P = 0.004 and P = 0.02). CONCLUSIONS: Lp-PLA2 mass and activity increase in patients with CKD. Elevated mass and activity of Lp-PLA2 related to inflammation and atherosclerosis may take part in the development of kidney injury and atherosclerosis in patients with CKD.

Mesenchymal stem cells, not conditioned medium, contribute to kidney repair after ischemia-reperfusion injury.

INTRODUCTION: Studies have shown that stem cells exert their therapeutic effects on acute kidney injury (AKI) through paracrine/endocrine actions. If the protective effect is mediated in an endocrine manner, the injection of the factors that these cells secrete could be effective, but the effect of conditioned medium (CM) remains controversial. METHODS: In this study, we cultured mesenchymal stem cells (MSCs) and then transplanted them into an ischemia-reperfusion (I/R) injury model. CM was also injected into mice, and the histological changes, level of cell proliferation, loss of peritubular capillaries and anti-inflammatory and anti-apoptotic effects were examined at different time points. RESULTS: The results showed that MSC infusion improved renal function and histological alterations, leading to significantly reduced mortality. MSC administration also promoted kidney microvasculature repair, attenuated kidney peritubular capillary loss, increased the proliferation of parenchymal cells and decreased CD68-positive macrophage infiltration and apoptotic cells. Although we determined that CM contained proangiogenic factors, including hepatocyte growth factor (HGF), vascular endothelial growth factor-A (VEGF-A) and insulin-like growth factor-1 (IGF-1), no favorable effects were observed during the course of repair. CONCLUSIONS: Our data show that MSC infusion promotes kidney repair in a variety of ways, including enhancement of the repair of peritubular capillaries and tubular epithelial cells and anti-inflammatory and anti-apoptotic effects. MSCs can secrete high levels of proangiogenic growth factors, but CM results in a nonsignificant improvement, indicating that MSCs play a role in kidney repair through paracrine rather than endocrine mechanisms. These results indicate that MSC infusion is a promising therapeutic strategy for promoting kidney repair after injury.

Efficacy and safety of Abelmoschus manihot for primary glomerular disease: a prospective, multicenter randomized controlled clinical trial.

BACKGROUND: Abelmoschus manihot, a single medicament of traditional Chinese medicine, has been widely used to treat kidney disease. This is the first randomized controlled clinical trial to assess its efficacy and safety in patients with primary glomerular disease. STUDY DESIGN: Prospective, open-label, multicenter, randomized, controlled, clinical trial. SETTING & PARTICIPANTS: From May 2010 to October 2011, a total of 417 patients with biopsy-proven primary glomerular disease from 26 hospitals participated in the study. INTERVENTIONS: A manihot in the form of a huangkui capsule, 2.5 g, 3 times per day; losartan potassium, 50mg/d; or combined treatment, a huangkui capsule at 2.5 g 3 times per day, was combined with losartan potassium, 50mg/d. The duration of intervention was 24 weeks. OUTCOMES & MEASUREMENTS: The primary outcome was change in 24-hour proteinuria from baseline after treatment. Change in estimated glomerular filtration rate (eGFR) from baseline after treatment was a secondary outcome. The 24-hour proteinuria was measured every 4 weeks and eGFR was measured at 0, 4, 12, and 24 weeks. RESULTS: Mean baseline urine protein excretion was 1,045, 1,084, and 1,073 mg/d in the A manihot, losartan, and combined groups, respectively, and mean eGFR was 108, 106, and 106 mL/min/1.73 m2, respectively. After 24 weeks of treatment, mean changes in proteinuria were protein excretion of -508, -376, and -545 mg/d, respectively (P=0.003 for A manihot vs losartan and P<0.001 for the combined treatment vs losartan). Mean eGFR did not change significantly. The incidence of adverse reactions was not different among the 3 groups (P>0.05), and there were no severe adverse events in any group. LIMITATIONS: Results cannot be generalized to those with nephrotic syndrome or reduced eGFR. CONCLUSIONS: A manihot is a promising therapy for patients with primary kidney disease (chronic kidney disease stages 1-2) with moderate proteinuria.

