肝硬化患者血、尿NAG检测的临床意义

目的探讨血、尿NAG水平对诊断肝硬化的价值.方法测定46例肝硬化患者及30例健康者晨尿、晨血NAC水平并经过统计学处理.结果肝硬化患者血、尿NAG水平明显高于正常对照,失代偿期明显高于代偿期.结论血、尿NAG活力测定及对其动态观察,可较灵敏反映肝硬化早期是否合并肾脏损害,并可间接判断肝硬化对肝功能的损害程度,对肝硬化的发展、预后、疗效监测具有重要价值.     

精浆生化指标在精液不液化致不育患者中的改变及其意义

目的:观察精浆生化指标在精浆不液化致不育患者中的变化,探讨其与精液不液化的相关性.方法:根据WHO对精浆不液化的定义,随机选取56例精液不液化患者及正常生育男性20例作为对照.各自留取精液并分离精浆后,分别测定pH、中性α-葡萄糖苷酶(NAG)、果糖(Fru)、锌(Zn)、柠檬酸、超氧化物歧化酶(SOD)和淀粉酶(AMY).结果:与正常组相比,精浆不液化(异常组)中除了果糖含量无差异外,其他生化指标都具有显著性差异,具有统计学意义.结论:前列腺分泌功能的损害是导致精浆不液化的主要病因之一,精浆生化检测是寻找精浆不液化病因的快捷、方便、准确、有效的临床手段,值得重视和推广.     

尿肾损伤分子-1在急性肾损伤诊断中的临床价值

目的探讨尿肾损伤分子-1(Kidney injury molecule-1,Kim-1)在急性肾损伤诊断中的敏感性及临床价值。方法选择2010年1月至2011年6月在我科住院的急性肾损伤患者58例作为病例组,健康体检者20例为对照组。尿Kim-1、微量白蛋白(mALB)测定采用酶联免疫吸附法(ELISA),尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG)测定采用对硝基苯酚(PNP)比色法。结果急性肾损伤组患者尿液中的Kim-1、NAG、mALB的测定浓度明显高于对照组,差异具有统计学意义(P<0.01),我们通过ROC曲线、诊断试验结果显示:尿Kim-1曲线下面积为0.956,95%可信区间为0.910～1.001,较尿NAG、mALB更具有敏感性(P<0.001),两组间患者年龄及男女比例差异均无统计学意义(P>0.05)。结论尿Kim-1在急性肾损伤诊断中起着重要的作用,检测尿Kim-1的浓度可以成为急性肾损伤患者无创并有效的检测手段,有助于急性肾损伤的早期监测,对预防急性肾损伤的发生、发展具有重要的临床价值。     

尿半胱氨酸蛋白酶抑制剂用于评价肾小管早期损伤的研究

目的探讨尿半胱氨酸蛋白酶抑制剞C（CYS-C）用于评估肾小管早期损伤的价值。方法对40例肾病患者测定尿中CYS-C、视黄醇结合蛋白（RBP）和N-乙酰-β-D-氨基葡萄糖苷酶（NAG）,分析阳性检出率及三者的相关性。结果所有患者的CYS-C阳性检出率为60．0％,RBP为57．5％,NAG为67．5％;CYS-C与RBP有显著相关性,差异有统计学意义（r=0．743、P〈0．01）,CYS-C与NAG无相关性,差异无统计学意义（r=0．289、P〉0．05）。结论尿CYS-C与RBP均是提示肾小管早期损伤有效的指标,而且CYS-C的敏感性和稳定性较RBP高,测定方法也优于RBP。     

微量NAG酶释放法鉴定牛血清促进细胞生长的活性

目的　检查牛血清促进细胞生长的活性。方法　微量NAG酶释放法。结果　在同一实验条件下 ,试验血清 (990 5 0 7,990 40 2 )与对照血清 (990 40 5 )对促进K5 6 2细胞生长的活性没有明显差别 ,但血清的促进细胞生长活性随着储存时间的增加而降低 ,如试验血清 (970 6 2 1)。结论　利用微量NAG酶释放法可以筛查新生牛血清促进细胞生长的活性     

