冠脉造影术后对比剂肾病的研究进展

随着人口老龄化以及饮食结构的改变,冠心病发病率逐年升高。冠状动脉造影技术在临床中广泛开展,导致对比剂肾病(contrast-induced nephropathy,CIN)的发病率不断上升。CIN的发生与患者本身的基础肾脏疾病及术前血糖水平等危险因素密切相关。对比剂会影响肾脏血流动力学,同时对肾小管有直接毒性作用,最新研究显示炎症反应参与了CIN的发生,但其具体发病机制尚未完全阐明。在CIN的早期诊断中,新的生化指标较血肌酐值可更早反应对比剂使用后肾功能的损害。除静脉水化疗法外,新型的药物在防治CIN中起到一定作用。CIN对患者的预后有重要影响,认识和熟悉CIN的高危因素、发病机制及早期诊断方法,对预防冠脉造影术后引发的肾脏损害尤为重要。该文就CIN的发病机制、高危因素、早期诊断、防治方法等方面的研究进展进行综述。     

冠状动脉粥样硬化性心脏病介入操作后造影剂肾病发病的相关因素分析

目的:分析行冠状动脉介入操作后的冠状动脉粥样硬化性心脏病患者发生造影剂肾病的相关性及危险因素.方法:收集我院心内科2011年9月至2012年3月共计325例使用造影剂威视派克对行介入操作的冠状动脉粥样硬化性心脏病患者的临床资料,分析入选病例的基线资料和造影剂肾病(contrast-induced nephropathy,CIN)的发病率,分组讨论CIN发生的相关危险因素.结果:325例行冠脉介入的冠状动脉粥样硬化性心脏病患者中有28例发生CIN(发病率为8,6％),高龄、合并高血压、2型糖尿病、左心收缩功能不全、eGFR＜60mL/min/1.73m2、使用较高剂量造影剂(≥95mL)、诊断为急性冠脉综合征、存在冠脉病变的患者CIN发病率较高(P＜0.05).logistic回归分析显示高血压(RR=5.11,P=0.036),诊断急性冠脉综合征(RR=2.67,P=0.049),eGFR＜60mL/min/1.73m2(RR=6.50,P=0.003)是CIN发病的危险因素.结论:高龄,高血压,2型糖尿病,左心收缩功能不全,eGFR＜60mL/min/1.73m2及造影剂剂量较大,诊断急性冠脉综合征,存在冠脉病变等高危因素的患者CIN发病率高.高血压,诊断急性冠脉综合征,eGFR＜60mL/min/1.73m2可能是CIN发生的危险因素.     

冠心病患者PCI术后对比剂肾病发生的预测因素的临床研究

目的:探讨冠心病患者PCI术后发生对比剂肾病(Contrast Media Induced Nephropathy,CIN)的预测因素。方法:入选2015年1月至2015年9月长海医院确诊为冠心病并接受PCI治疗的≥75岁老年患者共计317例,根据CIN评分分成CIN评分低分组(4-10分)、CIN评分中分组(11-16分)、CIN评分高分组(≥16分),分析比较不同CIN评分组患者的术后对比剂肾病的发生情况;对相关危险因素进行单因素及多因素分析,探讨冠心病PCI患者发生对比剂肾病的独立预测因子。结果:317例冠心病PCI患者中,14例发生CIN(4.4%),CIN评分高分组比例最高(4例,11.8%,P=0.042)。单因素分析表明,CIN风险评分、术前GFR、术前肌钙蛋白、术前总胆固醇、急性心肌梗死、Syntax评分在术后CIN发生中存在显著的统计学差异(P0.05),为独立的风险预测因素。多因素Logistic回归分析结果显示,CIN风险评分在术后CIN发生中存在显著的统计学差异(95%CI:1.37-7.78,P0.05),术前GFR在术后CIN发生中存在显著的统计学差异(95%CI:1.01-1.07P0.05),两者均为独立预测因子。结论:CIN风险评分、术前GFR是高龄冠心病患者PCI术后发生CIN的独立预测因子。     

