It has been verified that the red blood cell distribution width (RDW) is related to renal function. This study aimed to investigate the association of RDW with the residual renal function in peritoneal dialysis (PD) patients. The patients were categorized into three groups according to the quartiles of their baseline RDWs. The correlations between RDW and clinical parameters, dialysis adequacy, and residual renal function were analyzed. The clinical data, PD prescription and dialysis adequacy of 54 uremic patients on continuous ambulatory PD were collected. All the statistical analyses were performed using the Statistical Package for the Social Sciences program version 17.0. The baseline RDW of the patients was 13.56% ± 1.36%. No significant differences in the other indexes [hemoglobin, albumin, alkaline phosphatase, intact parathyroid hormone (iPTH), urea and creatinine] among the three groups were found. One month after beginning PD, the correlation between the RDW and the residual renal function has not been found in the multivariate regression model adjusted for the hemoglobin, albumin, and leukocyte. Three months after beginning the PD, a significant difference between Group 2 and Group 3 in iPTH was found. Multivariate regression analysis showed that the elevated RDW is associated with the declined residual glomerular filtration rate (heart rate = -0.587, 95% confidence interval -1.080 ~ -0.093) for the corresponding period after PD, adjusted for the hemoglobin, albumin, and leukocyte. This study showed that the RDW reflected the residual renal function in the corresponding period after PD in the PD patients.

To investigate whether myofibrillogenesis regulator 1 (MR-1) attenuates renal ischemia/reperfusion (I/R) injury via inhibiting phosphorylated Akt (p-Akt) mitochondrial translocation-mediated opening of the mitochondrial permeability transition pore (mPTP), we injected adenovirus containing MR-1 gene or its siRNAs to the left kidney subcapsular areas of Sprague-Dawley rats, which subsequently underwent experimental renal I/R injury. Renal functions and the severity of the tubular injury were evaluated by the serum creatinine and blood urea nitrogen levels and the pathological scores. We also examined the mitochondrial morphology and functions. Total/p-Akt were assessed by western blot using the mitochondrial and the cytosolic fractions of cortex of renal tissue, respectively. We found that mitochondrial and cytosolic MR-1 levels and mitochondrial p-Akt decreased, and cytosolic p-Akt increased after reperfusion. Subcapsular injection of adenovirus led to higher MR-1 expression in the mitochondria/cytosol, inhibited mPTP opening, and alleviated renal I/R injury; adenovirus injection also upregulated mitochondrial total and p-Akt levels more prominently compared with the normal saline (NS) group. Subcapsular injection of MR-1 siRNAs significantly lowered MR-1 expression and induced renal injury, with increased mPTP opening and mitochondrial damage, similar to I/R injury. MR-1 interacted with Akt in renal cortex homogenate. Wortmannin, a phosphatidylinositol 3 kinase (PI3K) inhibitor, abolished both mitochondrial p-Akt recruitment and the protective effect of MR-1 overexpression on I/R injury. To conclude, MR-1 protects kidney against I/R injury through inhibiting mPTP opening and maintaining mitochondrial integrity, through the recruitment of PI3K-dependent p-Akt to the mitochondria. MR-1 could be a new therapeutic strategy for renal I/R injury.

