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[讨论] 姜的假论文《肾衰长期血液透析肾囊肿与肾肿瘤的发生》

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发表于 2017-3-11 10:25 |显示全部帖子
 肾衰长期血液透析肾囊肿与肾肿瘤的发生
  姜埃利 马腾骧
  
  摘要 作者在12年间对887例血液透析患者中观察到512例继发后天性肾囊肿(57.7%),其中19例在肾囊肿的基础上发生了肾肿瘤,并且通过物理检查方 法、超声、CT和手术得到证实。作者探讨了长期血液透析患者肾囊肿与肾肿瘤演变过程和发生机理,认为肾萎缩后肾血流量降低、肾功能的丧失、尿液对肾小管的 冲刷作用降低及肾小管的阻塞是继发后天性肾囊肿的直接原因;而尿毒症所至机体免疫监视能力的下降,肾囊肿内容物长期物理和化学的作用,又是肾囊肿向肾肿瘤 演变的根源。作者认为,继发性肾囊肿是肾肿瘤的前驱病变。
  主题词 肾功能衰竭/治疗 血液透析 肾肿瘤/病因学 肾囊肿
  
  随着血液净化技术的不断提高和完善,慢性肾功能衰竭接受血液透析治疗患者的存活率也在提高,从1982~1994年我们共接收了887例病人,现就其肾脏原发病的病理改变进行分析和探讨。
  
  临床资料
   887例慢性肾功能衰竭尿毒症,男性532例,女性355例,平均年龄为43.5岁(14~82岁),887例的原发病:肾小球肾炎503例,慢性肾盂 肾炎257例,糖尿病肾病67例,胶原性肾病23例,原因不祥37例,多囊肾未统计在内。肾脏最终的病理改变均为肾萎缩,患者接受血液透析的平均时间为 7.5年(1~23年)。
  
  方法与结果
  对887例肾萎缩尿毒症血液透析的患者定期进行双肾B超和CT形态学检查,发现512例患者在维持性血液透析治疗中出现肾体积的增大,萎缩肾内发现单发或多发性的继发性肾囊肿。平均肾体积为176.8cm³(113.2~214.6cm³)。
  在512例继发性肾囊肿的病例中,19例经B超和CT检查提示有单侧肾内占位性病变,并进行了手术切除,证实肿瘤的发生,病理结果见附表。
  萎缩肾继发肾囊肿内容物生化检查提示:粘性浅黄色胶样液体,有陈旧性血块,含有大量蛋白、草酸盐、磷酸盐、钙盐和K、Na、Cl、Zn、Fe、Cu等离子成分。
  讨论
  30%~90%萎缩肾慢性肾功能衰竭尿毒症的患者在进行维持性血液透析治疗过程中会发生肾囊肿[1,2]。
   萎缩肾内继发肾囊肿可以是单发性的、多发行的或蜂窝样的,肾囊肿出现的频率和肾囊肿的大小与血液透析的时间年限有关。在我们的病例中,接受血液透析治疗 2年内萎缩肾体积似乎不变,或者有继续缩小的趋势,随着透析治疗时间的推移,大约2/3的病人萎缩肾体积开始增大,过程是缓慢的。肾体积的增大并不意味着 肾组织细胞的再生,而是肾囊肿形成所致。大多数肾囊肿为单发性的,直径小于1cm,最大的囊肿达2.4cm。B超检查对直径小于0.5cm的囊肿诊断困 难,而CT检查较容易发现囊肿的存在[3]。
  萎缩肾内继发肾囊肿出现的原因可能是:(1)肾萎缩后肾血流量降低,肾组织缺氧,肾内组织纤维化 [4,5]。(2)肾小球功能的丧失,尿液产生减少,对肾小管内的冲刷作用降低,大量的草酸盐、碳酸盐、磷酸盐和肾小管内变性坏死脱落的细胞颗粒组成细小 结石,阻塞肾小管,使小管内压力增加,最终形成肾囊肿。我们对肾内物进行了生化检查,分析结果也证实了这一点。
  Dunnill等[5]在1977年首次报道了慢性透析病人继发肾肿瘤。Matas[6]曾对慢性肾功能衰竭恶性肿瘤的发病进行过报道,认为血液透析患者恶性肿瘤的发病率高于正常人的7倍。
  