Efficacy and safety of Changfu peritoneal dialysis solution: a multi-center prospective randomized controlled trial.

BACKGROUND: A multi-center large scale study is needed to confirm the efficacy and safety of domestic peritoneal dialysis (PD) solutions. Some researchers believe that 6 L/d is enough for adequate dialysis, but there is no multi-center prospective study on Chinese population to confirm this. In this study, we evaluated the efficacy and safety of domestic PD solution (Changfu) and its difference between 6 L and 8 L dosage. METHODS: Adult PD patients who had taken PD therapy for at least one month were selected and divided into four groups according to two dialysis solution brands and two dialysis dosages, i.e., 6 L dose with Changfu dialysis solution, 6 L dose with Baxter dialysis solution, 8 L dose with Changfu dialysis solution, and 8 L dose with Baxter dialysis solution. After 48 weeks, the changes of primary and secondary efficacy indices were compared between different types and different dosages. We also analyzed the changes of safety indices. RESULTS: Changes of Kt/V from baseline to 48 weeks between Changfu and Baxter showed no statistical differences; so did those of creatinine clearance rate (Ccr). Normalized protein catabolic rate (nPCR) from baseline to 48 weeks between Changfu and Baxter showed no statistical differences; so did those of net ultrafiltration volume (nUF) and estimated glomerular filtration rate (eGFR). Changes of nPCR from baseline to 48 weeks between 6 L and 8 L showed no statistical differences; so did those of nUF and eGFR. The decline of Kt/V from baseline to 48 weeks in 6 L group was more than that in 8 L group. Change of Ccr was similar. During the 48-week period, the mean Kt/V was above 1.7/w, and mean Ccr was above 50 L×1.73 m(-2)×w(-1). More adverse events were found in Changfu group before Changfu Corporation commenced technology optimization, and the statistical differences disappeared after that. CONCLUSIONS: The domestic PD solution (Changfu) was proven to be as effective as Baxter dialysis solution. During 48-week period, a dosage of 6 L/d was enough for these patients to reach adequate PD. Clinical study promotes technological optimization, further helps to improve the safety indices of the medical products.

Epidemiology and risk factors for chronic kidney disease in patients with ischaemic stroke.

BACKGROUND: There is growing evidence for an association between chronic renal disease (CKD) and adverse cerebrovascular events because of the overlap of several risk factors. The purpose of this study is to examine the epidemiology of CKD and the characteristics of risk factors for CKD in the population with ischaemic stroke. METHODS: This retrospective study included 571 patients with ischaemic stroke. Estimated glomerular filtration rate (eGFR) was calculated by the Modification of Diet in Renal Disease (MDRD) study equation. Renal function was assessed according to the Kidney Disease Outcomes Quality Initiative (K/DOQI)-CKD classification. RESULTS: Study demonstrated that the major factors associated with CKD in the ischaemic stroke patients were age, diabetes mellitus, hypertension, systolic blood pressure, LDL cholesterol and serum uric acid. Diabetes mellitus (OR 4·146, 95% CI 1·047-16·418, P = 0·043), hypertension and diabetes mellitus (OR 3·574, 95% CI 1·248-10·234, P = 0·018), serum uric acid (OR 1·010, 95% CI 1·006-1·013, P < 0·001) and LDL cholesterol (OR 1·431, 95% CI 1·063-1·928, P = 0·018) were independent risk factors associated with CKD in the patients with ischaemic stroke. CONCLUSIONS: The patients with ischaemic stroke may be considered as a high-risk population for CKD and be aggressively managed for CKD prevention. The high prevalence of CKD in population with ischaemic stroke prompts the need for greater public awareness about risks of CKD.

