Perceptions of Home Dialysis Training and Experience Among US Nephrology Fellows

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Sex Disparities in Risk of Mortality Among Children With ESRD

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Inhibition of Intracellular Clusterin Attenuates Cell Death in Nephropathic Cystinosis

Nephropathic cystinosis, characterized by accumulation of cystine in the lysosomes, is caused by mutations in CTNS. The molecular and cellular mechanisms underlying proximal tubular dysfunction and progressive renal failure in nephropathic cystinosis are largely unclear, and increasing evidence supports the notion that cystine accumulation alone is not responsible for the end organ injury in cystinosis. We previously identified clusterin as potentially involved in nephropathic cystinosis. Here, we studied the expression of clusterin in renal proximal tubular epithelial cells obtained from patients with nephropathic cystinosis. The cytoprotective secretory form of clusterin, as evaluated by Western blot analysis, was low or absent in cystinosis cells compared with normal primary cells. Confocal microscopy revealed elevated levels of intracellular clusterin in cystinosis cells. Clusterin in cystinosis cells localized to the nucleus and cytoplasm and showed a filamentous and punctate aggresome-like pattern compared with diffuse cytoplasmic staining in normal cells. In kidney biopsy samples from patients with nephropathic cystinosis, clusterin protein expression was mainly limited to the proximal tubular cells. Furthermore, expression of clusterin overlapped with the expression of apoptotic proteins (apoptosis-inducing factor and cleaved caspase-3) and autophagy proteins (LC3 II and p62). Silencing of the clusterin gene resulted in a significant increase in cell viability and attenuation of apoptosis in cystinosis cells. Results of this study identify clusterin as a pivotal factor in the cell injury mechanism of nephropathic cystinosis and provide evidence linking cellular stress and injury to Fanconi syndrome and progressive renal injury in nephropathic cystinosis.     

The Workforce in Critical Care Nephrology: Challenges and Opportunities

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大剂量碘克沙醇对合并糖尿病患者冠状动脉介入术后肾功能的影响

目的 评估大剂量碘克沙醇(＞300 mL)对糖尿病患者经皮冠状动脉介入治疗(PCI)术后72 h内肾功能的影响。方法 顺序筛选2015年10月—2017年12月4个中心的987例冠状动脉介入治疗术中使用大剂量(＞300 mL)碘克沙醇的患者,最终204例合并糖尿病患者被纳入,进一步评价术后72 h内对比剂诱导的急性肾损伤(CI-AKI)的发生情况。结果 204例糖尿病患者使用大剂量碘克沙醇(＞300 mL)对比剂诱导的急性肾损伤总发生率为3.9%(8/204)。其中碘克沙醇300～500 mL亚组和＞500 mL亚组对比剂诱导的急性肾损伤发生率分别为4.3%(7/161)和2.3%(1/43)；基线eGFR＜60 mL/(min·1.73 m²)的患者对比剂诱导的急性肾损伤发生率为6.9%(2/29)。多因素Logistic回归分析显示,合并慢性肾功能不全、贫血、行急诊冠状动脉介入治疗术以及高Mehran评分是对比剂诱导的急性肾损伤的独立危险因素。对比剂诱导的急性肾损伤发生率与对比剂剂量的增加似乎无关。结论 合并糖尿病患者使用大剂量(＞300 mL)碘克沙醇后对比剂诱导的急性肾损伤发生率不高。     

经皮冠脉介入治疗应用培哚普利保护肾功能77例临床观察

目的 观察培哚普利在经皮冠状动脉介入治疗(PCI)前后对患者肾功能的影响.方法 将入选的147例行冠状动脉支架植入术的患者按随机数字表法分为培哚普利组(77例)和对照组(70例).培哚普利组术前服用培哚普利(4 mg· d-1)至少3d,术后继续服用培哚普利.对照组治疗期间不使用任何血管紧张素转换酶抑制剂(ACEI)类药物.两组患者术中均使用对比剂碘克沙醇造影.记录患者术前1d,术后1d、3d的肌酐、尿酸、血尿素氮(BUN)和肾小球滤过率,分析比较两组患者手术前后肾功能的变化和对比剂肾病(CIN)发生率的差异.结果 两组术前1d肌酐、肾小球滤过率、尿酸和BUN均差异无统计学意义(P＞0.05),但培哚普利组BUN术后3d较术前1d上升(P＜0.05).对照组肌酐术后3d较术前1d升高(P＜0.05),对照组尿酸术后3d较术前1d升高(P＜0.05),对照组肾小球滤过率术后3d较术前1d下降(P＜0.05).对照组各项肾功能主要指标术后1d较术前1d均差异无统计学意义(P＞0.05).两组患者CIN的发生率差异无统计学意义(P＞0.05).结论 培哚普利可预防患者冠脉PCI术后应用对比剂引起的肾功能损伤.     

术前血清胱抑素C、超敏C 反应蛋白对PCI 术后造影剂肾病的预测价值*

目的 探讨术前24 h血清胱抑素C（CysC）及超敏C反应蛋白（hs-CRP）对经皮冠状动脉介入术 （PCI）后造影剂肾病的预测价值。方法 选取2019年6月—2020年3月在河北中石油中心医院行PCI治疗的128例 冠状动脉硬化性心脏病（以下简称冠心病） 患者为研究对象,根据术后造影剂肾病诊断结果,将其分为病例组 （23例）和对照组（105例）。采用全自动生化分析仪测定两组术前24 h血清CysC、hs-CRP水平。采用Logistic回 归分析患者PCI术后造影剂肾病的危险因素,通过绘制受试者工作特征（ROC） 曲线评价术前24 h血清CysC、 hs-CRP及两者联合对造影剂肾病的预测价值。结果 病例组造影剂用量、合并糖尿病患者比例、术前24 h血清 CysC及hs-CRP水平高于对照组（P <0.05）。多因素Logistic回归分析显示,造影剂用量高［O＾R=1.843（95% CI： 1.322,2.758）］、合并糖尿病［O＾R =0.645（95% CI：0.510,0.892）］、术前24 h血清CysC升高［O＾R=1.801 （95% CI：1.139,2.448）］、术前24 h血清hs-CRP升高［O＾R=0.633（95%CI：0.479,0.880）］是PCI术后发生 造影剂肾病的独立危险因素（P <0.05）。术前24 h血清CysC（>1.322 mg/L）联合hs-CRP（>5.290 mg/L）预测 造影剂肾病的AUC最高,为0.916 （95% CI：0.897,0.986）,敏感性为91.3% （95% CI：0.883,0.936）,特异性 为82.9% （95% CI：0.795,0.850）。结论 PCI术后造影剂肾病的发生与造影剂用量、合并糖尿病情况及术前 24 h血清CysC、hs-CRP水平有关。术前24 h血清CysC、hs-CRP对PCI术后造影剂肾病具有较高的预测价值。