BACKGROUND:Low calcium dialysate with 1.25 mmol/l calcium concentration has been proposed to replace standard calcium dialysate in peritoneal dialysis patients taking calcium-containing phosphate binder to prevent hypercalcaemia. We conducted a meta-analysis to evaluate long term effects on mineral and bone metabolism by low versus standard calcium dialysate in peritoneal dialysis.METHOD:Clinical studies comparing low versus standard calcium dialysate in peritoneal dialysis patients were identified by searching PubMed (from 1990 to October 2013) and EMBASE (from 1990 to October 2013). Major outcomes extracted for meta-analysis were: serum total and ionized calcium, phosphate, parathyroid hormone and bone metabolism. Statistical analyses were performed using the Review Manager, version 5.1.0 (Cochrane Collaboration, Oxford, UK).RESULTS:Four studies were identified for meta-analysis. A total of 240 peritoneal dialysis patients received standard calcium dialysate and 106 patients were given low calcium dialysate. 1-2 year after peritoneal dialysis, both serum total and ionized calcium were lower in low calcium dialysate patients as compared with standard dialysate patients (Total calcium: MD, 0.09; 95% CI, 0.05 0.13; P < 0.0001; Ionized calcium: MD, 0.04; 95% CI, 0.02 0.06; P < 0.0001). No statistical difference was observed in phosphate level between two groups (MD, -0.05; 95% CI, -0.13 0.02; P = 0.19). Intact parathyroid hormone level was significantly increased in low calcium dialysate patients. No clinically significant long term change of bone metabolism was observed between low and standard calcium dialysate treated patients.CONCLUSION:Long term (1-2 year) use of low calcium dialysate with 1.25 mmol/l calcium concentration in peritoneal dialysis patients results in decrease of serum total and ionized calcium level and does not change serum phosphate level. No clinical significance in the change of bone metabolism was observed between low and standard calcium dialysate patients despite the increase of serum parathyroid hormone in low calcium dialysate group.

Background: Hypouricemia is caused by various diseases and disorders, such as hepatic failure, Fanconi renotubular syndrome, nutritional deficiencies and genetic defects. Genetic defects of the molybdoflavoprotein enzymes induce hypouricemia and xanthinuria. Here, we identified a patient whose plasma and urine uric acid levels were both extremely low and aimed to identify the pathogenic gene and verify its mechanism. Methods: Using next-generation sequencing (NGS), we detected a mutation in the human molybdenum cofactor sulfurase (MCSU) gene that may cause hypouricemia. We cultured L02 cells, knocked down MCSU with RNAi, and then detected the uric acid and MCSU concentrations, xanthine oxidase (XOD) and xanthine dehydrogenase (XDH) activity levels, and xanthine/hypoxanthine concentrations in cell lysates and culture supernatants. Results: The NGS results showed that the patient had a mutation in the human MCSU gene. The in vitro study showed that RNAi of MCSU caused the uric acid, human MCSU concentrations, the XOD and XDH activity levels among cellular proteins and culture supernatants to be extremely low relative to those of the control. However, the xanthine/hypoxanthine concentrations were much higher than those of the control. Conclusions: We strongly confirmed the pathogenicity of the human MCSU gene.

Gentamicin may cause acute kidney injury. The pathogenesis of gentamicin nephrotoxicity is unclear. Autophagy is a highly conserved physiological process involved in removing damaged or aged biological macromolecules and organelles from the cytoplasm. The role of autophagy in the pathogenesis of gentamicin nephrotoxicity is unclear. The miniature pigs are more similar to humans than are those of rodents, and thus they are more suitable as human disease models. Here we established the first gentamicin nephrotoxicity model in miniature pigs, investigated the role of autophagy in gentamicin-induced acute kidney injury, and determined the prevention potential of rapamycin against gentamicin-induced oxidative stress and renal dysfunction. At 0, 1, 3, 5, 7 and 10 days after gentamicin administration, changes in autophagy, oxidative damage, apoptosis and inflammation were assessed in the model group. Compared to the 0-day group, gentamicin administration caused marked nephrotoxicity in the 10-day group. In the kidneys of the 10-day group, the level of autophagy decreased, and oxidative damage and apoptosis were aggravated. After rapamycin intervention, autophagy activity was activated, renal damage in proximal tubules was markedly alleviated, and interstitium infiltration of inflammatory cells was decreased. These results suggest that rapamycin may ameliorate gentamicin-induced nephrotoxicity by enhancing autophagy.

