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Navigating nephrotoxic waters:A comprehensive overview of contrast-induced acute kidney injury prevention 被引量:1
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作者 Panagiotis Theofilis Rigas Kalaitzidis 《World Journal of Radiology》 2024年第6期168-183,共16页
Contrast-induced acute kidney injury(CI-AKI)is the third leading cause of acute kidney injury deriving from the intravascular administration of contrast media in diagnostic and therapeutic procedures and leading to lo... Contrast-induced acute kidney injury(CI-AKI)is the third leading cause of acute kidney injury deriving from the intravascular administration of contrast media in diagnostic and therapeutic procedures and leading to longer in-hospital stay and increased short and long-term mortality.Its pathophysiology,although not well-established,revolves around medullary hypoxia paired with the direct toxicity of the substance to the kidney.Critically ill patients,as well as those with pre-existing renal disease and cardiovascular comorbidities,are more susceptible to CI-AKI.Despite the continuous research in the field of CI-AKI prevention,clinical practice is based mostly on periprocedural hydration.In this review,all the investigated methods of prevention are presented,with an emphasis on the latest evidence regarding the potential of RenalGuard and contrast removal systems for CI-AKI prevention in high-risk individuals. 展开更多
关键词 Contrast-induced acute kidney injury Contrast media PREVENTION HYDRATION RenalGuard Dyevert
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Pilot study on the effect of flavonoids on arterial stiffness and oxidative stress in chronic kidney disease
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作者 Anastasia Vagopoulou Panagiotis Theofilis +4 位作者 Despina Karasavvidou Nasra Haddad Dimitris Makridis Stergios Tzimikas Rigas Kalaitzidis 《World Journal of Nephrology》 2024年第3期41-48,共8页
BACKGROUND Flavonoids,the main class of polyphenols,exhibit antioxidant and antihypertensive properties.AIM To prospectively investigate the impact of flavonoids on arterial stiffness in patients with chronic kidney d... BACKGROUND Flavonoids,the main class of polyphenols,exhibit antioxidant and antihypertensive properties.AIM To prospectively investigate the impact of flavonoids on arterial stiffness in patients with chronic kidney disease(CKD)stagesⅠ-Ⅳ.METHODS In this prospective,single-arm study,CKD patients with arterial hypertension and diabetes mellitus were enrolled.Baseline demographic,clinical,and laboratory variables were recorded.Patients received daily treatment with a phenol-rich dietary supplement for 3 months.Blood pressure,arterial stiffness(carotidfemoral pulse wave velocity,central pulse pressure),and oxidative stress markers(protein carbonyls,total phenolic compound,total antioxidant capacity)were measured at baseline and at study end.RESULTS Sixteen patients(mean age:62.5 years,87.5%male)completed the study.Following intervention,peripheral systolic blood pressure decreased significantly by 14 mmHg(P<0.001).Carotid-femoral pulse wave velocity decreased from 8.9 m/s(baseline)to 8.2 m/s(study end)(P<0.001),and central pulse pressure improved from 59 mmHg to 48 mmHg(P=0.003).Flavonoids also reduced oxidative stress markers including protein carbonyls(P<0.001),total phenolic compound(P=0.001),and total antioxidant capacity(P=0.013).CONCLUSION Flavonoid supplementation in CKD patients shows promise in improving blood pressure,arterial stiffness,and oxidative stress markers. 展开更多
