Chinese Journal of Nephrology

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Immunofecal occult blood test predicts the prognosis of patients with chronic kidney disease

ZHOU Hui;MOU Shan;YANG Hai-yun;WANG Qin;SHI Bei-li;GU Le-yi;HANG Ying;NI Zhao-hui.

2012, 28(6): 429-434.

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Objective To evaluate the value of immunofecal occult blood test(IFOBT) as a prognostic indicator in CKD patients with colorectal impairment. Methods A total of 176 CKD patients and 180 healthy adults as control were enrolled. Serum biochemistry was measured at baseline and gastrointestinal bleeding was determined by IFOBT. All the CKD patients were followed up for 4.5 years. Renal replacement therapy or death was defined as end-point event. The Logistic regression analysis was used for risk factors. Kaplan-Meier analysis and COX regression model were used for survival analysis. Results The positive rate of IFOBT in CKD patients was significantly higher than healthy control (17% vs 5.3%, χ2=13.236, P<0.01). When comparing with IFOBT negitive patients, IFOBT positive patients were older[(62.030±15.544) years old vs (48.660±19.018)years old, P<0.01], had higher ESR [(71.800±31.657) mm/h vs ( 57.210±32.712) mm/h, P<0.05], C-reactive protein[6.230(3.000～14.148) mg/L vs 3.000(3.000～6.833) mg/L, P<0.05], serum creatinine [419.100(103.200～546.625) μmol/L vs 175.100（68.150～462.950） μmol/L, P<0.05], and had lower hemoglobin level[(97.970±20.590) g/L vs (107.170±27.988) g/L, P<0.05] and eGFR [11.400 (8.671～53.544) ml•min-1•(1.73 m2)-1 vs 35.274 (10.961～82.145) ml•min-1•(1.73 m2)-1, P<0.01]. There was a negative correlation between IFOBT value and eGFR in CKD patients (r=-0.20, P<0.01). Positive correlations of IFOBT value with age (r=0.175, P<0.05) and serum creatinine (r=0.171, P<0.05) were found. Logistic regression and COX regression analysis showed that IFOBT value, eGFR and ESR were important factors that influenced the prognosis of CKD patients. Kaplan-Meier analysis revealed that IFOBT value >100 μg/L predicted progression of renal function. Conclusions The prevalence of gastrointestinal bleeding disorder is high in patients with CKD. Value of IFOBT independently predicts decline in renal function of CKD patients.

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Clinicopathological analysis of lupus nephritis with antinucleosome antibody

ZHENG Zhao-hui;LIU Wei-xia;LEI Yong-sheng;ZHANG Li-juan;LU Hua-qing;XING Guo-lan;QUAN Song-xia;LIU Zhang-suo.

2012, 28(6): 435-438.

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Objective To explore the clinicopathological characteristics of lupus nephritis (LN) with antinucleosome antibody (AnuA). Methods Data of 481 patients with biopsy-proven LN in the First Affiliated Hospital of Zhengzhou University from 2004 to 2011 were analyzed retrospectively. The patients were divided into two groups: AnuA-positive group (76 patients) and AnuA-negative group (405 patients). The clinical manifestations, laboratory examinations, histopathologic classes of LN, disease activity measured by SLE disease activity index (SLEDAI) of two groups were investigated and compared. Results There were 15 male patients in positive group (15/76, 19.74%) with mean age of (27.99±10.88) years and 45 patients in negative group (45/405, 11.11%) with mean age of (31.15±12.15) years respectively, which showed that male patients were more common in positive group (P＜0.05). Incidences of oral ulcer, fever, anemia, low complement and positive anti-dsDNA antibody were higher in positive group (P＜0.05). Percentage of diffuse proliferative lupus nephritis(class Ⅳ) and pathological activity index (AI) in positive group were higher compared to negative group (all P＜0.05), while no significant differences of other pathological types, chronic index (CI) and SLEDAI were found between two groups. Conclusion LN patients with positive AnuA have special clinicopathological characteristics and AnuA may be used as a promising biomarker for the proliferative LN.

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A retrospective study on management of gross hematuria in autosomal dominant polycystic kidney disease patients

MA Yi-yi;CHEN Dong-ping;MEI Chang-lin;YU Sheng-qiang;RONG Shu;ZHANG Tong;LI Lin.

