腹膜透析对转化生长因子β1在残存肾中表达的影响

探讨清除循环中毒素后生长因子和残存肾小球的改变。方法采用分子杂交技术和组织病理分析方法在肾次全切除的残存肾大鼠模型上研究腹膜透析（ＰＤ）对转化生长因子β１（ＴＧＦ－β１）ｍＲＮＡ在残存肾中表达的影响和肾小球硬化的变化。分模型组和ＰＤ组，第８周ＰＤ组开始作腹膜透析至第１２周。分别在第７周和１２周各组杀检６只作肾病理检查（ＨＥ．ＰＡＳ染色）和ＴＧＦ－β１ｃＤＮＡ缝隙点样杂交。结果在实验的第７周两组间肾小球硬化指数（ＧＳＩ）及ＴＧＦ－β１ｍＲＮＡ表达均无显著性差异。第十二周，ＰＤ组的ＧＳＩ及ＴＧＦ－β１ｍＲＮＡ表达均显著低于模型组。ＧＳＩ改变程度与ＴＧＦ－β１ｍＲＮＡ表达丰度变化呈明显正相关（ｒ＝０．６５Ｐ＜０．０５）。结论腹膜透析可明显减少ＴＧＦ－β１ｍＲＮＡ的表达并延缓残存肾小球的硬化     

黄芪对肾缺血再灌注损伤的保护作用

目的 探讨黄芪注射液对肾脏缺血再灌注损伤的影响。方法 观察黄芪注射液对肾缺血再灌注损伤大鼠血浆超氧化物歧化酶（ＳＯＤ）,脂质过氧化产物丙二醇（ＭＤＡ）,内以素－１（ＥＴ－１）,一氧化氮（ＮＯ）变化及肾组织病理改变。结果 黄芪治疗组血浆ＥＴ０－１,ＭＤＡ水平较缺血再灌注组显著下降,ＳＯＤ显著升高,且病理改变较轻。结论 黄芪对肾脏缺血再灌注损伤具有保护作用。．     

反应性氧代谢产物在大鼠庆大霉素肾毒性中的致病作用及其预防

研究反应性氧代谢产物（ＲＯＭ）在大鼠庆大霉素（ＧＭ）肾毒性中的致病作用及其预防，在腹腔注射庆大霉素的同时，分别给人参总皂甙（ＧＳ），去铁敏（ＤＦＯ）和丹参（ＳＭ），各组用药均为７天，结果显示各组尿ＮＡＧ酶和血肌酐均比正常组显著增高，且模型组更显著升高。血清和肾皮质匀浆中丙二醛（ＭＤＡ）含量模型组比其他各组显著升高，而各预防组与正常组之间差异不显著；各组血清及肾皮质匀浆中超氧化物歧化酶（ＳＯＤ）活性     

大鼠移植肾组织ICAM-1/LFA-1分子表达与急性排斥反应的关系

目的探讨移植肾组织内细胞间粘附分子－１（ＩＣＡＭ－１）／淋巴细胞功能相关抗原－１（ＬＦＡ－１）的异常表达与移植排斥的关系。方法采用改进的大鼠原位肾移植模型，分五个实验组，在不同的时间段、观测受体鼠存活、肾功能；以及移植肾组织用单克隆抗体免疫组织化学染色后，图象分析法定量测定移植肾组织ＩＣＡＭ－１／ＬＦＡ－１分子表达的水平。结果移植肾急性排斥组ＩＣＡＭ－１／ＬＦＡ－１分子水平显著高于同品系移植对照组和药物治疗组。结论移植肾组织活检同时检测组织内ＩＣＡＭ－１／ＬＦＡ－１分子的表达，在肾移植急性排斥的诊断和治疗方面具有极其重要的临床意义。     

膀胱癌多向耐药基因P－GP_（170）表达的研究

应用ＭＤＲ（Ａｂ－１）和Ｃ２１９单克隆抗体，免疫组化法对４２例膀胱癌ＭＤＲ１和ＭＤＲ３基因编码的Ｐ－ＧＰ１７０的表达进行了研究。结果发现，３０例膀胱初发瘤Ｐ－ＧＰ１７０的阳性表达率为７０％（２１／３０），其中８例（２７％）为强阳性染色，１２例（４３％）为阳性或部分阳性染色。１２例化疗后复发的肿瘤切片，Ｐ－ＧＰ１７０的阳性表达率为８３．３％，２４例Ｇ（１～２）肿瘤Ｐ－ＧＰ１７０阳性表达率为７９％（１９／２４）。而１８例Ｇ３肿瘤Ｐ－ＧＰ１７０的阳性表达率仅占４４％（８／１８）。４２例膀胱肿瘤总的Ｐ－ＧＰ１７０阳性表达率为７３．８％（３１／４２）。实验结果提示，Ｐ－ＧＰ１７０的表达水平与肿瘤的恶性度或病理组织学分级不相关。复发性肿瘤Ｐ－ＧＰ１７０的表达率高于初发肿瘤，可能是腔内灌注化疗失败的重要因素。     