Prevalence, awareness, treatment, and control of hypertension in the non-dialysis chronic kidney disease patients.

BACKGROUND: Data on the epidemiology of hypertension in Chinese non-dialysis chronic kidney disease (CKD) patients are limited. The aim of the present study was to investigate the prevalence, awareness, treatment, and control of hypertension in the non-dialysis CKD patients through a nationwide, multicenter study in China. METHODS: The survey was performed in 61 tertiary hospitals in 31 provinces, municipalities, and autonomous regions in China (except Hong Kong, Macao, and Taiwan). Trained physicians collected demographic and clinical data and measured blood pressure (BP) using a standardized protocol. Hypertension was defined as systolic BP ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg, and/or use of antihypertensive medications. BP < 140/90 mmHg and < 130/80 mmHg were used as the 2 thresholds of hypertension control. In multivariate logistic regression with adjustment for sex and age, we analyzed the association between CKD stages and uncontrolled hypertension in non-dialysis CKD patients. RESULTS: The analysis included 8927 non-dialysis CKD patients. The prevalence, awareness, and treatment of hypertension in non-dialysis CKD patients were 67.3%, 85.8%, and 81.0%, respectively. Of hypertensive CKD patients, 33.1% and 14.1% had controlled BP to < 140/90 mmHg and < 130/80 mmHg, respectively. With successive CKD stages, the prevalence of hypertension in non-dialysis CKD patients increased, but the control of hypertension decreased (P < 0.001). When the threshold of BP < 130/80 mmHg was considered, the risk of uncontrolled hypertension in CKD 2, 3a, 3b, 4, and 5 stages increased 1.3, 1.4, 1.4, 2.5, and 4.0 times compared with CKD 1 stage, respectively (P < 0.05). Using the threshold of < 140/90 mmHg, the risk of uncontrolled hypertension increased in advanced stages (P < 0.05). CONCLUSIONS: The prevalence of hypertension Chinese non-dialysis CKD patients was high, and the hypertension control was suboptimal. With successive CKD stages, the risk of uncontrolled hypertension increased.

Serum levels and activity of indoleamine2,3-dioxygenase and tryptophanyl-tRNA synthetase and their association with disease severity in patients with chronic kidney disease.

OBJECTIVE: This study aims to test the serum levels and activity of indoleamine2,3-dioxygenase(IDO) and tryptophanyl-tRNA synthetase (TTS) in patients with chronic kidney disease (CKD) and to evaluate their association with disease severity. METHOD: Serum concentrations of IDO and TTS in 61 patients with CKD and 16 healthy volunteers were tested by ELISA. Tryptophan and kynurenine concentrations were measured by high-performance liquid chromatography (HPLC). RESULTS: Patients with CKD showed higher serum levels of IDO and TTS in comparison to healthy controls (p = 0.001). Patients with CKD showed lower serum levels of tryptophan and higher serum levels of kynurenine in comparison to healthy controls (p < 0.001). The kyn/Trp ratio significantly correlated with the disease severity in CKD patients (r = 0.721; p < 0.001). CONCLUSIONS: IDO and TTS may play critical roles in the immune pathogenesis of CKD. The activity of IDO correlated with the disease severity of CKD.

Treatment of 5/6 nephrectomy rats with sulodexide: a novel therapy for chronic renal failure.