糖尿病合并急性心肌梗死患者PCI术后造影剂肾病的危险因素及SHI、HbA1c的预测价值研究

摘要 目的：探讨糖尿病合并急性心肌梗死（AMI）患者经皮冠状动脉介入治疗（PCI）术后造影剂肾病（CIN）的危险因素,并分析应激性高血糖指数（SHI）和糖化血红蛋白（HbA1c）对CIN的预测价值。方法：选取2019年1月～2022年1月我院收治的102例接受PCI治疗的糖尿病合并AMI患者,根据PCI术后是否发生CIN分为CIN组26例和非CIN组76例。收集患者基线资料和计算SHI,采用单因素和多因素Logistic回归分析糖尿病合并AMI患者PCI术后CIN的影响因素,受试者工作特征（ROC）曲线分析SHI、HbA1c对糖尿病合并AMI患者PCI术后CIN的预测价值。结果：单因素分析显示,CIN组年龄大于非CIN组,高血压比例、Killip分级≥Ⅱ级比例和心肌肌钙蛋白T、N末端B型利钠肽前体（NT-proBNP）、超敏C反应蛋白（hs-CRP）、血糖、HbA1c、血尿酸、血尿素氮、血肌酐、SHI高于非CIN组,淋巴细胞计数、白蛋白、估算肾小球滤过率（eGFR）低于非CIN组（P＜0.05）。多因素Logistic回归分析显示,年龄增加、高血压、Killip分级≥Ⅱ级、NT-proBNP升高、白蛋白降低、hs-CRP升高、HbA1c升高、血肌酐升高、eGFR降低、SHI升高为糖尿病合并AMI患者PCI术后CIN的独立危险因素（均P＜0.05）。ROC曲线分析显示,SHI、HbA1c联合预测糖尿病合并AMI患者PCI术后CIN的曲线下面积大于两者单独预测的曲线下面积。结论：年龄增加、高血压、Killip分级≥Ⅱ级、NT-proBNP、hs-CRP、HbA1c、血肌酐、SHI升高及白蛋白、eGFR降低为糖尿病合并AMI患者PCI术后CIN的独立危险因素,SHI联合HbA1c对糖尿病合并AMI患者PCI术后CIN的预测价值较高。     

冠状动脉介入术中对比剂应用对肾功能影响的研究

目的:观察冠状动脉介入术后患者肾功能变化情况、CIN发生率及其相关危险因素。方法:选择从2009年12月至2010年3月在新疆维吾尔自治区人民医院心内科接受冠状动脉介入术的患者131人,测定介入术前5天内任何一天和术后48小时的Scr,分析CIN危险因素。结果:131例患者中有8例发生CIN,发病率为6.1%,Logistic多因素回归分析均显示糖尿病、年龄大于70岁、LVEF小于45%是CIN发生的独立危险因素。结论:糖尿病、LVEF<45%、年龄>70岁是CIN的独立危险因素。     

高尿酸血症与肾脏疾病关系的研究进展

高尿酸血症(HUA)是血尿酸(UA)增高的一种疾病,也是常见的机体代谢紊乱,临床上大多数HUA患者无明显的症状。由于经济水平提高和生活方式的改变,其发病率有增高趋势,且男性高于女性。HUA多发于中老年人群,严重影响其生活质量,因此中老年人群HUA已经成为普遍关注的健康问题。近年来研究发现HUA是痛风的主要病因之一,并且血尿酸(UA)水平可导致肾功能减退。已有多项研究表明HUA与肾脏疾病的发生发展密切相关,HUA是Ig A肾病、糖尿病肾病、急性肾损伤等肾脏疾病的独立危险因素,本文主要从HUA的流行病学、危险因素、发病机制及其与肾脏疾病关系这几个方面展开综述。     

冠状动脉介入术中对比剂应用对肾功能影响的研究

目的：观察冠状动脉介入术后患者肾功能变化情况、CIN发生率及其相关危险因素。方法：选择从2009年12月至2010年3月在新疆维吾尔自治区人民医院心内科接受冠状动脉介入术的患者131人,测定介入术前5天内任何一天和术后48小时的Scr,分析CIN危险因素。结果：131例患者中有8例发生CIN,发病率为6.1%,Logistic多因素回归分析均显示糖尿病、年龄大于70岁、LVEF小于45%是CIN发生的独立危险因素。结论：糖尿病、LVEF〈45%、年龄〉70岁是CIN的独立危险因素。     

通心络对高血压患者颈动脉内膜中层厚度的影响

各种心血管危险因素造成靶器官损害,最终导致心脑血管疾病。高血压导致的左心室肥厚、颈动脉内膜中层厚度(CCA-IMT)增加或粥样斑块、微量白蛋白尿等靶器官损害,目前被公认是心脑血管疾病危险的重要标记。本研究通过无创伤性超声技术观察高血压患者应用通心络胶囊对其CCA-IMT的影响。     

