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尿肾损伤分子-1预示常染色体显性多囊肾病早期发展速度 被引量:2

Urine Kidney Injury Molecule-1 can Predict the Progression of Autosomal Dominant Polycystic Kidney Disease in Early Stage Patients
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摘要 目的:探讨尿KIM-1水平与早期ADPKD患者病情进展的相关性,及其预示作用。方法:(1)收集临床确诊为ADPKD患者(CKD1,2期)及体检健康人群各40例,并取其晨起后第2次尿液标本,采用ELISA方法测定尿液中Kim-1浓度,比较多囊肾病人群与正常人群在Kim-1表达程度的差异;(2)用多囊肾患者肾脏体积增长速度判断疾病进展状况,用MRI肾脏成像的方法计算6个月间隔后肾脏体积增长情况;(3)去除肾脏总体积大于1500cm3的患者,以肾脏体积半年增长率2.7%为界,将患者划分为高平均速度组和低平均速度组,比较两组间KIM-1水平差异。结果:(1)多囊肾患者与正常人群相比,eGFR水平(采用CKD-EPI公式计算)差异无统计学意义(P>0.05),但尿中Kim-1水平多囊肾病组显著升高[(837.9±821.5)pg/mlvs(440.3±270.2)pg/ml,P<0.05];(2)多囊肾患者半年肾脏体积增长速度为(4.88±3.86)%,显著高于国外报道的多囊肾患者半年体积增长速度;(3)高平均速度组KIM-1水平高于低平均速度组(P<0.05)。结论:Kim-1作为肾小管损伤后出现的一种重要的生物标记物在多囊肾病患者群中表达显著升高,能预示早期肾脏体积并未发展到一定程度的多囊肾患者肾体积的增长快慢,但Kim-1在疾病进展中的作用机制仍需要进一步的实验研究阐明。 Objective:To study the correlation between urine Kidney injury molecule-1(KIM-1)and the progression of Autosomal Dominant Polycystic Kidney Disease(ADPKD)in early stage patients.Methods:(1)Human KIM-1 Elisa kit was used to determine the different levels of urine KIM-1 in 40 ADPKD patients and 40 healthy individuals.All the patients were diagnosed with stage I or stage II chronic kidney disease at the time of enrollment.(2)We used the increasing rate of total kidney volume to evaluate the progression of ADPKD patients.Increases in kidney volume in ADPKD patients were detected within 6 months by magnetic resonance imaging measurements.(3)Four patients had a total kidney volume over 1500cm3,and were excluded from the study.And the other 36 patients were divided into two groups.One group was over the average increases rate of total kidney volume which was reported about 2.7% during 6 months in the foreign patients.The other group was just the opposite.We compared the urine KIM-1 levels in the two groups.Results:(1)Compared with healthy individuals,the ADPKD patients had a much higher level of urine KIM-1(837.9±821.5 pg/ml vs 440.3±270.2 pg/ml,P0.05)but a similar estimated glomerular filtration rate.(2)The increasing rate of total kidney volume was 4.88±3.86% during 6 months in Chinese Hans Patients with ADPKD,which was much higher than foreign patients.(3)There was a positive correlation between urine KIM-1 level and the increasing rate of total kidney volume.Conclusion:Urine Kidney injury molecule-1(KIM-1)can predict the progression of Autosomal Dominant Polycystic Kidney Disease in early stage patients.We should do more research to reveal the mechanism of KIM-1 interaction with the progression of ADPKD.
出处 《中国中西医结合肾病杂志》 2011年第5期403-406,共4页 Chinese Journal of Integrated Traditional and Western Nephrology
基金 上海市科委重大科技攻关项目(No.08dz1900601) 上海市重点学科建设项目(No.B902)
关键词 肾损伤分子-1 常染色体显性多囊肾病 早期诊断 Kidney injury molecule-1 Autosomal dominant polycystic kidney disease Early diagnosis
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参考文献15

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同被引文献27

  • 1张彤,梅长林.多囊蛋白1分子在多囊肾发病中的作用机制[J].中华肾脏病杂志,2005,21(5):300-302. 被引量:8
  • 2梅长林,戴兵.常染色体显性多囊肾病:挑战与策略[J].中华肾脏病杂志,2005,21(11):636-637. 被引量:13
  • 3DAI Bing MEI Chang-lin.Research on autosomal dominant polycystic kidney disease in China[J].Chinese Medical Journal,2006(22):1915-1924. 被引量:7
  • 4lbraghimov-Beskrovnaya O, Natoli TA. mTOR signaling in polycystic kidney disease. Trends Mol Med ,2011,17 ( 11 ) :625-633.
  • 5TorrosVE, Harris PC. Polycystic Kidney disease in 2011 : Connecting the dots toward a polyeystic kidney disease therapy. Nat Rov Nephrol, 2011,8(2) :66-68.
  • 6Winyard P, Jenkins D. Putative roles of cilia in polycystic kidney disease. Biochim Biophys Acta,2011,1812 (10) : 1256-1262.
  • 7Karihaloo A, Koraishy F, Huen SC, et al. Macrophages promote cyst growth in polycystic kidney disease. J Am Soc Nephml, 2011,22 (10) :1809-1814.
  • 8Schrier RW. Renal Volume, Renin-Angiotensin-Aldosterone System, Hypertension, and Left Ventricular Hypertrophy in Patients with Autosomal Dominant Polycystic Kidney Disease. J Am Soc Nephrol, 2009,20(9) :1888-1893.
  • 9Steinman TI. Polycystic kidney disease: a 2011 update. Curr Opin Nephrol Hypertens, 2012,21 ( 2 ) : 189 - 194.
  • 10Bae KT, Grantham JJ. Imaging for the prognosis of autosomal dominant polycystic kidney disease. Nat Rev Nephrol,2010,6 (2) :96-106.

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