AIM: Sulodexide, a glycosaminoglycan, could reduce albuminuria in diabetic patients. The aim of this study was to determine whether sulodexide could be used to treat chronic kidney failure in rats. METHODS: Sixty Wistar rats undergone 5/6 nephrectomy, then were randomly divided into 4 groups: the model group, sulodexide group (sulodexide 5 mg/kg per day, im), irbesartan group irbesartan (20 mg/kg per day, ig) and sulodexide plus irbesartan group. Another 12 rats were enrolled into the sham operation group. After the treatments for 4, 8 and 12 weeks, urinary protein and serum creatinine levels were measured. After 12 weeks, serum cholesterin and triglycerides levels were measured, and the degrees of glomerular sclerosis and renal tubulointerstitial fibrosis were scored. The expression of aminopeptidase P (JG-12) in the renal tissue was examined using immunohistochemical staining. The renal expressions of endothelial nitric oxide synthase (eNOS) and tissue type plasminogen activator (tPA) were detected with RT-PCR and Western blot. RESULTS: Proteinuria was markedly attenuated in the sulodexide-treated groups. After 4 and 8 weeks only the sulodexide-treated groups showed significant reduction in serum creatinine; while after 12 weeks all the three treatment groups showed significant reduction in serum creatinine. Furthermore, all the three treatment groups showed significant reduction in the scores of glomerular sclerosis and tubulointerstitial fibrosis. The glomerular expression of JG-12 was increased in both the sulodexide group and the sulodexide plus irbesartan group, but not in the irbesartan group. The eNOS mRNA and protein expression was decreased and the tPA mRNA and protein expression was significantly increased in the model group compared with Sham group. Sulodexide, irbesartan, and their combination reversed the decrease of eNOS expression but increased the tPA expression much more compared with model group. CONCLUSION: Sulodexide was similar to irbesartan that can decrease proteinuria and attenuate renal lesions in 5/6 nephrectomy rats. The renal protection by sulodexide might be achieved via its impact on renal vascular endothelial cells.

Prevalence and risk factors for chronic kidney disease in patients with coronary artery disease.

OBJECTIVES: Chronic renal disease (CKD) is recognized as a worldwide public health problem. Traditional risk factors for CKD are also present in coronary artery disease (CAD). The purpose of this study is to examine the prevalence and characteristics of risk factors for CKD in the population with CAD. METHODS: Renal function was evaluated in 527 patients with CAD in order to assess characteristics of the incidence, risk factors for CKD in the population with CAD. In the present study in order to concentrate on evaluation for eGFR of the patients with CAD proteinuria is not included in the definition of CKD. RESULTS: Univariate analysis demonstrated that the major risk factors associated with CKD in the patients with CAD were age (P ≤ 0.001), smoking (P = 0.016), diabetes mellitus (P = 0.021), hypertension (P ≤ 0.001), and systolic blood pressure (P = 0.004). The percentages of patients with both hypertension and diabetes mellitus were significantly greater in the CKD3-4 group (P < 0.001). The results of multivariable analysis showed that hypertension (OR 1.925, 95% CI 1.196-3.098, P = 0.007), diabetes mellitus (OR 1.744, 95% CI 1.044-2.914, P = 0.034) and serum uric acid (OR 1.008, 95% CI 1.006-1.010, P ≤ 0.001) were independent risk factors for reduced eGFR. CONCLUSIONS: CKD is common and has a high prevalence in the population with CAD. Several risk factors are known to simultaneously affect heart and kidney. The patients with CAD may be considered as a high-risk population for CKD.

[Atorvastatin attenuates parathyroid hormone 1-34 induced cardiomyocytes hypertrophy through downregulating K-Ras-ERK1/2 pathway].