Background/Aims: Ischemia/reperfusion (I/R) injury is characterized by cytoskeletal reorganization and loss of polarity in proximal tubule epithelial cells. Previously, we showed that myofibrillogenesis regulator (MR)-1 promoted actin organization in cardiomyocytes. MR-1 is also expressed in the kidney. Methods: In this study, we investigated MR-1 expression in acute renal failure induced by I/R in Sprague-Dawley rats. We determined the MR-1 expression and the ratio of fibrous actin (F-actin) to globular actin (G-actin). HK-2 cells were treated with or without hypoxia/reoxygenation (H/R), and MR-1 levels were increased by adenoviral overexpression or silenced by RNA interference. Results: I/R and H/R resulted in cellular injury and decreases of MR-1, the F-/G-actin ratio, and myosin light chain (MLC)-2. MR-1 overexpression attenuated H/R-induced cell injury and loss of surface membrane polarity of actin. MR-1 overexpression also increased the expression and phosphorylation of MLC-2 and MLC kinase, which were decreased in MR-1-silenced and H/R-treated cells. Conclusion: Together, these data show that MR-1 promoted actin polarity on the membrane surface and protected HK-2 cells from H/R injury. The mechanism might involve the rapid organization of F-actin through the upregulation and phosphorylation of MLC-2.

AimTo assess the effectiveness of supine/standing urinalysis for differential diagnosis of left renal vein entrapment syndrome (LRVES) combined with or without glomerulopathy.MethodsThe enrolled patients with abnormal urinalysis and LRVES demonstrated by Doppler sonography were guided to perform a supine/standing urinalysis.ResultsFifty-two patients were enrolled. Most of them were adolescents (aged 14-29 years, 73.1%) and with low body mass index (BMI, mean BMI, 19.82.4kg/m(2)). Seventeen cases (32.7%) manifested orthostatic urine abnormalities (OUA, proteinuria and/or haematuria show negative in supine while positive after 15min standing), two patients who had undergone renal biopsies both showed no evidence of kidney lesions, another two patients were changed from abnormal to normal urinalysis after weight gain. The remaining 35 cases (67.3%) manifested non-orthostatic urine abnormalities (NOUA, proteinuria and/or haematuria show positive both in supine and standing), 15 patients had undergone renal biopsies and showed different degrees of glomerulopathy. After prednisone/immunosuppression therapy, four patients with glomerulonephritis were changed from the NOUA to the OUA classification. Statistics analyses showed that serum total protein and albumin levels were significantly lower (P=0.028, 0.007, respectively) and urinary protein was significantly higher (P=0.007) in the NOUA group than in the OUA group.ConclusionAfter the indication of LRVES by ultrasound, patients with OUA likely have only LRVES, while patients with NOUA likely also have glomerulopathy. Supine/standing urinalysis combined with Doppler sonography can be helpful for differential diagnosis of LRVES combined with or without glomerulopathy.Summary at a Glance An interesting paper demonstrates supine/standing urinalysis combined with Doppler sonography can be helpful for differential diagnosis of left renal vein entrapment syndrome from glomerulopathy.

As an important complication of diabetic mellitus, diabetic nephropathy (DN) has been the main cause of end-stage renal disease. It is of great importance to diagnose DN early, and to identify the risk factors of disease progression in order to carry out in-time and effective therapies. Previous literatures have reported the role of several clinical factors in the diagnosis and progression of DN, including age, longer diabetes duration, diabetic retinopathy, higher level of hypertension and HbA1c, and so on. However, the significance of these clinical factors is still controversial and limited. This review aimed to evaluate the values and limitations of these factors in diagnosing and predicting the renal outcome of DN.

先天性肾上腺皮质增生症，是一种罕见的疾病，患病率为1/16000，这是一种常染色体隐性遗传性疾病，主要是6号染色体CYP21基因缺陷。其主要病变是肾上腺皮质激素生物合成过程中，由于某种必需的酶完全或不完全缺乏，致正常的皮质激素主要是皮质醇的合成不足，反馈抑制作用减弱致垂体促肾上腺皮质激素分泌增多，后者促使肾上腺皮质增生，合成过多的雄激素和（或）盐皮质激素，临床出现不同程度肾上腺皮质功能减退，以及男女性分化发育异常，女性出现男性化，男性则表现为性早熟。少见者因酶的缺陷同时影响到雌激素的合成，以致性不发育。下列任何一种酶缺陷均导致本病。常见类型：21-羟化酶（90%以上）、11β-羟化酶、3β-类固醇脱氢酶、17α-羟化酶缺陷等[1]。不同的酶缺陷产生的生化改变和临床症状不同。2013年1月解放军总医院收治1例患者，诊断为先天性肾上腺皮质增生症伴慢性肾衰竭，现就诊疗过程报道如下。