  血液透析患者在肾囊肿的基础上继发肾内实质肿瘤是一个事实。我们在512例患者中,手术证实19例(3.7%)。在这些患者中,肿瘤的发生于患者的性别和年龄无关,关且肿瘤在左、右肾脏发生的比率也没有差别,而与患者接受血液透析时间的长短有关。
  萎缩肾内肾囊肿继发肾肿瘤的原因可能是:(1)尿毒症患者自身免疫系统功能障碍,免疫监视能力下降,自身对细胞内DNA的突变杀伤能力减弱[6,7]。(2)肾囊肿内容物长期物理和化学的作用。(3)血清毒素和中分子毒素的长期作用。
  本组19例肾肿瘤都是在肾囊肿的基础上产生的,故萎缩肾内囊肿的形成常被认为肾内肿瘤发生的前驱病变[8~10]。
19例肿瘤.jpg

  
  参考文献
  1 Vaziri ND. Acquired renal cystic disease in dialysis patients. Int J Artif Organs, 1982, 5:336.
  2 Vaziri ND, Darwish R, Martin DC, et al. Acquired renal cystic disease in renal transplant recipients. Nephron, 1984, 37:203.
   3 Erich M, Dimiter T, Jan Z, et al. Acquired cystic disease of the kidnets in chronic hemodialyzed and renal transplant patients. Eur Urol, 1984, 10:245.
  4 Ishikawa I. Development of acquired cystic disease and adenocarcinoma of the kidney in glomerulonephritic chronic hemodialysis patients. Nephrology, 1980, 14:1.
  5 Dunnill MS, Millard PR, Oliver D. Acquired cystic disease of the Kidneys: a hazard of ling-term intermittent maintenance hemodiaysis. J Clin Path, 1977, 30:868.
  6 Matas AJ. Increased incidence of malignancy during chronic renal failure. The Lancet, 1975:19 April.
   7 Darmada EM, Offer J, Woodhouse MA. Toxic metabolic defect in polycystic disease of kidney. Evidence from microscopic studies. Lancet, 1970, 1:547.
  8 Hughson MD, Hennigar GR, McManus JFA. Atypical cysts acquired renal cystic disease and renal cell tumors in end stage dialysis kidneys. Lab Invest. 1980, 42:475.
  9 Colin C. Acquired renal cystic disease and renal neoplamsin hemodialysis patiens. Urol Radiol, 1984, 6:153.
   10 Adersen BL, Curry NS, Gobien RP. Sonography of evolving renal Cystic transformation associated with hemodialysis. AJR, 1983, 141:1003.
  
  (收稿: 1994-12-06 修回: 1995-01-28)
  
  OCCURRENCE OF RENAL CYST AND TUMOR IN PATIENTS UNDER LONGTERM HEMODIALYSIS
  
  Jiang Aili, Ma Tengxiang
  Research Center of Dialysis Institute of Urologic Surgery, 2nd Affiliated Hospital, Tianjin Medical University, Tianjin 300211
  
   In a period of 12 years, 887 renal failure patients were treated with hemodialysis in our research center. In 512 patients (57.7%) renal cysts were detected by ultrasonagraphy and/or CT. The cysts were apparently acquired during hemodialysis rather than congenital. More important is the fact that in 19 patients with renal cysts tumor subsequently developed. Surgical specimen confirmed that the tumor was malignant in 8 and benign in 11. The mechanism of genesis of renal cyst and tumor in patients under longterm hemodialysis is discussed. The failed kidneys become ischemic and fibrotic and the glomeruli are functionless or completely replaced by fibrotic tussue. Under this situation, the decreased washing-out effect of urinary flow in the renal tubules and tubular obstruction most likely account for cyst formation. The constant chemical and/or physical irritation by the cyst contents combined with the longterm uremia-induced immuno-suppression may contribute to the neoplastic transformation. From the sequence of events, renal cyst may be considered as a pre-cancerous manisfestation.       

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发表于 2017-3-20 14:49 |显示全部帖子
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