2012, 28(6): 439-443.

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Objective To search the ideal management for gross hematuria in autosomal dominant polycystic kidney disease (ADPKD). Methods ADPKD patients who were ever hospitalized and followed up in our department since 1993 were enrolled in the study. Demographic and clinical data were colloected, such as gender, age of gross hematuria, level of renal function, causative factors, management strategies, duration of gross hematuria, blood platelet count, activated partial thromboplastin time, prothrombin time, international normalized ratio, size of kidney cyst and so on. ADPKD patients were divided into different groups according to causative factors or management. The clinical data were compared among groups. Results A total of 905 ADPKD patients were screened, among whom 279 patients ever had gross hematuria (male/female:150/129). One hundred and forty-six patients had integrated therapeutic process records, while only 101 patients could provide relevant laboratory examination results. In these 101 patients, gross hematuria was found in any stage of chronic kidney disease (CKD); the average eGFR was (56.4±44.1) mml•min-1•(1.73 m2)-1; the duration of gross hematuria was (8.8±8.0) d; no significant difference between male and female in duration of gross hematuria existed [(8.2±7.3) d vs (9.5±8.8) d, P=0.426]; coagulation parameters were all normal. The platelet count was also normal in 91 patients. Duration of gross hematuria among groups divided according to different causative factors was significantly different (P<0.05). The patients in bed rest group had significantly shorter duration of gross hematuria compared with other groups (P<0.05). The platelet count, prothrombin time and international normalized ratio were all at similar level in different groups. Conclusions The causative factors in ADPKD patients with gross hematuria should be confirmed as the first step of management strategies. Bed rest is the key point in management. Antifibrinolytic agent is a proper choice in the cases receiving hemostatic drugs. It is unnecessary to use antibiotic agent for prevention.

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Epidemiologic investigation of chronic kidney disease in Chengdu urban population

GUO Zong-lin;WANG Qi-rong;ZHOU Ya-nan;LIANG Jiang-hong;DONG Jun-yi;FU Bin;YANG Fu-hua;LU Xiao-qiong;SU Xiao-yu;FU Ping.

2012, 28(6): 444-449.

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Objective To investigate the prevalence and risk factors of chronic kidney disease (CKD) in Chengdu urban population and the prevalence of CKD in risk population. Methods Questionnaire (anamnesis, smoking, drink) of risk factors of CKD and somatoscopy (blood pressure, body height and body weight) were carried out in railman of Chengdu urban. Their blood and urine indicators (blood sugar, blood lipid, blood uric acid, blood creatinine, uromicroprotein/creatinine ratio, routine urine examination, etc) were measured. The prevalence and risk factors of CKD in Chengdu urban population and the prevalence of CKD in risk population were elucidated. Results Eligible data of 5326 subjects were enrolled in the study． After the adjustment of age and gender component, the prevalence of albuminuria was 11.54%, reduced eGFR was 5.54%, hematuria was 3.87%, and CKD was 18.32%; the recognition was 1.93%. In addition, the prevalence of albuminuria was respectively 23.79%, 28.00%, 14.08%; prevalence of reduced eGFR was respectively 4.76%, 4.53%, 3.26%; prevalence of hematuria was respectively 2.94%, 3.20%, 2.37% in 3098 people with hypertension, diabetes or hyperlipaemia. Independent risk factors of albuminuria were female, hypertension, diabetes, hyperlipemia and high BMI. Independent risk factors of reduced eGFR were female, age, hyperuricemia and hypertension. Drink was negatively correlated with reduced eGFR. Independent risk factors of hematuria were female and age. Conclusions The prevalence of CKD is quite high and the recognition rate is low in the Chengdu urban populaton. Risk factors of CKD are age, female, diabetes, hypertension, hyperlipemia, hyperuricemia and high BMI. Control of the development of metabolic disease can reduce the CKD.

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Analysis of the incidence and risk factors of acute kidney injury in respiratory failure patients

YANG Qian-hua;YAN Yu-cheng;CHE Miao-lin;ZHANG Wei-ming;WANG Qin;LU Ren-hua;ZHU Ming-li;NI Zhao-hui;QIAN Jia-qi.

2012, 28(6): 450-454.

