2型糖尿病合并終末期腎病外周血細(xì)胞水平的臨床研究

何宴清 楊萍 文莉 鄭雪松 肖麗

·論著·

何宴清 楊萍 文莉 鄭雪松 肖麗

目的分析CD+34細(xì)胞與糖尿病腎病代謝參數(shù)的相關(guān)性及其與糖尿病腎病發(fā)病的關(guān)系。方法選擇終末期腎病患者100例，根據(jù)是否合并2型糖尿病分為合并糖尿病的終末期腎病組(n=55)，為終末期腎病組(n=45)。糖尿病組(n=50)。同時(shí)選取體檢中心健康體檢者作為健康對(duì)照組(n=60)。比較4組三酰甘油(TG)、膽固醇(TC)、空腹血糖(FPG)、餐后2 h血糖(2 hFPG)、糖化血紅蛋白(HbA1c)、CD+34細(xì)胞/單核細(xì)胞值，尿微量白蛋白、肌酐(Cr)水平測(cè)定，腎小球?yàn)V過(guò)率的差異，以及各指標(biāo)間的相關(guān)性。結(jié)果與陰性健康對(duì)照組比較，3個(gè)試驗(yàn)組CD+34細(xì)胞在單核細(xì)胞中的比值降低(P<0.05)；糖尿病組高于終末期腎病組、糖尿病合并終末期腎病組(P<0.05)。糖尿病合并終末期腎病組外周血 CD+34/單核細(xì)胞值與HBA1c、Cr、FPG、微量白蛋白、2 hFPG呈負(fù)相關(guān)(r值分別為-0.439、-0.241、-0.298、-0.342、-0.447，P<0.05)。結(jié)論CD+34細(xì)胞可能是腎病患者的危險(xiǎn)因素，參與腎病的發(fā)生，監(jiān)測(cè) CD+34細(xì)胞水平變化也許能用來(lái)預(yù)測(cè) 2 型糖尿病患者合并終末期腎病的發(fā)生發(fā)展，其中糖尿病可能進(jìn)一步導(dǎo)致CD+34細(xì)胞數(shù)量的下降。

CD34+細(xì)胞；2型糖尿病；終末期腎病

1 資料與方法

1.1 一般資料 選擇2012年1月至2013年1月在我院腎病內(nèi)科住院的終末期腎病患者100例，根據(jù)是否合并糖尿病分為2組:糖尿病合并終末期腎病組55例，男30例，女25例；終末期腎病組45例，男23例，女22例，為終末期腎病無(wú)糖尿病病史。糖尿病組為50例2型糖尿病患者無(wú)腎病病史。同時(shí)選取體檢中心的60例健康體檢者作為健康對(duì)照組。4組一般資料比較有可比性。見(jiàn)表1。

表1 4組一般資料比較 ±s

2 結(jié)果

組別CD+34/PMNC健康對(duì)照組(n=60)0．094±0．032糖尿病組(n=50)0．075±0．022?終末期腎病組(n=45)0．038±0．020?#糖尿病合并終末期腎病組(n=55)0．035±0．020?#

注：與健康對(duì)照組比較，*P<0.05；與糖尿病組比較，#P<0.05

2.2 4組FPG、2 hFPG、HbA1c水平比較 健康對(duì)照組與糖尿病組、糖尿病合并終末期腎病組比較差異有統(tǒng)計(jì)學(xué)意義(P<0.05)，與終末期腎病組比較差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)；糖尿病組與終末期腎病組、糖尿病合并終末期腎病組比較有統(tǒng)計(jì)學(xué)意義(P<0.05)；終末期腎病組與糖尿病合并終末期腎病組比較差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。見(jiàn)表3。

組別FPG(mmol/L)2hFPG(mmol/L)HbA1c(%)健康對(duì)照組(n=60)4．3±0．87．2±0．64．9±0．5糖尿病組(n=50)8．0±2．19．8±2．38．5±0．6終末期腎病組(n=45)5．7±1．2#8．3±2．4#5．6±0．9#糖尿病合并終末期腎病組(n=55)9．5±3．0?#△13．6±3．6?#△10．5±0．7?#△

注：與健康對(duì)照組比較，*P<0.05；與糖尿病組比較，#P<0.05；與終末期腎病組比較，△P<0.05

2.3 4組患者微量白蛋白、Cr、eGFR比較 終末期腎病組及糖尿病合并終末期腎病組微量白蛋白、Cr、eGFR與健康組比較差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。糖尿病組與健康對(duì)照組比較差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)，糖尿病組與終末期腎病組及2型糖尿病合并終末期腎病組微量白蛋白、Cr、eGFR差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。終末期腎病組及糖尿病合并終末期腎病組比較，差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)。見(jiàn)表4。

組別Cr(μmol/L)微量白蛋白(mg/L)eGFR(%)健康對(duì)照組(n=60)60±65．4±2．998±7?糖尿病組(n=50)80±86．9±3．295±8?終末期腎病組(n=45)795±8?1014．3±50．2?9．0±0．8?糖尿病合并終末期腎病組(n=55)804±10?986．1±40．0?9．5±1．2?

注：與健康對(duì)照組比較，*P<0.05

表5 CD34+細(xì)胞與各指標(biāo)相關(guān)分析

3 討論

1 Garg AX,Kibexd BA,Clark WF,et al.Albuminufia and renalinsufficiency prevalence guides population screening: results from the NHANESIII.Kindney Int,2002,61:2165-2175.