关键词 FLAVONOIDS Chronic kidney disease Arterial stiffness Oxidative stress Carotid-femoral pulse wave velocity
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炎症干扰PPARγ-LXRα-ABCA1途径介导的肾小球系膜细胞胆固醇外流 被引量:7
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作者 陈昱杨 陈曜 +3 位作者 赵蕾 李青 阮雄中 陈压西 《中国病理生理杂志》 CAS CSCD 北大核心 2010年第12期2400-2404,共5页
目的:观察炎症能否干扰过氧化物酶体增殖物活化受体γ(PPARγ)-肝X受体α(LXRα)-三磷酸腺苷结合盒转运体A1(ABCA1)途径介导的人肾小球系膜细胞(HMCs)的胆固醇外流。方法:将HMCs分为4组:对照组、高脂组[细胞给予100 mg/L低密度脂蛋白(L... 目的:观察炎症能否干扰过氧化物酶体增殖物活化受体γ(PPARγ)-肝X受体α(LXRα)-三磷酸腺苷结合盒转运体A1(ABCA1)途径介导的人肾小球系膜细胞(HMCs)的胆固醇外流。方法:将HMCs分为4组:对照组、高脂组[细胞给予100 mg/L低密度脂蛋白(LDL)处理]、炎症组[细胞给予20μg/L肿瘤坏死因子-α(TNF-α)处理]、联合干预组(细胞给予20μg/L TNF-α+100 mg/L LDL处理)。采用实时定量PCR和W esternb lotting方法检测PPARγ、LXRα和ABCA1的mRNA及蛋白表达水平。用[3H]标记胆固醇,液体闪烁计数法检测胆固醇外流量。用油红O染色法及化学酶促-比色法观察HMCs中脂质积聚情况。结果:与对照组相比,高脂组PPARγ、LXRα和ABCA1 mRNA及蛋白的表达明显增加,单纯的炎症刺激可下调它们的表达,而联合干预组中上述各基因和蛋白表达量比高脂组明显下降。胆固醇外流测定结果显示:与对照组相比,高脂组胆固醇外流量增加,而炎症组胆固醇外流量降低,联合干预组比高脂组胆固醇外流量明显减少。油红O染色提示联合干预组细胞内脂质积聚明显高于其余3组。细胞内胆固醇含量测定亦显示炎症能进一步加重胞内脂质积聚。结论:炎症因子可通过抑制PPARγ-LXRα-ABCA1表达导致HMCs胆固醇外流减少,加重细胞内脂质积聚。 展开更多
关键词 炎症 核受体 三磷酸腺苷结合盒转运体A1 人肾小球系膜细胞 胆固醇外流
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Can non-invasive measurements aid clinical assessment of volume in patients with cirrhosis? 被引量:3
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作者 Andrew Davenport Banwari Argawal +5 位作者 Gavin Wright Konstantinos Mantzoukis Rumyana Dimitrova Joseph Davar Panayota Vasianopoulou Andrew K Burroughs 《World Journal of Hepatology》 CAS 2013年第8期433-438,共6页
AIM:To evaluate the non-invasive assessments of volume status in patients with cirrhosis.METHODS:Echocardiography and multifrequency bioimpedance analysis measurements and short synacthen tests were made in 20 stable ... AIM:To evaluate the non-invasive assessments of volume status in patients with cirrhosis.METHODS:Echocardiography and multifrequency bioimpedance analysis measurements and short synacthen tests were made in 20 stable and 25 acutely decompensated patients with cirrhosis.RESULTS:Both groups had similar clinical assessments,cortisol response and total body water(TBW),however the ratio of extracellular water(ECW)/TBW was significantly greater in the trunk(0.420±0.004 vs0.404±0.005),and limbs(R leg 0.41±0.003 vs 0.398±0.003,P<0.05,and L leg 0.412±0.003 vs 0.399±0.003)with decompensated cirrhosis compared to stable cirrhotics,P<0.05).Echocardiogram derived right atrial and ventricular filling and end diastolic pressures and presence of increased left ventricular end diastolic volume and diastolic dysfunction were similar in both groups.The decompensated group had lower systemic blood pressure,mean systolic 101.8±4.3 vs122.4±5.3 and diastolic 58.4±4.1 mmHg vs 68.8±3.1 mmHg respectively,P<0.01,and serum albumin30(27-33)vs 32(31-40.5)g/L,P<0.01.CONCLUSION:Decompensated cirrhotics had greater leg and truncal ECW expansion with lower serum albumin levels consistent with intravascular volume depletion and increased vascular permeability. 展开更多
关键词 CIRRHOSIS BIOIMPEDANCE ECHOCARDIOGRAPHY EXTRACELLULAR water ASCITES CORTISOL
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The role of mycophenolate in the treatment of antineutrophil cytoplasmic antibody-associated vasculitis 被引量:2