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Objective To determine the incidence and risk factors of acute kidney injury(AKI) in respiratory failure patients. Method Clinical data of 235 patients diagnosed as respiratory failure admitted in respiratory division and internal medicine intensive care unit in Renji Hospital from January 2006 to December 2008 were analyzed retrospectively. Patients' demographics, clinical data and laboratory examinations before and after respiratory failure were collected. The incidence, clinical risk factors and hospital mortality of AKI in the respiratory failure patients were analyzed. Multivariate Logistic regression analysis was used to investigate the independent risk factors of AKI in these patients. Results Of the total 235 patients, the average age was (70.05±12.85) years old, the ratio of male to female was 1.90∶1. Seventy-seven patients developed AKI and the incidence was 32.8%. The incidence of AKI in those with hypertension (44.4% vs 26.6%, P<0.01) or chronic kidney disease(66.7% vs 31.3%, P<0.01) was significantly higher. The incidence of AKI in patients with mechanical ventilation was much higher than those without mechanical ventilation（44.8% vs 13.3%, P<0.01). The incidence of multi-organ system failure (33.8% vs 5.7%, P<0.01), the failure of weaning from mechanical ventilation(69.2% vs 32.5%，P<0.01) and the mortality (51.9% vs 13.3%, P<0.01) in AKI patients were higher than those without AKI. Multivariate Logistic regression analysis showed that age (OR=1.668), anemia (OR=0.980), baseline serum creatinine (OR=1.071) and mechanical ventilation (OR=3.222) were independent risk factors of AKI. Conclusions Incidence and mortality of AKI are quite high in respiratory failure patients. Age, baseline serum creatinine, anemia and mechanical ventilation are independent risk factors of AKI.

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Effect of donor age on prognosis of living donor kidney transplantation

CHEN Guo-dong;ZHANG Xiao-dan;SHI Lei;WANG Xiao-qin;ZHAI Jie;CHEN Li-zhong.

2012, 28(6): 455-459.

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Objective To assess the impact of donor age on the outcome of living donor kidney transplantation. Methods A total of 217 patients undergoing living donor kidney transplantation during 2004 to 2011 were enrolled in our retrospective study. The recipients were divided into different groups according to their donors’ age or the age gaps between donors and recipients. A follow-up survey was conducted to evaluate the serum creatinine level and the incidence of complications after transplantation. Results As the donors age grew, the recipients’ serum creatinine increased. The serum creatinine levels of patients with older donors(age gap>5 years) at 1 month[(143.5±42.1) μmol/L vs (114.4±30.4) μmol/L], 3 months (139.9±36.6) μmol/L vs (110.6±33.3) μmol/L], 1 year [(132.1±22.1) μmol/L vs (105.5±35.9) μmol/L] and 2 years (132.0±45.4) μmol/L vs (97.2±17.5) μmol/L] after operation were significantly higher than those with younger donors(age gap<-5)(P<0.05). The incidence of acute rejection (19.4% vs 9.7%, P<0.05) and chronic rejection (9.7% vs 1.4%, P<0.05) was significantly higher in the group with donors older than 50 years old than those with donors younger than 50 years old. But no significant difference was observed in the survival of the grafts or the recipients. Age gap between the donor and recipient was an independent risk factor for abnormal serum creatinine level at 2 years after transplantation (OR=5.010, P<0.05). Conclusions Donor age is an important impact factor on the outcome of living donor kidney transplantation. Recipients of older living donation have poorer prognosis.

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Anemia aggravates clinical and pathological changes in patients with IgA nephropathy

HE Ting;MAO Hai-ping;LI Zhi-bin;GUO Na;XU Ri-cong;YANG Xiao;YU Xue-qing;LI Zhi-jian.

2012, 28(6): 460-463.

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Objective To analyze the changes of clinical and pathological features in the patients of IgA nephropathy with anemia. Methods Four hundred and nine patients of IgA nephropathy diagnosed by renal biopsy were classified into two groups: IgA nephropathy with non-anemia (group 1) and IgA nephropathy with anemia (group 2). Changes were studied retrospectively between the groups. Results Serum hemoglobin level was correlated with the clinical parameters of IgA nephropathy. Compared to group 1, changes in group 2 were as followed: serum creatinine increased, eGFR decreased, proteinuria increased; the global sclerosis, segmental sclerosis, crescents and tubulointerstitial lesions worsened. The glomerular and tubulointerstitial lesions were negatively correlated with serum hemoglobin and eGFR, but positively correlated with serum uric acid and proteinuria (P<0.05). Multivariate Logistic regression analysis revealed that anemia was an independent risk factor for the tubulointerstitial lesion. Conclusion Clinical feature and pathological damages in the patients of IgA nephropathy with anemia are more serious than those with non-anemia.