RENAL TUBULAR PEPTIDE CATABOLISM IN CHRONIC VASCULAR REJECTION

Chronic vascular rejection (CR) is the commonest cause of renal transplant loss, with few clues to etiology, but proteinuria is a common feature. In diseased native kidneys, proteinuria and progression to failure are linked. We proposed a pathogenic role for this excess protein at a tubular level in kidney diseases of dissimilar origin. We demonstrated in both nephrotic patients with normal function and in those with failing kidneys increased renal tubular catabolisman and turnover rates of a peptide marker, Aprotinin (Apr), linked to increased ammonia excretion and tubular injury. These potentially injurious processes were suppressed by reducing proteinuria with Lisinopril. Do similar mechanisms of renal injury and such a linkage also occur in proteinuric transplanted patients with CR, and if so, is Lisinopril then of beneficial value? We now examine these aspects in 11 patients with moderate/severe renal impairment (⁵¹CrEDTA clearance 26.2 ± 3.3 mL/min/1.73m²), proteinuria (6.1 ± 1.5 g/24 h) and biopsy proven CR. Lisinopril (10–40 mg) was given daily for 2 months in 7 patients. Four others were given oral sodium bicarbonate (Na HCO₃) for 2 months before adding Lisinopril. Renal tubular catabolism of intravenous ^99mTc-Apr (Apr^* 0.5 mg, 80 MBq), was measured before and after Lisinopril by γ-ray renal imaging and urinary radioactivity of the free radiolabel over 26 h. Fractional degradation was calculated from these data. Total 24 h urinary N-acetyl-β-glucoaminidase (NAG) and ammonia excretion in fresh timed urine collections were also measured every two weeks from two months before treatment. After Lisinopril proteinuria fell significantly (from 7.8 ± 2.2 to 3.4 ± 1.9 g/24 h, p < 0.05). This was associated with a reduction in metabolism of Apr^* over 26 h (from 0.5 ± 0.05 to 0.3 ± 0.005% dose/h, p < 0.02), and in fractional degradation (from 0.04 ± 0.009 to 0.02 ± 0.005/h, p <0.01). Urinary ammonia fell, but surprisingly not significantly and this was explained by the increased clinical acidosis after Lisinopril, (plasma bicarbonate fell from 19.1 ± 0.7 to 17.4 ± 0.8 mmol/L, p <0.01), an original observation. Total urinary NAG did fall significantly from a median of 2108 (range 1044–3816) to 1008 (76–2147) μmol/L, p < 0.05. There was no significant change in blood pressure or in measurements of glomerular hemodynamics. In the 4 patients who were given Na HCO₃ before adding Lisinopril, both acidosis (and hyperkalemia) were reversed and neither recurred after adding Lisinopril. These observations in proteinuric transplanted patients after Lisinopril treatment have not been previously described.     

参黄草合剂治疗早期肾损伤的临床研究

目的：观察参黄草合剂对早期肾损伤的临床疗效。方法：用尿液酶学改变检测出早期肾损伤患者74例，分为两组，治疗组64例，在治疗原发病的基础上加服参黄草合剂；对照组10例，单纯治疗原发病。治疗14d后，观察两组治疗前后尿酶的变化，结果：治疗组尿酶恢复正常者占80％，而对照组仅为10％，组间比较差异显著（P＜0．01）。结论：参黄草合剂对早期肾损伤有较好的治疗作用。     

尿系列酶检测对新生儿肺炎肾功能的评价

目的　 探讨新生儿肺炎时尿系列酶的改变作为评价肾小管功能的指标。 方法 　检测早产、足月新生儿肺炎尿系列酶NAG、GAL、GGT、ALP、LDH活性 ,与正常组进行对照。同时检测血BUN ,SCr作为肾小球功能的指标 ,GAL/NAG比值动态观察作为肾功能恢复的指标。 结果 　早产儿组尿酶NAG、GAL、GGT、ALP、LDH活性与对照组比较明显增高 ,有显著差异 (P <0 0 0 1) ,足月儿组尿酶NAG、ALP、LDH活性与对照组比较明显增高 ,有显著差异 (P <0 0 0 1)。尿酶GAL/NAG比值恢复期与对照组比较有统计学差异 (P <0 0 5 )。 结论 　尿酶NAG、GAL、GGT、ALP、LDH活性增高可作为新生儿肺炎时肾小管功能受累的指标 ,GAL/NAG比值升高提示新生儿肺炎肾功能的恢复     

接触有机氟作业工人尿N-乙酰-β-D-氨基葡萄糖苷酶活性测定

对194名接触有机氟作业工人进行了尿NAG活性测定,结果表明,长期接触有机氟作业工人尿NAG活性明显高于非接氟作业的对照组。不同性别、不同工龄和不同工种之间尿NAG活性未见明显差异,但对照组工人尿NAG活性随年龄增加而升高。提示长期接触有机氟作业可能对工人肾脏产生一定的损害。