OBJECTIVE: To investigate the effects of atorvastatin on parathyroid hormone 1-34 (PTH1-34) induced neonatal rat cardiomyocytes hypertrophy and on the expression changes of small GTP-binding protein (K-Ras) and extracellular signal regulated protein kinases 1/2 (ERK1/2). METHODS: Neonatal rat cardiomyocytes hypertrophy was established with 10(-7) mol/L rPTH1-34 in the presence or absence of 10(-5) mol/L atorvastatin or 10(-4) mol/L mevalonic acid (MVA). Cardiomyocyte diameter was measured by Motic Images Advanced 3.0 software, the synthetic rate of protein in cardiomyocytes was determined by (3)H-leucine incorporation and single-cell protein content was measured by BCA. The concentration of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were determined by ELISA. Protein expression of ERK1/2, p-ERK1/2 and K-Ras was detected by Western blot. RESULTS: Compared to PTH1-34 group, cellular diameter was decreased 12.07 µm, (3)H-leucine incorporation decreased 1622 cpm/well and single-cell protein content decreased 84.34 pg, ANP or BNP concentration reduced 7.13 µg/L or 20.04 µg/L, protein expression of K-Ras, ERK1/2 or p-ERK1/2 downregulated 0.81, 0.19 and 1.44 fold, respectively, in PTH1-34 plus atrovastatin co-treated cardiomyocytes (all P < 0.05). Compared to PTH1-34 plus atrovastatin co-treated group, cardiomyocyte diameter increased 4.95 µm, (3)H-leucine incorporation increased 750 cpm/well and single-cell protein content increased 49.08 pg, ANP or BNP increased 3.12 µg/L or 9.35 µg/L and protein expression of K-Ras, ERK1/2 or p-ERK1/2 upregulated 0.52, 0.06 and 1.19 fold (all P < 0.05) in MVA, PTH1-34 and atrovastatin co-treated cardiomyocytes. CONCLUSIONS: Atrovastatin attenuates PTH1-34 induced neonatal rat cardiomyocytes hypertrophy through downregulating K-Ras and ERK1/2 pathway.

Characterization of interleukin-33 and soluble ST2 in serum and their association with disease severity in patients with chronic kidney disease.

INTRODUCTION: This study aims to test the serum levels of interleukin-33 (IL-33) and soluble ST2 (sST2) in patients with chronic kidney disease (CKD) and to evaluate their association with disease severity. METHODS: Sixty-nine patients with CKD were enrolled, disease severity was assessed, and clinical data were collected. Twelve healthy volunteers served as healthy individuals. Serum IL-33 and sST2 were tested by enzyme-linked immunosorbent assay. RESULTS: The patients were classified into five categories based on their estimated glomerular filtration rate (eGFR). No difference was found as to the serum concentration of IL-33 between CKD patients and healthy individuals (p = 0.656), while a higher serum level of sST2 was found in CKD patients (p = 0.003). The correlation analysis revealed a significant correlation between the serum level of sST2 and disease severity (r = 0.586; p < 0.001). A higher level of sST2 was found in CKD patients with elevated parathyroid hormone (p = 0.001). Serum sST2 correlated with parathyroid hormone (r = 0.412; p < 0.001), serum phosphorus (r = 0.545; p < 0.001), and serum calcium (r = -0.494; p < 0.001). CONCLUSION: An elevated concentration of serum sST2 is found in CKD patients and correlates with disease severity. Serum sST2 may be also associated with parathyroid hormone disorder of CKD. The sST2 may have an important role in the development of CKD or as a marker of disease severity.

An evaluation of the RIFLE criteria for acute kidney injury after myeloablative allogeneic haematopoietic stem cell transplantation.

BACKGROUND: Patients undergoing myeloablative allogeneic haematopoietic stem cell transplantation (HSCT) have a higher incidence of acute kidney injury (AKI). RIFLE is a newly developed classification for AKI that includes three grades of severity - AKI-R, AKI-I, AKI-F. OBJECTIVE: The purpose of this study was to analyse retrospectively major risk factors for AKI at the time of myeloablative allo-HSCT and to use the RIFLE criteria to predict mortality in myeloablative allo-HSCT. METHODS: Renal function was evaluated in 143 patients with allo-HSCT by RIFLE criteria in order to assess the incidence, risk factors and mortality rate of various degrees of AKI. RESULTS: The results of this study showed that patients with hepatic veno-occlusive disease (HVOD) have a higher incidence of AKI-F than those without HVOD (P = 0.002). The incidence of AKI-I and AKI-F in patients with grade III-IV acute graft-versus-host disease (aGVHD) and increased total bilirubin was significantly higher than in those without (P = 0.001, P <0.001). HVOD was an independent risk factor of AKI-F (OR 5.058, 95% CI 1.317-19.424, P = 0.018), and increased total bilirubin was an independent risk factor for AKI-F (OR 5.126, 95% CI 1.403-18.998, P = 0.014). Worsening RIFLE category was associated with increased mortality of the patients in the 100 days post-transplant (P = 0.003). In addition, 180-day survival of patients in different AKI classes was significantly different (P = 0.0095). CONCLUSION: AKI is common in patients with myeloablative allo-HSCT and is associated with increased risk of death. The RIFLE criteria appear to be an important tool for stratification of these patients on the basis of death risk.