急性胰腺炎大鼠肝,肾超微结构的改变及其与氧自由基的关系

用制作十二指肠闭袢的方法复制大鼠急性胰腺炎模型，于术后８ｈ、１６ｈ和２４观察急性胰腺炎大鼠肝、肾超微结构的改变；同时测定肝、肾组织的超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）及血浆ＭＤＡ的水平。结果提示氧自由基及其引发的脂质过氧化反应参与了急性胰腺炎并发的肝、肾损害的病理过程。     

特异性环加氧酶2抑制剂对肾大部切除大鼠肾脏的保护作用

目的 探讨特异性环加氧酶（ＣＯＸ）－２抑制剂（ｒｏｆｅｃｏｘｉｂ）对５／６肾切除大鼠肾脏病变的保护作用。方法 大鼠随机分为 ４组，１假手术组，Ⅱ肾切除（ＳＮＸ）组，皿 ＳＮＸ＋ｒｏｆｅｃｏｘｉｂ组，Ⅱ ＳＮＸ＋蚓哚美辛组。６周后检测大鼠血压、肾功能、尿蛋白及尿血栓烷Ｂ。（ＴＸＢ_２），观察肾组织病理改变，并应用ＲＴ－ＰＣＲ的方法检测肾皮质内ＴＧＦ－βｍＲＮＡ的表达；免疫沉淀方法检测ＴＧＦ－β１蛋白质的表达。结果ｒｏｆｅｃｏｘｉｂ组大鼠蛋白尿水平较ＳＮＸ组显著降低（Ｐ＜０．０５）；肾小球硬化及肾小球基底膜增生程度比ＳＮＸ组明显减轻（Ｐ＜０．０５）；肾皮质ＴＧＦ－βｒｍ ＲＮＲ及蛋白质表达水平较ＳＮＸ组分别下调４０．８２％（Ｐ＜０．０１）和５６．８４％（Ｐ＜０．００１）。吲跺美辛组大鼠蛋白尿水平虽较ＳＮＸ组降低，肾皮质ＴＧＦ－β１ｍＲＮＡ及其蛋白质的表达水平较ＳＮＸ组分别下调１６．４２％和１５ ．７６％（Ｐ＞０．０５），但均无统计学意义；肾小球硬化虽较ＳＮＸ组轻，但肾间质纤维化程度较ＳＮＸ组加重。结论 特异性ＣＯＸ－２抑制剂对５／６肾大部切除大鼠肾脏病变有部分保护作用。要明确ＣＯＸ－２抑制剂产生肾保护的机制尚待进一步研究     

汉防己甲素和维拉帕米对环孢素A肾毒性的防护作用

了解中药汉防己甲素（Ｔｅｔ）和维拉帕米（Ｖｅｒ）对环孢素Ａ肾毒性（ＣｓＡ－ＮＴ）的防护作用。方法一组大鼠用ＣｓＡ５０ｍｇ·ｋｇ－１／ｄ灌胃７天导致急性ＣｓＡ中毒，另二组在给ＣｓＡ前，分别给Ｖｅｒ及Ｔｅｔ。结果ＣｓＡ中毒大鼠表现为血清肌酐升高３４．８％，Ｃｃｒ下降３９．４％，并出现近曲小管大片空泡变性。同时，肾皮质丙二醛（ＭＤＡ）含量显著升高，超氧化物歧化酶（ＳＯＤ）活性显著下降。给予Ｔｅｔ或Ｖｅｒ均能使上述肾功能和脂质过氧化指标明显改善，Ｔｅｔ还能减轻ＣｓＡ所致的组织学损害。结论Ｔｅｔ能有效地保护ＣｓＡ对肾的毒害     