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Effects of a novel PPARγ agonist on Wnt-β-catenin pathway in ADPKD cystic-lining epithelial cells

FU Li-li;LIU Mo-yan;LIU Chun-yan;HU Hui-min;MEI Chang-lin.

2012, 28(6): 464-468.

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Objective To investigate the effects of a novel PPARγ agonist DH9 on Wnt-β-catenin pathway in human polycystic kidney cystic-lining epithelial cells(WT9-12). Methods WT9-12 cells were treated with different concentrations of DH9 for 72 hours and the proliferation was assessed by MTT. WT9-12 cells were pretreated with SB216763 or GW9662 for two hours and then treated with DH9 for 72 hours. Western blotting was applied to detect the protein expression of β-catenin, phospho-β-catenin, GSK3β, phospho-GSK3β. Results DH9 could effectively inhibit the proliferation of the cells. 60μmol/L DH9 could facilitate β-catenin down-regulation(P<0.01) and phospho-β-catenin up-regulation(P<0.01). Inhibition of GSK3β by SB216763 could protect WT9-12 cells against DH9-facilitated β-catenin repression in a dose-dependent manner despite phosphorylating deactivation, but PPARγ inhibitor GW9662 couldn’t. Conclusions DH9 can effectively block the proliferation of WT9-12 cells. The effect may be mediated by facilitating the down-regulation of β-catenin via GSK3β-dependent mechanism.

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The interaction between Cdc42-interacting protein 4 and β-catenin in renal tubular epithelial-mesenchymal transition

XU Chu-ou;ZHANG Ya-min;LIU Ping;ZHOU Qiao-dan;ZENG Rui;BAI Shou-jun;PEI Guang-chang;HAN Min;LIU Li-li;XU Gang.

2012, 28(6): 469-475.

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Objective To investigate the expression and distribution of Cdc42-interacting protein 4 (CIP4) in renal fibrotic tissue, and the interaction between CIP4 and β-catenin in transforming growth factor β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) model of HK-2 cell line. Methods In vivo, the model of renal fibrosis was induced by 5/6 subtotal nephrectomy in rat. Masson staining was used to evaluate the level of renal tissue fibrosis. The expression and distribution of CIP4 was detected by immunohistochemistry. In vitro, the EMT model of HK-2 cell line was induced by TGF-β1 (10 μg/L) for 72 h. Western blotting was used to observe the expression of E-cadherin, β-catenin, CIP4 and α-SMA. Colocalization and interaction of CIP4 and β-catenin were detected by immunofluorescence and immunoprecipitation respectively. Results Compared to sham group, CIP4 expression was increased in group of 5/6 subtotal nephrectomy, CIP4 was mainly distributed in basolateral side of renal tubular epithelia. In vitro, expressions of α-SMA and CIP4 were increased in HK-2 cells stimulated by TGF-β1 for 72 h (2.5 and 1.8 folds, respectively) (all P<0.05), expression of E-cadherin was decreased(P<0.05). Partial colocalization between CIP4 and β-catenin was detected by immunofluorescence. In control group, CIP4 and β-catenin partially colocalized at the cell membrane. After the stimulation of TGF-β1, translocation to nucleus of CIP4 and β-catenin were increased, and partially colocalized in nucleus. The interaction between CIP4 and β-catenin was observed by immunoprecipitation in both control and TGF-β1 stimulated groups. Conclusions Expression of CIP4 in renal fibrotic tissue is increased, which is mainly distributed in basolateral side of renal tubular epithelia. CIP4 and β-catenin partially colocalize and interact with each other. CIP4 may play a role in EMT process through the interaction with β-catenin.

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Effect of losartan on the glomerular protein expression profile of type 2 diabetic KKAy mice

FAN Qiu-ling;YANG Gang;LIU Xiao-dan;MA Jian-fei;FENG Jiang-min;JIANG Yi;WANG Li-ning.

2012, 28(6): 476-483.

