铅性肾病的流行病学分析

我们检查了铅接触人员１０２３名，发现铅性肾病８４例，患病率８．２％。女性３４例（７．２％），男性５０例（９％），男女铅性肾病患病率无显著性差异。印刷厂空气铅浓度平均０．００６９ｍｇ／ｍ３，蓄电池厂为０．１００５ｍｇ／ｍ３，铅矿为０．５ｍｇ／ｍ３。铅性肾病患病率分别为４．７３％，８．３％和２８．５７％（Ｐ＜０．００５）。分析铅性肾病患病率与年龄和铅接触年限的关系。年龄小于３０岁，～４０岁，～５０岁和大于５０岁者，铅性肾病患病率分别为５．５％，８．６％，１２．１％，和１５．６％（Ｐ＜０．０５）。铅接触年限小于１０年，～２０年和大于２０年者，铅性肾病患病率分别为６．６％，９．９％和１３．１％（Ｐ＜０．０５）。     

糖尿病大鼠肺病理改变及同期肾脏病理变化对比

目的:观察糖尿病(DM)大鼠肺组织改变及与同期肾脏变化的关系.方法:链脲菌素腹腔注射制作糖尿病大鼠模型,4周后胶原、网状纤维染色及透射电镜方法观察糖尿病大鼠肺组织基底膜病理改变,同期观察肾脏改变.结果:DM大鼠4周后肺组织病理改变为毛细血管基底膜及Ⅱ型肺泡上皮细胞基底膜不同程度的增厚及肺间质胶原成分等细胞外基质的增多,与同期糖尿病肾脏病变相平行.结论:DM大鼠4周后肺组织与糖尿病肾病相似,主要表现为微血管病变.     

Comparison of histopathological characteristics of allograft biopsy between responder and non-responder to antiproteinuric effect of angiotensin-converting enzyme inhibitor (ACEI)

Abstract:  Angiotensin-converting enzyme inhibitor (ACEI) has become recognized as agents that have renoprotective effects in the treatment of progressive renal diseases including post-transplant kidneys. Previously we demonstrated the safety and effectiveness of ACEI treatment on the hypertensive proteinuric post-transplant patients ( N  = 10) who had been followed up for 12 months. However, not all patients show good response in urinary protein reduction. We aimed to analyse the histopathological factor(s) affecting the responsiveness of proteinuria to ACEI treatment. Fourteen post-transplant patients with proteinuria who were treated with ACEI and underwent allograft biopsy were analysed. Eight patients showed 50% or more reduction in proteinuria (responder). The other 6 patients showed less (< 50%) reduction in proteinuria (non-responder). There was no difference in clinical characteristics (BP, renal function, donor age, recipient body mass index), dietary sodium or protein intake, and diuretic use between the two groups. As a histopathological characteristic, glomerular size in responder group was significantly larger than that in non-responder group. This suggests that the large glomerular size at least partly contributes to the responsiveness in urinary protein reduction to ACEI treatment in kidney allograft recipients with proteinuria.     

简易立体定位仪定位微创治疗高血压脑出血

目的　探讨高血压脑出血微创治疗的方法和手术时机的选择对该病疗效的影响。方法　对 12例高血压脑出血患者 ,采用脑内血肿定位仪微创血肿穿刺引流术清除血肿 ,观察疗效。结果　ADL1～ 3级 75 % ,病死率 8.3%。结论　颅内血肿定位仪定位微创血肿穿刺引流术 ,具有效果肯定、定位准确、损伤轻微、适应症广的特点 ,超早期治疗是预后的关键     

罗格列酮对实验性慢性环孢素肾病的作用

目的 探讨罗格列酮（RSG）对慢性环孢素肾病（CCN）大鼠模型的肾保护作用。 方法 低盐饮食基础上建立CCN大鼠模型，其中1组模型鼠用RSG同时灌胃。分别在实验开始后第14天和第35天处死动物，检测血浆和肾组织血管紧张素Ⅱ（AngⅡ）、AngⅡ1型受体(AT1R)、转化生长因子β1(TGF-β1)、细胞外调节蛋白激酶（p-ERK）、α-SMA和纤连蛋白（FN）的表达。在体外用不同浓度的CsA和RSG孵育NRK细胞。RT-PCR检测肾皮质TGF-β1，Western印迹分析检测FN、AT1R、p-ERK水平。 结果 RSG可改善环孢素A导致的大鼠肌酐清除率的下降[（0.586±0.094）比(1.072±0.105)ml&#8226;min^-1&#8226;kg^-1，P < 0.01]、血浆和肾组织AngⅡ水平增加（P < 0.01）、肾间质单核细胞浸润（P < 0.01）、肾间质纤维化（1.707±0.019 比 2.335±0.022，P < 0.01）、肾组织α-SMA表达增加（P < 0.01）、肾皮质TGF-β1 mRNA水平增加（P < 0.01）、NRK细胞FN、AT1R和p-ERK蛋白水平增加（P < 0.05）。 结论 RSG可能通过减轻炎细胞浸润、影响AngⅡ作用和下调TGF-β1等途径减轻CsA所致的肾组织损伤。     