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作者 Maria Koukoulaki Christos Iatrou 《World Journal of Nephrology》 2019年第4期75-82,共8页
Mycophenolic acid, the active metabolite for mycophenolate mofetil and mycophenolic sodium, is a strong, noncompetitive, reversible inhibitor of inosine monophosphate dehydrogenase, the key enzyme in de novo synthesis... Mycophenolic acid, the active metabolite for mycophenolate mofetil and mycophenolic sodium, is a strong, noncompetitive, reversible inhibitor of inosine monophosphate dehydrogenase, the key enzyme in de novo synthesis of guanosine nucleotides leading to selective inhibition of lymphocyte proliferation. Mycophenolic acid has been evaluated as induction and remission maintenance agent in the treatment of antineutrophil cytoplasmic antibody-associated vasculitis (AAV). Since the course of disease of AAV usually requires long term immunosuppression, mycophenolate has been explored as a less toxic agent compared to cyclophosphamide and azathioprine. Mycophenolate is a potent immunosuppressive agent in the therapy of AAV, non-inferior to other available drugs with comparable side effect profile. Therefore, it could be a valuable alternative in cases of toxicity with life threatening side effects or intolerance to cyclophosphamide or azathioprine, in cases with high cumulative dose of cyclophosphamide, but also in cases with insufficient response. Several studies have shown a higher relapse rate following discontinuation of mycophenolate or in mycophenolate treated subjects that raises concerns about its usefulness in the treatment of AAV. This review describes the efficacy of mycophenolate in AAV as remission induction agent, as remission maintenance agent, and as therapeutic option in relapsing AAV disease, the relapse rate following discontinuation of mycophenolate, and the adverse events related to mycophenolate treatment. 展开更多
关键词 Mycophenolic acid MYCOPHENOLATE mofetil MYCOPHENOLATE sodium Antineutrophil CYTOPLASMIC antibody-associated VASCULITIS Microscopic polyangiitis GRANULOMATOSIS with polyangiitis induction REMISSION Relapse
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Interplay between metabolic dysfunction-associated fatty liver disease and chronic kidney disease:Epidemiology,pathophysiologic mechanisms,and treatment considerations 被引量:1
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作者 Panagiotis Theofilis Aikaterini Vordoni Rigas G Kalaitzidis 《World Journal of Gastroenterology》 SCIE CAS 2022年第39期5691-5706,共16页
The recently proposed nomenclature change from non-alcoholic fatty liver disease to metabolic dysfunction-associated fatty liver disease(MAFLD)has resulted in the reappraisal of epidemiological trends and associations... The recently proposed nomenclature change from non-alcoholic fatty liver disease to metabolic dysfunction-associated fatty liver disease(MAFLD)has resulted in the reappraisal of epidemiological trends and associations with other chronic diseases.In this context,MAFLD appears to be tightly linked to incident chronic kidney disease(CKD).This association may be attributed to multiple shared risk factors including type 2 diabetes mellitus,arterial hypertension,obesity,dyslipidemia,and insulin resistance.Moreover,similarities in their molecular