预防造影剂肾病水化时机选择的Meta分析

目的评价预防造影剂肾病(CIN)不同口服水化时机选择的效果,为降低CIN发生率提供依据。方法运用计算机检索PubMed、EMbase、The Cochrane Library、中国知网、万方数据库、维普数据库以及中国生物医学文献数据库关于口服水化预防造影剂肾病的随机对照试验(RCT),检索时间从建库至2020年9月。由2名研究人员独立筛选文献、提取基本资料并根据Cochrane手册评价文献的质量,采用RevMan 5.3软件进行Meta分析。结果共纳入11个CRT研究,1927例患者。Meta分析结果显示,术后6 h内定时定量饮水可降低CIN的发病率[RR=0.33,95%CI(0.20,0.54),P<0.01],同时定时定量饮水可减少尿潴留的发生[RR=0.48,95%CI(0.30,0.77),P=0.003]及胃部不适感[RR=0.57,95%CI(0.38,0.85),P=0.006]。结论有计划定时定量饮水进行水化疗法可降低造影剂肾病的发生率,减少了尿潴留的发生及胃部不适感。     

宫颈癌患者HPV16/18型病毒感染及阴道菌群观察

目的探讨宫颈癌与人乳头瘤病毒(HPV)感染高危型HPV(HPV16/18)表达及阴道菌群的关系。方法回顾性分析我院2018年1月-2020年1月收治的37例宫颈癌患者的临床资料,将其设为宫颈癌组。纳入同期于我院治疗的43例宫颈上皮内瘤变(CIN)患者的临床资料设为CIN组。比较两组基础资料(年龄、绝经情况、孕次、产次、HPV16/18阳性表达、阴道菌群、饮食卫生习惯和家族遗传史)差异,并对有差异信息进行赋值,以多因素Logistic回归模型分析宫颈癌发生的危险因素。结果经单因素分析,两组患者年龄、绝经情况、孕次和产次比较,差异无统计学意义(P>0.05)；宫颈癌组HPV16/18阳性、阴道菌群失调、饮食卫生习惯较差以及存在家族遗传史患者数显著多于CIN组(P<0.05)。经多因素Logistic回归分析证实HPV16/18阳性、阴道菌群失调、饮食卫生习惯较差以及存在家族遗传史是宫颈癌发生的危险因素(P<0.05)。结论宫颈癌发生危险因素较多,临床应针对存在危险因素的患者加强监测并给予相应干预从而降低宫颈癌发生风险。     

Mechanisms for an effect of acetylcysteine on renal function after exposure to radio-graphic contrast material: study protocol

Background

Contrast-induced nephropathy is a common complication of contrast administration in patients with chronic kidney disease and diabetes. Its pathophysiology is not well understood; similarly the role of intravenous or oral acetylcysteine is unclear. Randomized controlled trials to date have been conducted without detailed knowledge of the effect of acetylcysteine on renal function. We are conducting a detailed mechanistic study of acetylcysteine on normal and impaired kidneys, both with and without contrast. This information would guide the choice of dose, route, and appropriate outcome measure for future clinical trials in patients with chronic kidney disease.

Methods/Design

We designed a 4-part study. We have set up randomised controlled cross-over studies to assess the effect of intravenous (50 mg/kg/hr for 2 hrs before contrast exposure, then 20 mg/kg/hr for 5 hrs) or oral acetylcysteine (1200 mg twice daily for 2 days, starting the day before contrast exposure) on renal function in normal and diseased kidneys, and normal kidneys exposed to contrast. We have also set up a parallel-group randomized controlled trial to assess the effect of intravenous or oral acetylcysteine on patients with chronic kidney disease stage III undergoing elective coronary angiography. The primary outcome is change in renal blood flow; secondary outcomes include change in glomerular filtration rate, tubular function, urinary proteins, and oxidative balance.

Discussion

Contrast-induced nephropathy represents a significant source of hospital morbidity and mortality. Over the last ten years, acetylcysteine has been administered prior to contrast to reduce the risk of contrast-induced nephropathy. Randomized controlled trials, however, have not reliably demonstrated renoprotection; a recent large randomized controlled trial assessing a dose of oral acetylcysteine selected without mechanistic insight did not reduce the incidence of contrast-induced nephropathy. Our study should reveal the mechanism of effect of acetylcysteine on renal function and identify an appropriate route for future dose response studies and in time randomized controlled trials.

Trial registration

Clinical Trials.gov: NCT00558142; EudraCT: 2006-003509-18.     