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Objective To investigate the effects of angiotensin receptor blocker (ARB) losartan on the glomerular protein expression profile of spontaneous type 2 diabetic KKAy mice by two-dimensional differential gel electrophoresis and MALDI-TOF mass spectrometry. Methods 8-week-old spontaneous type 2 diabetic KKAy mice were randomly divided into losartan (10 mg• kg-1•d-1 given in drinking water) treatment group and non-treatment group. Eight-week-old C57BL/6 mice were used as normal control. The glomeruli were separated by magnetic bead perfusion through thoracic aorta at age of 20 weeks, then glomerular protein was extracted. The glomerular protein expression profile was investigated by CyDyes minimal fluorescence labelling, two-dimensional differential gel electrophoresis and MALDI-TOF mass spectrometry. Results KKAy mice developed higher body weight and blood glucose, higher urinary microalbumin creatinine ratio at age of 20 weeks than C57BL/6 mice at the same age (all P<0.05). Losartan treatment markedly reduced urinary microalbumin creatinine ratio [(539.71±100.23)mg/g vs (728±177.19) mg/g], attenuated mesangial expansion and the thickening of glomerular basement membrane, but had no effect on the blood glucose. By DeCyder 2-D differential analysis software, 62 protein spots of differential expression were found in glomeruli between losartan treatment and non-treatment KKAy mice at age of 20 weeks. Among them, 41 proteins were identified by peptide mass fingerprinting. The expressions of 28 proteins were up-regulated by losartan treatment, including glycerokinase, sulfite oxidase, glycine amidinotransferase, adenosylhomocysteinase, etc. The expressions of 13 proteins were down-regulated by losartan treatment, including 3-mercaptopyruvate sulfurtransferase, ATP synthase subunit d, 60 000 heat shock protein, stress-70 protein(alternative name 75 000 glucose-regulated protein, GRP75), etc. Six differentially expressed proteins were found in glomeruli between non-treatment KKAy mice and C57BL/6 mice, and the differential expressions were suppressed by losartan treatment, including dihydrolipoyllysine-residue acetyltransferase component of pyruvate dehydrogenase complex, succinyl-CoA ligase (GDP-forming) subunit beta, mitochondrial, ATP synthase subunit d, GRP75, nucleoside diphosphate-linked moiety X motif 19 and selenium-binding protein 1. Conclusions Losartan significantly reduces the urinary protein excretion rate and renal pathological lesion of spontaneous type 2 diabetic KKAy mice, and suppresses the differential expression of mitochondrial ATP synthase subunit d, GRP75, selenium-binding protein 1, etc in glomeruli. Losartan may play a renoprotective role by reducing glomerular mitochondrial reactive oxygen species genesis and inhibiting oxidative stress.

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Impact of peptide binding domain of heat shock protein 72 on epithelial to mesenchymal transition

CAO Tao;CAO Shi-rong;LI Hui-yan;XIONG Li-ping;FAN Jin-jin;YU Xue-qing;MAO Hai-ping.

2012, 28(6): 484-488.

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Objective To investigate the effects of peptide-binding domain (PBD) of heat shock protein (HSP) 72 on epithelial to mesenchymal transition (EMT) in rat renal tubular epithelial cells. Methods The expressions of wild-type HSP72, mutant of HSP72 lacking peptide binding domain (HSP72 -△PBD) and HSP72-PBD were induced by plasmid transfection. NRK-52E cells were stimulated by TGF-β1 for 48 h. The expressions of α-smooth muscle actin (α-SMA), E-cadherin, HSP72 and Smad3/p-Smad3 were detected by Western blot and immunofluorescence. Results After NRK-52E cells were stimulated by TGF-β 1 (10 μg/L) for 48 h, the expression of α-SMA was increased and the protein level of E-cadherin was decreased. Western blotting and immunofluorescence showed that over-expression of both HSP72 and PBD inhibited TGF-β1-induced up-regulation of protein α-SMA expression, down-regulation of protein E-cadherin. However, over-expression of HSP72-△PBD did not change the protein level of E-cadherin and α-SMA. In addition, over-expression of HSP72 and PBD significantly inhibited the phosphorylation of Smad3. Conclusion Inhibition of Smad3 activation and EMT by HSP72 is associated with the function of PBD.

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临床研究

基础研究

临床研究

基础研究