The mechanism of mesenchymal stem cell therapy in acute kidney injury remains uncertain. Previous studies indicated that mesenchymal stem cells could attenuate inflammation-related organ injury by induction of regulatory T cells. Whether regulatory T-cell induction is a potential mechanism of mesenchymal stem cell therapy in ischemic acute kidney injury and how these induced regulatory T cells orchestrate local inflammation are unknown. Here we found that mesenchymal stem cells decrease serum creatinine and urea nitrogen levels, improve tubular injury, and downregulate IFN-γ production of T cells in the ischemic kidney. In addition to the lung, mesenchymal stem cells persisted mostly in the spleen. Mesenchymal stem cells increased the percentage of regulatory T cells in the spleen and the ischemic kidney. Antibody-dependent depletion of regulatory T cells blunted the therapeutic effect of mesenchymal stem cells, while coculture of splenocytes with mesenchymal stem cells caused an increase in the percentage of regulatory T cells. Splenectomy abrogated attenuation of ischemic injury, and downregulated IFN-γ production and the induction of regulatory T cells by mesenchymal stem cells. Thus, mesenchymal stem cells ameliorate ischemic acute kidney injury by inducing regulatory T cells through interactions with splenocytes. Accumulated regulatory T cells in ischemic kidney might be involved in the downregulation of IFN-γ production.

Conflicting results have been reported regarding the effects of donor age, recipient age and donor-recipient age difference on short-and long-term outcomes after kidney transplantation. The aim of this study was to evaluate the effects of recipient age on graft function, oxidative stress, and gene expression after renal transplantation. Fifty male Fischer 344 rats [25 young (Y, 4 months), 25 senior (S, 16 months)] were randomized to 6 groups: 2 sham groups (Y and S, n = 5 in each group) and 4 renal transplant groups[young-to-young (Y-Y), young-to-senior (Y-S), senior-to-young (S-Y), senior-to-senior (S-S), (n = 10 in each group)]. The left kidneys were transplanted from donor to recipient. After 12 weeks, systematic blood pressure, graft weight, graft function, histology and oxidative stress were measured. Microarray analysis and quantitative real-time PCR confirmation were performed to study gene expression in the grafts. There were no differences in renal graft function between young and senior kidney cross-transplantation. Transplanted kidneys showed no significant differences in glomerulosclerosis index compared to non-transplanted kidneys but had significantly different tubulointerstitium scores compared to age-matched controls. Senior rats had lower SOD activity and higher MDA content than young rats. SOD activity was significantly lower and MDA content significantly higher in the Y-S group than in the Y-Y group. There were 548 transcript differences between senior and young kidneys with 36 upregulated and 512 downregulated transcripts. There were 492 transcript differences between Y-S and Y-Y groups with 127 upregulated and 365 downregulated transcripts. There were 1244 transcript differences between the S-Y and S-S groups with 680 upregulated and 574 downregulated transcripts. Oxidative stress and gene expression profile was significantly different in the Y-S compared to the S-Y group. The identified differences were mainly in the MAPK and insulin signal pathways, making these potential targets for therapeutic intervention.

Activation of reactive oxygen species and inflammation are implicated in renal ischemia/reperfusion (I/R) injuries. This study investigated whether grape seed proanthocyanidin extract (GSPE) protects against renal I/R injury by its effect on reactive oxygen species and the inflammation pathway. Wistar rats were administered GSPE before renal ischemia, followed by reperfusion for 24 hours. Plasma concentrations of urea, creatinine and cystatin C were measured for renal dysfunction. Serum and tissue superoxide dismutase activity and glutathione peroxidase and malondialdehyde levels were measured. Renal sections were analyzed for histological grading of renal injury, and nuclear factor-κB activity was determined. GSPE significantly reduced increases in urea, creatinine and cystatin C; increased kidney superoxide dismutase activity and glutathione peroxidase levels and reduced malondialdehyde levels. GSPE reduced histological renal damage and nuclear factor-κB activity. These results suggest that GSPE reduces renal dysfunction and injury caused by renal I/R.