pathophysiologic mechanisms can be detected,since inflammation,oxidative stress,fibrosis,and gut dysbiosis are highly prevalent in these pathologic states.At the same time,lines of evidence suggest a genetic predisposition to MAFLD due to gene polymorphisms,such as the PNPLA3 rs738409 G allele polymorphism,which may also propagate renal dysfunction.Concerning their management,available treatment considerations for obesity(bariatric surgery)and novel antidiabetic agents(glucagon-like peptide 1 receptor agonists,sodiumglucose co-transporter 2 inhibitors)appear beneficial in preclinical and clinical studies of MAFLD and CKD modeling.Moreover,alternative approaches such as melatonin supplementation,farnesoid X receptor agonists,and gut microbiota modulation may represent attractive options in the future.With a look to the future,additional adequately sized studies are required,focusing on preventing renal complications in patients with MAFLD and the appropriate management of individuals with concomitant MAFLD and CKD. 展开更多
关键词 Metabolic dysfunction-associated fatty liver disease Chronic kidney disease Hepatic steatosis inflammation Type 2 diabetes mellitus Obesity
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SM22启动SCAP真核表达质粒的构建及其在CHO细胞中的表达 被引量:3
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作者 王媛媛 胡接力 +3 位作者 崔静 黄爱龙 阮雄中 陈压西 《生物工程学报》 CAS CSCD 北大核心 2010年第1期114-120,共7页
为建立平滑肌特异的固醇调节元件结合蛋白(SREBP)的裂解激活蛋白(SCAP)超表达的转基因小鼠,深入探讨SCAP的功能,本实验构建了由平滑肌特异蛋白SM22启动子(pSM22)启动仓鼠SCAP443位点突变体——SCAP(D443N)的真核表达质粒,并在仓鼠卵巢细... 为建立平滑肌特异的固醇调节元件结合蛋白(SREBP)的裂解激活蛋白(SCAP)超表达的转基因小鼠,深入探讨SCAP的功能,本实验构建了由平滑肌特异蛋白SM22启动子(pSM22)启动仓鼠SCAP443位点突变体——SCAP(D443N)的真核表达质粒,并在仓鼠卵巢细胞(CHO)验证其表达。利用巢式PCR从小鼠肝脏组织提取的基因组中扩增得到pSM22基因。先将其插入pMD-T载体,构建T-SM22,对pSM22测序后,通过双酶切将pSM22克隆到pGL3-control-Luc中,成为pGL3-SM22-Luc。转染pGL3-SM22-Luc到血管平滑肌(VSMCs)中,通过检测荧光素酶(Luc)值观察pSM22在VSMCs内的启动活性。利用PCR从pTK-HSV-SCAP(D443N)质粒中扩增出SCAP(D443N)后克隆入pGL3-control中,成为pGL3-SCAP。然后再将pSM22克隆入pGL3-SCAP中,成为表达质粒pGL3-SM22-SCAP(D443N)。转染表达质粒到CHO细胞,用real-timePCR和Western blotting验证SCAP(D443N)的表达。结果证实pSM22在体外VSMCs中能启动Luc的表达;表达质粒pGL3-SM22-SCAP(D443N)酶切及测序结果正确;将其转染到CHO细胞后,与转染pGL3-control的对照细胞相比SCAP(D443)mRNA和蛋白表达显著增强。 展开更多
关键词 SM22 启动子 SREBP裂解激活蛋白 质粒构建 基因表达 转染
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炎症干扰胆固醇调节元件结合蛋白2致ApoE/SRA/CD36三基因敲除小鼠肝脏脂质的异常积聚 被引量:1
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作者 闫凤 黄爱龙 +2 位作者 徐珍娥 阮雄中 陈压西 《中华肝脏病杂志》 CAS CSCD 北大核心 2010年第5期366-370,共5页
目的 研究炎症是否通过干扰核转录因子胆固醇调节元件结合蛋白2(SREBP-2)而致ApoE/SRA/CD36三基因敲除小鼠肝脏胆固醇的异常积聚.方法 将8周龄ApoE/SRA/CD36三基因敲除雄性小鼠随机分为对照组(n=8)和炎症组(n=8),2组均喂以西方饮... 目的 研究炎症是否通过干扰核转录因子胆固醇调节元件结合蛋白2(SREBP-2)而致ApoE/SRA/CD36三基因敲除小鼠肝脏胆固醇的异常积聚.方法 将8周龄ApoE/SRA/CD36三基因敲除雄性小鼠随机分为对照组(n=8)和炎症组(n=8),2组均喂以西方饮食(Western diet),炎症组小鼠皮下注射10%酪蛋白建立慢性炎症模型,对照组注射相应量磷酸盐缓冲液,14周后处死,测定血清中炎症介质和脂质的水平及肝组织中胆固醇含量,油红O、免疫组织化学染色后观察肝脂质沉积程度以及组织形态变化,实时定量PCR法检测肝脏SREBP裂解激活蛋白(SCAP)、SREBP-2及其下游基因低密度脂蛋白受体(LDLr)mRNA水平.对计量资料采用两样本均数比较的t检验进行统计学分析.结果 炎症状态下,血清中总胆固醇[(7.72±1.70)mmol/L]、低密度脂蛋白胆固醇[(2.94±0.44)mmol/L]、高密度脂蛋白胆固醇[(2.24±0.63)mmol/L]水平均显著降低,与对照组[分别为(13.23±3.61)mmol/L、(9.28±3.66)mmol/L、(4.13±0.42)mmol/L]比较,t值分别为3.383、4.245、5.937,P值均<0.05;肝组织中胆固醇含量显著增加;油红O染色表明,胆固醇在肝脏中的沉积异常增多(t=2.707,P<0.05);实时定量PCR和免疫组织化学检测结果表明胆固醇代谢相关基因SREBP2、LDLr和SCAP的mRNA和蛋白质表达水平显著增加. 结论炎症可以通过干扰SREBP-2导致低密度脂蛋白胆固醇摄取异常,造成肝脏脂质沉积增多和损害. 展开更多
关键词 炎症 肝脏 SREBP-2 ApoE/SRA/CD36三基因敲除小鼠
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