Cardiovascular disease in patients with diabetic nephropathy

Diabetic nephropathy, which represents a major form of chronic kidney disease (CKD), is a leading cause of end-stage renal disease worldwide, and is also a risk factor for cardiovascular disease (CVD). Patients with diabetes and CKD have poorer outcomes after myocardial infarction. The underlying pathogenic mechanism that links diabetic nephropathy to a high risk of CVD remains unclear. In addition to traditional risk factors, including hypertension, hyperglycemia, and dyslipidemia, identification of novel modifiable risk factors is important in preventing CVD in people with diabetes. Inflammation/oxidative stress are known to be associated with an increased risk for CVD in patients with diabetic nephropathy. Moreover, homocysteine, advanced glycation end products, asymmetric dimethylarginine, and anemia may play a role in the development and progression of atherosclerosis in patients with diabetic nephropathy. This review summarizes the epidemiologic evidence, molecular mechanisms responsible for the increased risk for CVD in patients with diabetic nephropathy, and therapeutic intervention for diabetic nephropathy as evidenced by large-scale clinical trials.     

Relationship Between Hyperuricemia and Chronic Kidney Disease

Because approximately 70% of uric acid is excreted from the kidney, hyperuricemia occurs when renal function deteriorates. Until now, it has not been clear if the hyperuricemia seen in such renal diseases plays a role in the progression of renal disease. However, recent clinical studies show that the serum uric acid value is closely associated with hypertension in hyperuricemic patients (cross-sectional study), and also with the onset of hypertension (longitudinal study). Furthermore, one interesting report shows that treatment of hyperuricemia with allopurinol lowers blood pressure in juvenile essential hypertension patients with hyperuricemia. In addition, it is well known that hyperuricemia is closely associated with chronic kidney disease (CKD), is a risk factor for renal insufficiency in general populations, and is a poor prognostic factor of renal function in patients who also have IgA nephropathy. On the other hand, in intervention studies on hyperuricemia, the treatment of hyperuricemia with allopurinol in CKD has resulted in a fall in blood pressure and inhibition of the progression of renal damage. Conversely, the cessation of allopurinol treatment in CKD was followed by a rise in blood pressure and the development of renal damage. Furthermore, the rise of blood pressure and development of renal damage following cessation of allopurinol treatment are only seen in patients not receiving angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB). This suggests that the renin angiotensin (RA) system plays an important role in the development of hypertension and renal damage from hyperuricemia.     

Independent Role of Underlying Kidney Disease on Renal Prognosis of Patients with Chronic Kidney Disease under Nephrology Care

Primary kidney disease is suggested to affect renal prognosis of CKD patients; however, whether nephrology care modifies this association is unknown. We studied patients with CKD stage I-IV treated in a renal clinic and with established diagnosis of CKD cause to evaluate whether the risk of renal event (composite of end-stage renal disease and eGFR decline ≥40%) linked to the specific diagnosis is modified by the achievement or maintenance in the first year of nephrology care of therapeutic goals for hypertension (BP ≤130/80 mmHg in patients with proteinuria ≥150 mg/24h and/or diabetes and ≤140/90 in those with proteinuria <150 mg/24h and without diabetes) anemia (hemoglobin, Hb ≥11 g/dL), and proteinuria (≤0.5 g/24h). Survival analysis started after first year of nephrology care. We studied 729 patients (age 64±15 y; males 59.1%; diabetes 34.7%; cardiovascular disease (CVD) 44.9%; hypertensive nephropathy, HTN 53.8%; glomerulonephritis, GN 17.3%; diabetic nephropathy, DN 15.9%; tubule-interstitial nephropathy, TIN 9.5%; polycystic kidney disease, PKD 3.6%). During first year of Nephrology care, therapy was overall intensified in most patients and prevalence of main therapeutic goals generally improved. During subsequent follow up (median 3.3 years, IQR 1.9-5.1), 163 renal events occurred. Cox analysis disclosed a higher risk for PKD (Hazard Ratio 5.46, 95% Confidence Intervals 2.28–10.6) and DN (1.28,2.99–3.05), versus HTN (reference), independently of age, gender, CVD, BMI, eGFR or CKD stage, use of RAS inhibitors and achievement or maintenance in the first year of nephrology care of each of the three main therapeutic goals. No interaction was found on the risk of CKD progression between diagnostic categories and month-12 eGFR (P=0.737), as with control of BP (P=0.374), Hb (P=0.248) or proteinuria (P=0.590). Therefore, in CKD patients under nephrology care, diagnosis of kidney disease should be considered in conjunction with the main risk factors to refine renal risk stratification.     