The mTOR deregulation has a role in chronic kidney disease including diabetic nephropathy. SIRT1 is an important participant in renal cytoprotective responses to aging and stress. However, whether both mTOR and SIRT1 are involved in high glucose-inducing mesangial cells (MCs) senescence still remains to be explored. Hence we investigate the potential functional interrelationship between these two proteins in high glucose-inducing MCs senescence. High glucose increased mTOR expression and activity, but decreased SIRT1 expression and activity. The level of mTOR was increased significantly, while the SIRT1 expression and activity was declined significantly with serial cell culture passage. The siRNA-SIRT1 and nicotinamide promoted MCs senescence. NAD or resveratrol arrested high glucose-inducing MCs senescence. Meanwhile, the effects of NAD or resveratrol on high glucose-inducing MCs senescence were also completely blocked by SiRNA-SIRT1. Rapamycin arrested MCs senescence induced by high glucose and prevented MCs senescence with serial cell culture passage, and meanwhile increased the SIRT1 expression and activity. Moreover, the effects of rapamycin on MCs senescence induced by high glucose were also completely blocked by treating cells with niacinamide or siRNA-SIRT1. These findings provide support for the hypothesis that SIRT1 is required for the effects of rapamycin on high glucose-inducing MCs senescence.

Background: Uric acid (UA) has proven to be a causal agent in endothelial dysfunction in which ROS production plays an important role. Calcium overload in mitochondria can promote the mitochondrial production of ROS. We hypothesize that calcium transduction in mitochondria contributes to UA-induced endothelial dysfunction.Methods and results: We first demonstrated that high concentrations of UA cause endothelial dysfunction, marked by a reduction in eNOS protein expression and NO release in vitro. We further found that a high concentration of UA increased levels of [Ca2+](mito), total intracellular ROS, H2O2, and mitochondrial O-2(center dot-), and Delta psi(mito) but not the [Ca2+](cyt) level. When the mitochondrial calcium channels NCXmito and MCU were blocked by CGP-37157 and Ru360, respectively, the UA-induced increases in the levels of [Ca2+](mito) and total intracellular ROS were significantly reduced. Mitochondrial levels of O-2(center dot-) and Delta psi(mito) were reduced by inhibition of NCXmito but not of MCU. Moreover, inhibition of NCXmito, but not of MCU, blocked the UA-induced reductions in eNOS protein expression and NO release.Conclusions: The increased generation of mitochondrial O-2(center dot-) induced by a high concentration of UA is triggered by mitochondrial calcium overload and ultimately leads to endothelial dysfunction. In this process, the activation of NCXmito is the major cause of the influx of calcium into mitochondria. Our results provide a new pathophysiological mechanism for UA-induced endothelial dysfunction and may offer a new therapeutic target for clinicians. (C) 2012 Elsevier Ltd. All rights reserved.

BACKGROUND/AIMS:The Kruppel-like factor-15 (KLF15), a DNA-binding transcription factor, is highly expressed in endothelial and mesangial cells of the kidney. However, its effects on mesangial cell proliferation have not previously been investigated. In this study, we investigated the effect of KLF15 on mesangial cell proliferation.METHODS:We established a classic rat anti-Thy1 mesangial proliferative nephritis model. Affymetrix rat U230 2.0 chip was used to detect the gene expression profiles at different time point in the model. The different expression of KLF15 was shown during mesangial cell proliferation period and proliferation declined period of anti-Thy1 nephritis model by microarray analysis, Real-time PCR and Western blotting. Then we determined the effects of KLF15 and its downstream target, cell cycle regulation factor E2F1 on the proliferation of mesangial cells and the expression of the positive-acting cell cycle regulatory proteins, cyclinD1 and CDK2, by means of positive and negative interference experiments in cultured rat mesangial cells. We detected also protein expression of E2F1, cyclinD1 and CDK2 in vivo.RESULTS:By real-time PCR, Western blotting, and microarray analysis, KLF15 expression was shown to be lower during mesangial cell proliferation period and higher during proliferation declined period and under normal conditions. The mesangial cell proliferation was reduced and the expression of E2F1, cyclin D1 and CDK2 was downregulated in mesangial cells overexpressing KLF15. When KLF15 expression was inhibited by siRNA, the expression of E2F1, cyclin D1 and CDK2 and mesangial cell proliferation were increased. When E2F1 was inhibited by siRNA, protein level of CDK2 and cyclin D1 were lower than control. When siE2F1 was co-transfected with siKLF15 into mesangial cells, the increase of cell proliferation induced by siKLF15 was eliminated partly by siE2F1. Moreover, E2F1, cyclin D1 and CDK2 were higher expression during mesangial cell proliferation period, and were downregulated during proliferation declined period in vivo.CONCLUSIONS:These results suggest that KLF15 inhibits mesangial cell proliferation, possibly by regulating the expression of cell cycle regulation proteins through E2F1. Thus, KLF15 may be a useful target for therapeutic intervention in mesangial proliferative glomerulonephritis.