一氧化氮在糖尿病肾病中的作用

目的探讨糖尿病（ＤＭ）和高血压大鼠肾脏一氧化氮（ＮＯ）途径与ＤＭ肾病的关系。方法将自发性高血压大鼠（ＳＨＲ）制成链脲佐菌素（ＳＴＺ）ＤＭ模型。设ＷＫＹ、ＳＨＲ和ＳＨＲＤＭ三组。除形态学观察外,还测定各组大鼠肌酐清除率（Ｃｃｒ）、２４小时尿蛋白、血及肾组织ＮＯ含量、肾脏ＮＯ合成酶（ＮＯＳ）活性和ＮＯＳｍＲＮＡ表达水平。结果ＳＨＲＤＭ组大鼠２４小时尿蛋白定量２０周时明显高于其余两组,Ｃｃｒ无明显改变。血ＮＯ水平升高,肾ＮＯ含量降低。肾脏结构型ＮＯＳ（ｃＮＯＳ）活性下降,诱导型ＮＯＳ（ｉＮＯＳ）活性或ｉＮＯＳ／ｃＮＯＳ（ｉ／ｃ）比值增加。肾小球ＮＯＳｍＲＮＡ表达面积扩大,入球动脉及小叶间动脉ＮＯＳ基因表达明显下降。肾小球系膜增生,有形成ＫＷ结节或纤维蛋白帽的趋势,系膜区基质增多,基底膜增厚,肾小动脉壁厚腔窄。结论（１）ＳＴＺＳＨＲＤＭ模型出现的２４小时尿蛋白增加、肾小球系膜及肾小血管病变提示ＤＭ肾病的产生;（２）肾脏ＮＯ系统异常与ＤＭ肾病有关。     

阻抑治疗胃癌前病变的研究

采用自制甲硝基亚硝胍（ＭＮＮＧ）液（１００μｇ／ｍｌ）喂以１６０只Ｗｉｓｔａｒ大鼠，以诱发腺胃癌前病变；并在此基础上，随机抽样分组，分别予口服全反式维甲酸（ＡＴＲＡ）、β－胡萝卜素（ＢＣ）、倍半氧化羟乙基锗（Ｇｅ－１３２）和硒酵母（Ｙｓｅ），以观察这些药物对腺胃癌前病变演变至胃癌过程的影响。结果显示Ａ－ＴＲＡ、Ｇｅ－１３２及Ｙｓｅ对由ＭＮＮＧ溶液所诱发大鼠腺胃癌的发生率、癌肿的浸润程度等均有不同效应的阻抑作用；ＢＣ的作用不明显可能与观察时间过短有关。同时对建立大鼠腺胃癌前病变模型的方法亦进行了初步探讨。     

Clinical evaluation of renal cell carcinoma and acquired cystic disease of the kidney in long-term dialysis patients

Long-term dialysis patients frequently develop acquired cystic disease of the kidneys (ACDK). One hundred and sixty-seven dialysis patients were classified into two groups according to the presence or absence of ACDK, and the two groups were compared with regard to the dialysis period, laboratory findings, and so forth. Among the 167 dialysis patients, 37.7% showed ACDK and had an average dialysis duration of 10.3 years, which was significantly longer than the 5.0 years for patients without ACDK. The proportion of patients with ACDK rose with increasing duration of dialysis; 64.6% of the patients on dialysis for more than 10 years had ACDK. The values of hemoglobin and hematocrit of patients with ACDK were significantly higher than those without ACDK. Of 12 dialysis patients who were operated upon because of suspected renal tumor, pathological examination confirmed renal cell carcinoma in 8 and adenoma in one. One of these patients had been treated with chronic ambulatory peritoneal dialysis, and another had bilateral renal tumor. Among the 8 patients with renal cell carcinoma, ACDK was detected in 5 by means of CT and ultrasound tomography, and cystic changes were observed in two on light microscopic examination of the resected kidneys. Pathological examination of the non-tumorous renal tissues revealed hyperplastic or adenomatous changes in the cyst epithelium in 5 patients undergoing dialysis for more than 7.5 years. These changes were thought to be pre-neoplastic. The high incidence of ACDK and the development of renal tumors in long-term dialysis patients indicates the necessity of intensive monitoring.     