Relationship between hyperuricemia and chronic kidney disease

Because approximately 70% of uric acid is excreted from the kidney, hyperuricemia occurs when renal function deteriorates. Until now, it has not been clear if the hyperuricemia seen in such renal diseases plays a role in the progression of renal disease. However, recent clinical studies show that the serum uric acid value is closely associated with hypertension in hyperuricemic patients (cross-sectional study), and also with the onset of hypertension (longitudinal study). Furthermore, one interesting report shows that treatment of hyperuricemia with allopurinol lowers blood pressure in juvenile essential hypertension patients with hyperuricemia. In addition, it is well known that hyperuricemia is closely associated with chronic kidney disease (CKD), is a risk factor for renal insufficiency in general populations, and is a poor prognostic factor of renal function in patients who also have IgA nephropathy. On the other hand, in intervention studies on hyperuricemia, the treatment of hyperuricemia with allopurinol in CKD has resulted in a fall in blood pressure and inhibition of the progression of renal damage. Conversely, the cessation of allopurinol treatment in CKD was followed by a rise in blood pressure and the development of renal damage. Furthermore, the rise of blood pressure and development of renal damage following cessation of allopurinol treatment are only seen in patients not receiving angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB). This suggests that the renin angiotensin (RA) system plays an important role in the development of hypertension and renal damage from hyperuricemia.     

糖尿病肾病动物模型的研究进展

糖尿病肾病是终末期肾衰的主要原因,也是糖尿病致命的重要原因。但是糖尿病肾病的致病机制迄今尚不完全明了,理想的动物模型无疑可对糖尿病肾病的研究提供重要线索。糖尿病肾病动物模型包括诱发性、自发性和转基因等多种类型的动物模型,各种类型的动物模型在疾病的发生发展、病理生理变化等多个方面与人类糖尿病肾病具有相似的特征。应用这些模型有助于开展对糖尿病肾病的防治、发病机理、相关药物的开发等多方面的研究。     

脂代谢异常对肾病的影响

肾脏疾病发展为慢性肾衰竭是个不可逆的过程,脂质代谢的异常,对肾病患者具有重要的影响。多项实验已经证实,即使在肾病的早期阶段,也会出现不同程度的脂质及脂类代谢的异常,高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、脂联素、瘦素等脂类代谢相关物质发生改变,不仅对血浆脂代谢产生影响,对于肾小球及肾小管的结构及功能也会有一定的损伤作用。肾病患者,如肾病综合征、慢性肾衰竭等疾病,多数有肾小球及肾小管间质的损伤,肾脏的脂毒性加重肾单位的破坏。随着人们对于慢性肾脏病认识的逐渐深入,降脂治疗的普遍应用,人们普遍认为改善血浆中脂类的水平,对于肾病的治疗,尤其对于慢性肾衰竭的预防具有重要作用。     

Role of Contrast Media on Oxidative Stress, Ca2+ Signaling and Apoptosis in Kidney

Contrast media (CM)-induced nephropathy is a common cause of iatrogenic acute renal failure. The aim of the present review was to discuss the mechanisms and risk factors of CM, to summarize the controlled studies evaluating measures for prevention and to conclude with evidence-based strategies for prevention. A review of the relevant literature and results from recent clinical studies as well as critical analyses of published systematic reviews used MEDLINE and the Science Citation Index. The cytotoxicity induced by CM leads to apoptosis and death of endothelial and tubular cells and may be initiated by cell membrane damage together with reactive oxygen species (ROS) and inflammation. Cell damage may be aggravated by factors such as tissue hypoxia, properties of individual CM such as ionic strength, high osmolarity and/or viscosity. Clinical studies indeed support this possibility, suggesting a protective effect of ROS scavenging with the administration of N-acetylcysteine, ascorbic acid erdosteine, glutathione and bicarbonate infusion. The interaction between extracellular Ca²⁺, which plays a central role in intercellular contacts and production of ROS, and the in vitro toxicity of CM was also reviewed. The current review addresses the role of oxidative stress in the pathogenesis of CM in the kidney as well as current and potential novel treatment modalities for the prevention of neutrophil activation and CM-induced kidney degeneration in patients. ROS production through CM-induced renal hypoxia may exert direct tubular and vascular endothelial injury. Preventive strategies via antioxidant supplementation include inhibition of ROS generation or scavenging.