The molecular basis for aging of the kidney is not well understood. MicroRNAs (miRNAs) contribute to processes such as development, differentiation, and apoptosis, but their contribution to the aging process is unknown. Here, we analyzed the miRNA expression profile of young (3-month) and old (24-month) rat kidneys and identified the biologic pathways and genes regulated by differentially expressed miRNAs. We observed upregulation of 18 miRNAs with aging, mainly regulating the genes associated with energy metabolism, cell proliferation, antioxidative defense, and extracellular matrix degradation; in contrast, we observed downregulation of 7 miRNAs with aging, principally targeting the genes associated with the immune inflammatory response and cell-cycle arrest. Bioinformatics analysis suggested that superoxide dismutase 2 (SOD2) and thioredoxin reductase 2 (Txnrd2), located in the mitochondria, are potential targets of miR-335 and miR-34a, respectively. Aging mesangial cells exhibited significant upregulation of miR-335 and miR-34a and marked downregulation of SOD2 and Txnrd2. miR-335 and miR-34a inhibited expression of SOD2 and Txnrd2 by binding to the 3'-untranslated regions of each gene, respectively. Overexpression of miR-335 and miR-34a induced premature senescence of young mesangial cells via suppression of SOD2 and Txnrd2 with a concomitant increase in reactive oxygen species (ROS). Conversely, antisense miR-335 and miR-34a inhibited senescence of old mesangial cells via upregulation of SOD2 and Txnrd2 with a concomitant decrease in ROS. In conclusion, these results suggest that miRNAs may contribute to renal aging by inhibiting intracellular pathways such as those involving the mitochondrial antioxidative enzymes SOD2 and Txnrd2.

OBJECTIVE:To evaluate the effects of erythropoietin (EPO) combined with granulocyte-colony stimulating factor (G-CSF) on left ventricular function and ventricular remodeling after acute myocardial infarction (AMI) and investigate the possible mechanism.METHODS:The experimental design consisted of 5 groups of rats, namely the sham, myocardial infarction (MI) model, MI with EPO treatment, MI with G-CSF treatment, and MI with EPO plus G-CSF treatment groups. Apoptosis of the cardiomyocytes was detected by TUNEL staining, and HE staining, Masson trichrome staining, scarlatinum staining, and VIII agent staining were used to evaluate the survival, scar collagen deposition, and angiogenic effects. The cardiac structure and function of the rats after the treatments were assessed by echocardiography and hemodynamic examination.RESULTS:Echocardiography indicated that LVEF and FS were improved in all the intervention groups 7 days after MI, and the rats in EPO plus G-CSF treatment group showed the most obvious reduction of LVESD and LVESV (P<0.01). On day 28 after MI, all the intervention groups showed improvements in LVEF, FS, LVESD, LVEDD, LVESV and LVEDV, which were especially obvious in the combined treatment group; the interventions, especially the combined treatment, also resulted in decreased LVEDP and increased LVSP and +dP/dtmax. On day 1 after MI, the number of apoptotic cells was significantly greater in the MI model group than in EPO and G-CSF groups, and was the fewest in the combined treatment group (P<0.01). On day 28, the number of new vessels increased and the scar and collagen deposition reduced in the EPO and G-CSF groups, and these changes were more obvious in the combined treatment group.CONCLUSIONS:EPO combined with G-CSF can prevent left ventricular remodeling and improve cardiac systolic and diastolic functions by inhibiting cardiomyocyte apoptosis, reducing tissue collagen deposition and inducing neovascularisation.