The regulation of CD4+ T cell immune responses toward Th2 cell development by prostaglandin E2.

As an important immune mediator, PGE2 plays an important role in the immune tolerance, autoimmune diseases, immune regulation and tumor immunotolerance. PGE2 is considered to be a promising candidate for the control of the immune diseases. To further understand the immuno-modulating effects of PGE2 on CD4+ T cells, in vitro investigation was conducted in the present study. The results showed that PGE2 inhibited the proliferation of T cells in vitro in a dose-dependent manner. Gene expression profiling showed that 1716 genes were down regulated and 73 genes were up regulated with a change of 1.5 fold. Several signal transduction pathways were involved, such as TNF-α and NF-kB signaling pathway, T cell receptor signaling pathway, IL-2 signaling pathway, and MAPK pathway. The results showed that PGE2 inhibited IFN-γ, TNF-α and IL-4 production by CD4+ T cells 24h after cell culture. A comparison between IFN-γ and IL-4 production showed that PGE2 enhanced the relative ratio of IL-4 to IFN-γ in CD4+ T cells culture, and regulated CD4+ T cells toward Th2 cell development. The results of the present study indicated that PGE2 has the potential to treat Th1-mediated inflammatory diseases by regulating CD4+ T cells toward Th2 cell immune response.

[Effect of telmisartan on tubulointerstitial injury and expression of PPARγ in rat renal tissue of IgA nephropathy model].

OBJECTIVE: To observe the effect of telmisartan on the expression of PPARγ in rat renal tissue of IgA nephropathy model and clarify the possible mechanism of telmisartan in tubulointerstitial injury. METHODS: The experimental rat model with IgA nephropathy was induced by bovine serum albumin (BSA), lipopolysaccharide (LPS) and carbon tetrachloride (CCl4). Forty male SD rats were randomly divided into control group, IgA model group, rosiglitazone group, telmisartan group and losartan group. At pre-administration, Weeks 4, 8 and 10, the quantity of 24-hour proteinuria was measured. The morphologic changes of renal tissues were evaluated by electron microscope. Immunohistochemistry was used to observe the expressions of PPARγ, TGF-ß1 and α-smooth muscle actin (α-SMA) in different groups and RT-PCR to detect the expressions of PPARγ, TGF-ß1 and monocyte chemoattractant protein-1 (MCP-1) in different groups. RESULTS: Compared with control group, 24-hour proteinuria(mg) increased markedly in IgA model group (14.14 ± 1.99 vs 1.59 ± 0.18), but rosiglitazone group (2.35 ± 0.33), telmisartan group (1.88 ± 0.09) and losartan group (2.82 ± 0.34) was much lower and telmisartan had the most significant effect (all P < 0.05). Compared with control group, there were varying degrees of mesangial proliferation and infiltration of inflammatory cell in IgA model group (3.10 ± 0.18). The tubulointerstitial injury was notably alleviated in rosiglitazone group (1.97 ± 0.23), telmisartan group (1.57 ± 0.14) and losartan group (2.15 ± 0.22) while telmisartan had the most significant effect (all P < 0.01). With immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), PPARγ, TGF-ß1, α-SMA and MCP-1 had minimal expression on tubule and interstitium in normal group. But there was a high expression in model group. There was no difference between losartan and model groups. There was a lowered expression in rosiglitazone and telmisartan groups. CONCLUSION: Possibly through two separate passway of stimulating PPARγ and preventing Angiotensin II receptor, telmisartan shows special protective function in tubulointerstitial injury.