2 Coresh J,Selvin E,Stevens LA,et al.Prevalence of chronic kidney disease in the United States.JAMA,2007,298:2038-2047.

3 Chadban SJ,Briganti EM,Kerr PG,et al.Prevalence of kidney damage in Australian adults: the AusDiab kidney study.J Am Soc Nephrol,2003,14:S131-138.

4 Kunitoshi I,Kentaro K,Atsushi S,et al.Changes in the demographics and prevalence of chronic kidney disease in Okinawa.Japan(1993 to 2003).Hypertens Res,2007,30:55-62.

5 Xue JL,Ma JZ,Louis TA,et al.Forecast of the number of patientswith end-stage renal disease in the United States to the year 2010.JAm Soc Nephrol,2001,12:2753-2758.

6 Ati AS,Remuzzi G.Chronic renal diseases as a public health problem: Epidemiology,social,and economic implications.Kidney Int,2005,68:7-10.

7 National Kidney Foundation.K/DOQI clinical practice guidelines for chronic kidney disease: evaluation,classification and stratification.Am J Kidney Dis,2002,39:S1-S266.

8 Zuo L,Ma CHY,Wang M,et al.Appfieation of glomerular filtration rate estimating equations in chinses with chronic kidneydisease.Am J Kidney Dis,2005,45:463-472.

9 Cepeda FJ,Fernandez E,Pobes A,et al.Utility of cystatin-C in hospitalized patients.Comparing with diferent methods of assessing renal function.Nefrologia,2007,27:168-174.

10 Yang YS,Peng CH,Liu CK,et al.Use of serum eystatin C to detect Early- decline of glomerular filtration rate in type 2 diabetes.Intern Med,2007,46:801-806.

11 Hooligan CA,Tsalam an dris C,Akdeniz A,et al.Albumin to ereatinine ratio:a screening test with limirations.Am J Ki dneyDis,2002,39:1183-1189.

12 Skalova S.The diagnostic role of urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in the detection of renal tubular impairment.Acta Medica (Hradec Kralove),2005,48:75-80.

13 Sawshima K,Mizuno S,Mizuno HY,et al.Protein restriction ameliorates renaltubulointerstitial nephritis and reducesrenal transforming groeth factor beta expression in unilateraluretral obstruction.Exp Nephro1,2002,10:7-18.

14 Prakash S，Pande DP,Shanna S,et al.Randomized,double- blind,place-bo-controlled trial to evaluate efficacy of keto dietin predialytic chlonic renal failure.J Ren Nutr,2004,14:89-96.

15 Giordano M,De Feo P,Lucidi P.Effects of dietary protein restriction on fibrinogen and albumin metabolism in ne-phritic patients.Kidney Int,2001,60:235-242.

16 Kaplan NM.Kaplan’s-clinical hypertension 9th ed.Lippincott Wilkins.2006.373.

17 Fair DE,Ogbem MR,Weiler HA,et al.Dietary soy protein attenuates renal disease progression after 1 and 3 weeks in Han:SPRD-cy weaning rats.Nutr,2004,134:1504-1507.

18 Jamerson K,Weker MA,Bakris GL,et al.Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients.Engl J of Med,2008,359:2417-2428.

19 KDOQL Clinical Practice Guidelines and Clinical Practice Recommendations for Diabetes and Chronic Kidney Disease.Am J Kidney Dis,2007,49(2 Suppl 2):S12-154.

20 Dasgupta I,Porter C,Innes A,et al.“Benign”hypertensive nephrosclerosis.QJM,2007,100:113-119.

ClinicalstudyonthechangesofCD+34cellsinpatientswithtype2diabetesmellituscomplicatedbyterminalstagenephropathy

HEYanqing,YANGPing,WENLi,etal.

DepartmentofDermatology,TaiheHospitalAffiliatedtoHubeiMedicalCollage,Hubei,Shiyan442000,China

ObjectiveTo analyze the correlation between CD+34cells and the parameters of diabetic nephropathy as well as the pathogenesis of diabetic nephropathy.MethodsOne hundred patients with terminal stage nephropathy were divided terminal stage nephropathy A group (with diabetes,n=55) and terminal stage nephropathy B group (without diabetes,n=45),simple diabetes group (n=50),at the same time,60 healthy subjects were enrolled as control group.The TG,TC,FPG,2 hFPG,HbA1c,ratio of CD+34cells/monocytes,urine microcontent albumin,muscle anhydride levels,glomerular filtration rate were detected and comparted in the four groups.ResultsAs compard with that in control group,the ratio of CD+34cells/monocytes in three experimental groups were obviously decreased (P<0.05),which in diabetes group was significantly higher than that in terminal stage nephropathy A group and terminal stage nephropathy B group (P<0.05).The ratio of CD+34cells/monocytes was negatively correlated to HbA1c,Cr,FPG in terminal stage nephropathy A group (r=-0.439,-0.241,-0.241,-0.342,-0.298,respectively,P<0.05).ConclusionCD+34cells may be risk factors for patients with diabetic nephropathy,which may be involved in the pathiogenesis of diabetic nephropathy,so monitoring the changes of CD+34cells may predict the pathogenesis and development of type 2 diabetes mellitus complicated by terminal stage nephropathy,in which diabetes mellitus may result in further decrease of CD+34cells.

CD+34 cells;type 2 diabetes mellitus;terminal stage nephropathy

10.3969/j.issn.1002-7386.2014.23.003

442000 湖北省十堰市，湖北醫(yī)藥學(xué)院附屬太和醫(yī)院皮膚科

R 587.1

A

1002-7386(2014)23-3531-04

2014-05-13)