三磷酸腺苷结合盒运转体A1与颈动脉粥样硬化斑块的关系

目的 探讨三磷酸腺苷结合盒运转体A1(ATP binding cassette transporter A1,ABCA1)在人颈动脉粥样硬化斑块中的表达变化及作用机制.方法 收集24例人颈动脉粥样硬化斑块标本和10例肠系膜动脉标本(对照组),采用RT-PCR测定ABCA1 mRNA和视黄酸X受体α(RXRα)mRNA表达水平,并采用Western Blot检测ABCA1及RXRα的蛋白表达水平.24例人颈动脉粥样硬化斑块标本按病理分级,比较病理组织为Ⅲ级和Ⅰ级动脉粥样硬化组织间ABCA1 mRNA、RXRαmRNA表达水平及蛋白表达水平.结果 颈动脉粥样硬化斑块组的ABCA1 mRNA(0.79±0.04)和RXRα mRNA(0.73±0.04)表达与对照组相比上调,差异有统计学意义(P＜0.05);ABCA1 mRNA与RXRα mRNA增加水平相关(P＜0.05);颈动脉粥样硬化斑块的ABCA1蛋白表达(0.22±0.03)下调水平与对照组(0.53±0.03)相比差异有统计学意义(P＜0.05);Ⅲ级和Ⅰ级动脉硬化斑块ABCA1mRNA、RXRα mRNA及蛋白表达水平差异有统计学意义(P＜0.05).结论 ABCA1及RXRα蛋白表达水平下调可能是进展性动脉粥样硬化损害的关键因素.     

肾综合征出血热发病机制研究进展

肾综合征出血热发病机制至今仍未完全阐明,病毒、病毒受体、细胞因子、自由基、特异性CTL反应、HLA差异性均可能与发病有关.此文对近年来的研究进展进行了综述.     

慢性肾衰竭急性加重的临床特征及相关因素分析

目的：探讨慢性肾衰竭（CRF）急性加重因素及其治疗措施对预后的影响。方法：对2001年1月～2005年6月住院治疗的CRF急性加重患者42例，按其加重原因、基础疾病、治疗方式和疗效进行回顾性总结。结果：CRF急性加重因素依次为各种感染（45．2％）、原发病加重（19．0％）、高血压未控制（14．3％）、水电解质紊乱（11．9％）、肾毒性药物（11．9％）、心功能不全（9．5％）、尿路梗阻（4．8％）、血高粘滞状态（2．4%），7例同时存在≥2种上述病因（16．7％）。CRF急性加重原发病以慢性肾小球肾炎（52．4％）和糖尿病肾病（11．9％）为主。积极治疗后肾功能恢复达到或接近原来水平者40例，死亡2例，死亡2例的年龄均在60岁以上。结论：对于CRF肾功能急剧恶化的患者，应积极寻找其加重因素，并采取非透析和透析相结合治疗，改善肾功能，降低病死率，延长患者生命。     

异丙酚和异氟醚对非体外循环搭桥术患者围术期细胞因子的影响

目的:研究异丙酚和异氟醚对非体外循环搭桥术患者围术期炎性与抗炎性细胞因子平衡的影响。方法:择期非体外循环搭桥患者50例,随机分为2组。异丙酚组微量泵输入剂量为4～6mg·kg-·1h-1,异氟醚组吸入浓度为1%～1.5%。检测诱导前、打开心包、旁路血管开放30min,术后2h、24h血清白细胞介素6(IL-6)、白细胞介素10(IL-10)和肿瘤坏死因子α(TNF-α)的浓度。结果:2组患者旁路血管开放后IL-6浓度较术前升高(P<0.01),术后2h达高峰;术后2h异氟醚组高于异丙酚组(P<0.05)。IL-10浓度变化趋势与IL-6相似,旁路血管开放后、术后2h和24h异丙酚组高于异氟醚组(P<0.05)。2组患者TNF-α水平均无显著变化。结论:异丙酚麻醉促进IL-10的产生,抑制IL-6的产生,控制术中应激反应异丙酚优于异氟醚。     

糖化血红蛋白及糖化血清蛋白与糖尿病肾功能衰竭患者的血糖监测

糖化血红蛋白(Hb)A1c是血糖监测的苇要指标,反映检测前2～3个月的平均血糖水平.慢性肾功能衰竭(CRF)患者存在贫血、酸中毒、氧化应激、胰岛素抵抗、血液透析及促红细胞生成素(EPO)的应用等因素,对HbA1c的测定会造成影响.糖化血清蛋白(GSP)反映检测前2～3周的平均血糖水平,仅受血浆蛋白的影响,几乎不受血红蛋白和EPO治疗等以上因素的影响,且对短时间内的血糖变化更为敏感.将GSP作为糖尿病肾功能衰竭患者血糖监测指标可能比HbA1c更理想.     