[Expression and significance of CD80/CD86 in renal tissue of lupus nephritis].

OBJECTIVE: To measure the expression of CD80 and CD86 in renal tissue of lupus nephritis (LN) and explore its mechanism in the development of LN. METHODS: Forty-nine patients with active LN and 9 patients with minor glomerular abnormalities tissues as controls were studied. The expression of CD80 and CD86 in renal tissues was detected by immunohistochemical methods. RESULTS: CD86 was expressed extensively in glomerulus, periglomerular area, tubular epithelial cells and peritubular interstitium, while CD80 was expressed only in tubular epithelial cells and peritubular interstitium. Moreover, the percentage of CD80+ and CD86+ cells in tubular epithelial cells and peritubular interstitium showed a tendency to increase with tubulointerstitial damage. The expression of CD80 and CD86 in renal tissue correlated with the systemic lupus erythematosus (SLE) disease activity index score, the degree of proteinuria, creatinine clearance and anti-dsDNA antibody. CONCLUSIONS: This study shows that increased CD80 and CD86 expression with the progression of tubulointerstitial lesion might play an important role in the development of lupus nephropathy, and the tubulointerstitial expression of CD80 and CD86 could potentially serve as a surrogate marker of SLE disease activity. The co-stimulatory molecules CD80 and CD86 might play an important role in the pathogenesis of LN.

[The research on the relationship between the polymorphism of 1082A/G, anti-inflammatory interleukin-10 gene promoter with its effect of preventing ESRD patients from microinflammation and arteriosclerosis].

OBJECTIVE: We do this investigation in order to reveal the relationship between the polymorphism of 1082A/G, anti-inflammatory interleukin-10 gene promoter, and end stage renal disease (ESRD) patients microinflammatory state and arteriosclerosis (AS). METHODS: We used PCR-RFLP to measure the various kinds of distribution of IL-10 gene-1082A/G genotype and relevant indexes of microinflammatory state and AS of 870 ESRD patients and 1000 healthy persons of control group and to analyze the mechanism of its protection effect keeping ESRD patients away from microinflammation and arteriosclerosis. RESULTS: Compared with the control group, CRP, TNF-alpha, CH50, C3, IL-10 and Alb of ESRD group were in the normal range, but still significantly higher than those of the control group, while IL-10, Alb were significant lower (P < 0.05). The genotype distribution and allele frequency of IL-10A/G gene had no significant differences between the healthy group and the control group (P > 0.05). Levels of CRP, TNF-alpha, CH50 and C3 of ESRD patients with IL-10A/A genotype were significantly higher than those of ESRD patients with G/G and G/A genotype (P < 0.05), while IL-10 and Alb were significantly lower (P < 0.01). The production of IL-10 in serum from patients with IL-10A/A genotype was significantly lower than that of patients with G/G and G/A genotype (P < 0.01). The incidence rate of AS of patients with IL-10-1082A/A genotype was significantly higher than that of patients with G/G and G/A genotype (P < 0.01). The raise of AS incidence rate was correspondent with the decline of serum IL-10 and raise of serum CRP and Fib. CONCLUSION: The IL-10A/A genotype is a predictable factor of microinflammatory state and high AS incidence rate in ESRD patients. We use IL-10G/G genotype to modulate the high production of serum IL-10, to decline inflammatory reaction and to keep away from microinflammation and AS in ESRD patients. We should work hard on improving the dialysis membrane to reduce the anti-inflammatory factors in uremia for chronic renal failure patients with high arteriosclerosis risk.