Uremic acquired cystic disease of kidney

Multiple cystic disease occurring in the diseased kidneys of patients with end-stage renal insufficiency is called uremic acquired cystic disease of the kidney. In male patients undergoing long-term hemodialysis the incidence of ACDK is markedly high. ACDK is known to be accompanied by tumor, bleeding, calculus, abscess, etc., and the complication of cancer of the kidney is a special problem. In patients undergoing hemodialysis, occurrence of ACDK, tumor, and kidney cancer are observed respectively at the rate of 47.1, 4.8, and 1.5 per cent. When hemodialysis patients show gross hematuria, flank pain, rapid decrease in hematocrit, and sustained fever, ACDK or its complications should be investigated. Since the risk accompanied by kidney cancer is high in spite of a lack of symptoms, regular screening by ultrasonic examination or CT scan is needed. Renal transplantation is also recommended because of the regression of ACDK after successful renal transplantation. In the future, it appears that ACDK should be considered one disease entity and added to the categories of renal cystic diseases. In addition, ACDK can be studied as a model for clarification of the mechanism of cyst and tumor occurrence.     

Renal carcinoma in hemodialysis patients. Specially concerned with acquired cyst

Acquired cystic disease of the kidney (ACDK) with carcinoma in the original kidney is one sensational complication of long-term hemodialysis patients. The rate of incidence is about forty times higher than that in the general population and especially high in the young male group. From Dec. 1978 to Nov. 1990, we identified 8 patients of ACDK by computerized tomography (CT) scan, sonographic examination and angiography. Most patients had no clinical symptoms. The mean term of hemodialysis of the patients was 8 yrs. And one patient was diagnosed as having ACDK and tumor 8 yrs after kidney transplantation and then the kidney was removed. Their mean age was about 32 y.o. and the tumor size 1-3 cm in diameter. All tumors were inside the renal capsule. (Robson-1) Pathohistologically, the tumor area consisted of mainly clear cell carcinoma and the epithelium of the cyst wall showed multi-layered or papillary hyperplasia. In the 1st and 7th cases, simple nephrectomy was performed by transperitoneal approach. In the other cases it was performed by flank incision. All cases have had no recurrence and no metastasis of renal carcinoma. The etiology of ACDK and carcinoma occurrence has not been clarified yet, but it is suggested that uremic metabolite and deficiency of immuno-surveillance may cause the pathological changes in kidney tissue.     

Renal neoplasias in patients receiving dialysis and renal transplantation: clinico-pathological features and p53 gene mutations.

BACKGROUND: In Japan, the relative risk for renal cell carcinoma (RCC) in renal transplants was about 80-fold higher than that in the general population. Depressed immune surveillance due to the use of immunosuppressive agents was considered to cause cancer. Before renal transplantation, a vast majority of patients received hemodialysis, a known causative factor for acquired cystic disease of kidney (ACDK). Because ACDK is also considered to predispose to RCC, at least two risk factors for cancer accumulate in renal transplants. METHODS: In our study, clinicopathological features together with p53 gene mutations were analyzed in 218 patients with RCC: 22 received dialysis followed by renal transplantation, 39 received dialysis alone, and 157 sporadic RCC. P53 mutations were analyzed on DNA extracted from paraffin-embedded specimens with use of single strand conformation polymorphism, followed by direct sequencing. RESULTS: RCC in transplants shared several clinicopathological features with those in dialysis patients, which included small size and multiplicity of tumor, relatively high frequency of presence of ACDK, and papillary type of RCC. p53 gene mutations were infrequent in RCC of any clinical setting. CONCLUSIONS: Atrophic kidney at the end-stage of renal failure and under dialysis have lesions of ACDK that might predispose to RCC in dialysis and transplant patients.     

Chromophobe cell renal carcinoma with acquired cystic disease of the kidney in a long-term hemodialysis patient

We report a rare case of chromophobe cell renal carcinoma found in a 52-year-old female who had received hemodialysis therapy for 13 years. She was diagnosed as having a left renal tumor 7.5 cm in diameter with acquired cystic disease of the kidney (ACDK) by ultrasonographic examination during periodical systemic screening. As abdominal computed tomography scanning and enhanced color Doppler ultrasonography suspected that the hypervascular tumor was renal cell carcinoma, she underwent translumbar nephrectomy in July 2000. The histopathological diagnosis was chromophobe cell carcinoma with pT2 and grade 2 malignancy. Chromophobe cell carcinoma is uncommon among renal tumors with ACDK found in long-term hemodialysis patients.     