2 121例老年急性冠脉综合征患者血清脂类浓度的分析

目的分析60岁以上老年人血清脂类水平的参考值,并探讨急性冠脉综合征与血脂指标的相关性.方法将3 766例健康成人分为≤60岁和＞60岁的两个年龄段,采用生物化学的方法测量他们的血脂水平,找出60岁以上老年人的脂类参考值.同时分析2 121例老年急性冠脉综合征病人的脂类指标.结果 60岁以上老年人血脂参考值为:TC 4.65±1.96×1.05mmol/L;TG 1.02±1.96×0.45mmol/L;HDL-C 1.47±1.96×0.40mmol/L;LDL-C 2.98±1.96×0.56mmol/L;ApoA1 1.32±1.96×0.25g/L;ApoB 0.99±1.96×0.35g/L,并且急性心肌梗死和不稳定性心绞痛病人血清脂类各项指标之间没有显著性差异.结论血清LDL-C/HDL-C＞5和TG ≥1.9mmol/L这两项联合指标比其他单独指标与老年人急性冠脉综合征关系更密切.     

肾综合征出血热患者T细胞亚群数量与白细胞介素2,4水平变化的关系

采用ABC免疫组化染色法及单克隆抗体夹心法ELISA，同步检测了34例肾综合征出血热（HFRS）患者外周血T细胞亚群数量和血清白细胞介素2和4（IL－2、IL－4）水平。发现HFRS病程中各T细胞亚群数量均有不同程度的升高，其中CDS阳性T细胞在各病期均有升高。IL－4水平升高仅见于发热期．而IL－2的升高主要在低血压期和少尿期。病程中有CD4／CD8比值的下降甚至倒置。这种比值的变化与IL－2和IL－4的动态变化有一定的相关性。结果揭示，在HFRS发病机理中存在Thl型和Th2型免疫反应等多种免疫病理机制。     

Neonatal renal failure due to obstructive candidal bezoars

Acute renal failure (ARF) developed in a 7-week-old infant due to bilateral candidal bezoars (fungal balls) causing obstruction at the pelviureteric junction. The baby was born at term with an appropriate birthweight, and had been treated with broad-spectrum antibiotics for respiratory distress and septicemia during the 1st week of life. Recovery from ARF followed renal decompression with bilateral nephrostomy tube placement and parenteral administration of amphotericin B and 5-flucytosine. Received August 21, 1996; received in revised form and accepted January 3, 1997     

Distal Penile Gangrene in a Patient with Chronic Renal Failure

To date, only 10 cases of distal penile gangrene in patients with chronic renal failure have been reported. This rare condition is believed to result from progressive vascular calcification due to secondary hyperparathyroidism in patients with chronic renal failure. We report an additional case of distal penile gangrene in a 41-year-old man who presented with chronic renal disease and pulmonary tuberculosis. Since some authors have emphasized that aggressive surgical treatment in such cases has a significant mortality rate, we took a more conservative approach to treatment.     

Cibenzoline-induced respiratory muscular paralysis in a hemodialysis patient

A 69-year-old man was admitted to our kidney center with endstage renal failure. We started intermittent peritoneal dialysis immediately because of severe azotemia, hyperkalemia, and metabolic acidosis. Two weeks after admission, he developed uremic pericarditis with frequent ventricular premature contractions and supraventricular premature contractions. The intermittent peritoneal dialysis was then replaced by intensive hemodialysis, and oral administration of 300 mg/d of cibenzoline was started. Four days later, he developed thirst, weakness, and dyspnea due to respiratory muscular paralysis. We initiated respiratory support with a respirator because analysis of his blood gases revealed marked hypercapnia and hypoxia. He also developed hypoglycemia and prolonged PQ and QRS intervals on the electrocardiogram, which we believed were due to cibenzoline intoxication; we discontinued the cibenzoline immediately. All symptoms improved, and he was extubated 5 days later. After 2 months, his pericardial effusion disappeared. He now continues maintenance hemodialysis as an outpatient. We suspect that the cibenzoline induced the respiratory muscular paralysis for 2 reasons: 1) the patient experienced the respiratory muscular paralysis, at the same time he also experienced thirst, weakness, hypoglycemia, and prolonged PQ and QRS intervals on electrocardiogram, and all of these symptoms improved after the discontinuation of cibenzoline, and 2) his plasma concentration of cibenzoline became remarkably elevated, to 20 times above the standard therapeutic level. This patient's clinical course indicates that hemodialysis might be superior to intermittent peritoneal dialysis for treatment of cibenzoline intoxication.