高糖对大鼠系膜细胞肝细胞生长因子受体表达的影响及其机制研究

目的 观察高糖作用下大鼠系膜细胞(MsC)肝细胞生长因子（HGF）受体c-Met的表达，并探讨其机制和意义。 方法 用RT-PCR和Western 印迹方法检测高糖作用大鼠MsC的不同时间点（0、12、24、48、96 h）c-Met的表达。分别用光辉霉素A（mithramycin A）和SU11274抑制转录因子Sp1的DNA结合活性和阻断c-Met。用电泳迁移率改变实验(EMSA)观察Sp1与c-Met基因启动子的结合活性。以荧光探剂二氯双氢荧光素二乙酸酯(DCFH-DA)捕获细胞内活性氧。 结果 大鼠MsC的c-Met表达在高糖作用12、24和48 h都明显上升，96 h开始下降。光辉霉素A呈浓度依赖性抑制高糖作用下大鼠MsC的c-Met表达上调。大鼠MsC内Sp1与c-Met基因启动子的结合活性在高糖作用下明显增强。HGF及c-Met显著抑制高糖诱导的大鼠MsC内活性氧的增多。 结论 高糖作用下大鼠MsC的c-Met表达增强，其机制可能是通过Sp1介导。HGF-c-Met信号通路激活能抑制高糖所致大鼠MsC内的氧化应激反应。     

尿视黄醇结合蛋白在2型糖尿病肾病早期诊断中的意义

目的　探讨检测尿视黄醇结合蛋白 (RBP)在糖尿病肾病 (DN)早期诊断中的临床意义。方法　分别对 4 2例 2型糖尿病患者及 36例健康对照者用酶联免疫法 (ELISA)测定尿RBP ,用放射免疫法测定尿α1 微球蛋白 (α1 M )、β2 微球蛋白 (β2 M)。结果　糖尿病组三种尿微量蛋白排泄量明显高于健康对照组 ,且以尿RBP敏感性最高。结论　尿RBP的检测可敏感反映早期糖尿病患者肾小管损伤。     

C3 Deposition in IgA Nephropathy in Children and Adolescents

The aim of this study was to assess the significance of C3 deposition in IgA nephropathy in children and adolescents. One hundred and two patients aged 5–21 years (57 male and 45 female) were studied. The findings of C3 deposition were classified into 8 groups by immunofluorescent (IF) pattern and intensity as follows: group MC3+ (N = 12): mesangiocapillary pattern and 3+ in intensity; group MC2+ (N = 13): mesangiocapillary and 2+; group MC1 + (N = 4): mesangiocapillary and 1 +; group M3+ (N = 11): mesangial and 3+; group M2+ (N = 24): mesangial and 2+; group M1 + (N=18): mesangial 1 +; group S (N = 12): only segmentally positive; and group N (N = 8): negative. Histological changes were scored semiquantitatively as an activity index (cellular proliferation, necrosis, interstitial cell infiltration, and cellular crescents) and a chronicity index (mesangial sclerosis, segmental and global glomerular sclerosis, fibrous crescents, adhesion and tubulo-interstitial change). IF findings were scored semiquantitatively and laboratory findings were also studied. The following results were obtained: 1) The scores of total activity index in MC groups were higher than in the M, S or N groups, and the greater the degree of C3 deposition, the higher the score; 2) Such result was not evident in the chronicity index; 3) High IF scores of IgG and IgM were found in the MC3+ and MC2+ groups; 4) Hematuria was more severe in MC3+ and MC2+ than in other groups, and proteinuria was more prominent in the MC than other groups. Thus the degree of C3 deposition was parallel with histological activity and urinary findings.     

Pattern of renal dysfunction in analgesic nephropathy--comparison with glomerulonephritis.

Comprehensive renal function tests were performed in 84 patients with analgesic nephropathy, 33 glomerulonephritis patients matched for creatinine clearance, and 30 control subjects. A system of 1-day renal function tests including urine microscopy, creatinine clearance, phenolsulphonphthalein excretion, urine concentration and acidification, and electrolyte excretion, was used. Patients with analgesic nephropathy were found to have significant sterile pyuria and haematuria, even those with mild renal insufficiency, significantly reduced concentrating ability and a distal acidifying defect, and a tendency to impaired sodium conservation. These function defects are consistent with the primary lesion of renal papillary necrosis in analgesic nephropathy; the detection of these defects have implications in patient management.