目的 观察氯沙坦和厄贝沙坦分别联合前列地尔对早期糖尿病肾病蛋白尿的疗效.方法 早期糖尿病肾病患者55例按随机数字表法分为A组(氯沙坦+前列地尔,29例)和B组(厄贝沙坦+前列地尔,26例),氯沙坦基础剂量为50mg/d,厄贝沙坦基础剂量为150mg/d,两组均静脉滴注前列地尔注射液10μg/d,治疗前和治疗2周后监测血压,检测血肌酐、血尿素氮、血尿酸、24 h尿蛋白.结果 A组和B组治疗后24 h尿蛋白较治疗前均明显下降[分别为(0.46±0.21)g比(0.85±0.32)g、(0.38±0.19)g比(0.91±0.37)g],差异有统计学意义(P＜0.01),但两组治疗前后比较差异无统计学意义(P＞0.05),两组治疗前后血肌酐、血尿素氮、血尿酸无明显改变.A组伴有高尿酸血症16例患者血尿酸水平治疗后较治疗前显著下降[(445±58)μmol/L 比(527±69)μmol/L](P＜0.05),B组伴有高尿酸血症11例患者血尿酸水平治疗前后比较差异无统计学意义(P＞0.05).结论 在血糖控制平稳,血压控制达标情况下,血管紧张素Ⅱ受体抑制剂联合前列地尔治疗能有效降低早期糖尿病肾病患者的尿蛋白;氯沙坦更能显著降低血尿酸,在伴有高尿酸血症的患者中更具保护作用.

Objective To report a case of shrinking men syndrome(SMS) accompanying physiognomy change caused by renal osteodystrophy in a female patient with uremia undergoing dialysis and to analyze its pathogenesis.Methods Clinical and imaging data about the patient were analyzed.Clinical characteristics of SMS as well as its prevention and treatment were studied by reviewing the related literature.Results The iPTH of the patient increased to 2 208pg/L one year after regular renal dialysis.She was treated with 2.0μg Rocaltrol,twice a week for 4 weeks.Malformation of her face and articulations of both hands occurred and exacerbated accompanying left spinal bending,severe bone pain,and skin itching 2 years later.Spontaneous left femoral fracture occurred 6 years later.Her body height was 8cm shorter after dialysis.After high-volume blood dialysis,subtotal parathyroidec-tomy,correction of Ca and P metabolic disturbance,her bone pain and skin itching were significantly relived with her iPTH decreased to 160pg/L.Conclusion The quality of life in patients with SMS can be improved by early intervention of calcium and phosphorus metabolism,rational supplement of active VitD3,control of parathyroid hormone at the target range,and reduction of severe renal osteodystrophy incidence.

Objective:To explore the protective effects of Putian capsule on renal ischemia reperfusion injury(I/R)rats models.Methods:Twenty-four Wistar male rats were divided evenly into 3 groups randomly:the Sham-operated group(group Sham),the renal ischemia reperfusion injury group(group I/R)and the Putian preconditioning group(group PT).The rats in group I/R and PT were made I/R models by operation and the ischemia time was 1 hour.The PT group were treated by PT 160 mg·kg-1·d-1 before the operation.The levels of serum creatinine(Scr),blood urea nitrogen(BUN)and albumin(Alb)were detected respectively at 24,48 and 72 hour after ischemia and reperfusion(I/R)happened.Pathological changes in the different time were also noted by light microscope.Results:Compared with those in the sham group,the Scr and BUN were much higher in the control group after I/R at 24,48 and 72 hour,while these were not significantly elevated in PT group.The renal pathological changes were more severe in the model group than that of PT group.Conclusion:The results demonstrated that Putian capsule could protect the renal function against renal ischemia reperfusion injury and it could be used as a valuable clinical product.