获得性肾囊肿的囊内液体对细胞增殖的抑制作用

目的 观察获得性肾囊肿（ＡＣＤＫ）的囊液对培养细胞增殖的影响，探讨ＡＣＤＫ发生肾癌的可能原因。方法 将ＬＬＣ－ＰＫ１，Ｈｅｌａ，Ｔ２４，Ｃａｋｉ－１和成纤维细胞接种于９６孔培养板中，经过２４ｈ培养，加入不同浓度的ＡＣＤＫ和单纯肾囊肿的囊内液作用２４ｈ，用ＭＴＴ法测定培养细胞的增殖活性，比较两者之间对细胞增殖的抑制作用。结果 在培养细胞中加入１０％，２０％，４０％的获得性肾囊肿囊内液，结果显示随浓度     

Oncocytoma associated with acquired cystic disease of kidney (ACDK): a case report

A case of renal oncocytoma associated with acquired cystic disease of kidney (ACDK) in a 56-year-old man is reported. He had received hemodialysis for 15 years because of chronic renal failure. Computed tomography (CT) was performed because of distention in the upper abdomen, revealing a right renal tumor. He underwent laparoscopic right nephrectomy, and was diagnosed with renal oncocytoma. There have been reported 8 cases of renal oncocytoma in hemodialysis patients, and our case was the third one associated with ACDK in the literature.     

Xanthogranulomatous pyelonephritis with acquired cystic disease of the kidney in a haemodialysis patient

SUMMARY:   A 54-year-old-female patient who had received regular haemodialysis therapy for 12 years was referred to our hospital for evaluation of a left renal mass. Imaging examinations revealed acquired cystic disease of the kidney (ACDK) and a tumour-like lesion in the left kidney. Because of the preoperative diagnosis of the left renal cell carcinoma, the patient underwent a left nephrectomy. Pathological examination revealed xanthogranulomatous pyelonephritis. It was difficult to distinguish xanthogranulomatous pyelonephritis from renal cell carcinoma in our case, because it is very rare for xanthogranulomatous pyelonephritis to occur in ACDK.     

Ultrasonographic study on kidneys in patients with chronic renal failure. Part II. Acquired cystic disease of the kidneys

Ultrasonic examination of the kidney was performed on 280 patients undergoing chronic dialysis. Acquired cystic disease of the kidney (ACDK) was detected in 107 of 529 kidneys (20.2%). This paper presents an analysis of ultrasonotomograms of ACDK. Ultrasonic measurement of the size of ACDK was 72.5 +/- 15.2 mm in length and 41.7 +/- 9.8 mm in thickness. The size of ACDK was significantly greater than that of contracted kidneys by ultrasonographic diagnosis. With regard to sex distinction the length and thickness of ACDK were significantly greater in males than in females. As for laboratory data, patients with ACDK showed significantly higher values of red blood cell count, hematocrit and serum creatinine concentration compared with contracted kidneys. Prolongation of the dialysis peirod increased the incidence of ACDK. The size of ACDK showed a tendency to increase with duration of dialysis. However, no correlation was noted statistically between the incidence of ACDK and duration of dialysis and between the size of ACDK and duration of dialysis. There was a significantly lower incidence of ACDK in patients with diabetic nephropathy than those with chronic glomerulonephritis. A sonographic feature of ACDK is irregularity of the renal contour because of cystic transformation. Renal imaging, identification of the corticomedullary border, identification of the central echoes and increased parenchymal echogenicity were similar to other dialyzed kidneys. The main complications of ACDK are hemorrhage and tumor formation. We observed two retroperitoneal hematomas and one renal cell carcinoma developed within two years after this examination. The incidence of complications of ACDK was 5.1 per cent. We believe that patients with ACDK should be watched carefully by regular ultrasonic examination for early diagnosis and treatment of these complications.     

Acquired cystic disease of kidney associated with renal cell carcinoma in chronic dialysis patients.

We describe 2 cases of acquired cystic disease of the kidney (ACDK) associated with renal cell carcinoma in patients treated with long-term hemodialysis. Both patients have had dialysis for five and eight years, respectively. Renal cell carcinomas of these patients are small, averaging 2 cm in diameter. They are clear cell type. Atypical epithelial hyperplasia arising from cystic areas can be seen intermingling with carcinoma. This confirms that atypical epithelial hyperplasia is a precursor of renal cell carcinoma. Although the incidence of renal cell carcinoma arising in ACDK is on the rise, the issue of how to manage patients with ACDK remained unsettled and required further study.