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慢性肾衰竭与血浆胃泌素胃动素的相关性分析

2014-08-08刘永明许翠萍

中国当代医药 2014年14期
关键词:胃泌素慢性肾衰竭相关性

刘永明+许翠萍

[摘要] 目的 探讨慢性肾衰竭与血浆胃泌素、胃动素的相关性。 方法 选择本院2013年1~12月收治的90例慢性肾衰竭患者与9例正常健康者,以肾小球滤过率分组并与血浆胃泌素、胃动素进行相关性统计分析。 结果 慢性肾衰竭组测定的血浆胃泌素、胃动素的指标均高于对照组;慢性肾衰竭五组的胃泌素与对照组比较差异有统计学意义(P<0.01);除GFR3、GFR4组胃动素与对照组比较差异有统计学意义(P<0.01),其余3组胃动素均差异无统计学意义(P>0.05);GFR1、GFR2、GFR3、GFR4、GFR5组及对照组的GFR与胃泌素呈正相关;GFR1、GFR2、GFR5组及对照组的GFR与胃动素呈正相关,GFR3、GFR4组的GFR与胃动素呈负相关。 结论 肾脏损害可能会导致胃泌素和胃动素的升高,但是并不能证明胃泌素和胃动素的升高就是肾脏损害的严重征兆,胃泌素和胃动素是消化道疾病的测定指标,可以衡量消化系统功能的损害程度,虽然它们的分泌与肾脏损害有一定程度的相关性,但不能单纯用胃泌素与胃动素的测定指标来衡量肾脏实质的损伤。

[关键词] 慢性肾衰竭;胃泌素;胃动素;相关性;指标

[中图分类号] R692.5[文献标识码] A[文章编号] 1674-4721(2014)05(b)-0032-05

Correlation analysis of gastrin and motilin of plasma with chronic renal failure

LIU Yong-Ming1 XU Cui-Ping2▲

1.Shanxi Medical University,Taiyuan 030001,China;2.Department of Gastroenterology,Shanxi Medical University,the First Clinical Hospital,Taiyuan 030001,China

[Abstract] Objective To investigate the correlation analysis of gastrin and motilin of plasma with chronic renal failure. Methods 90 cases of chronic renal failure patients and 9 normal healthy were selected in our hospital from January 2013 to December 2013,they were grouped by glomerular filtration rate,and the test parameters of gastrin and motilin of plasma were correlation statistical analyzed. Results The indicators of gastrin and motilin in chronic renal failure group were higher than those of the control group,the gastrin in five chronic renal failure group compared with the control group,the difference was statistically significant (P<0.01),the motilin:except GFR3,GFR4 group compared with control group,the difference was statistically significant (P<0.01),the rest of the three groups,the difference was no statistically significant (P>0.05).The GFR were positively associated with gastrin in GFR1,GFR2,GFR3,GFR4,GFR5 groups and control group.The GFR were positively associated with motilin in GFR1,GFR2,GFR5 groups and control group,but there were negatively associated with motilin in GFR3,GFR4 groups. Conclusion Kidney damage may ead to elevated gastrin and motilin,but does not prove that the rise of gastrin and motilin is kidney damage serious symptom,but does not prove that the rise of gastrin and motilin is the kidney damage serious symptom,gastrin and motilin is the determination of the digestive tract disease indexes,to measure the digestive system function damage degree,although they secrete has a certain degree of correlation with kidney damage,but you can′t simply use gastrin and motilin measurement indicators to measure renal parenchymal damage.

[Key words] Chronic renal failure;Gastrin;Motilin;Relevance;Index

慢性肾衰竭(chronic renal failure,CRF)是一种常见的临床综合征,可以由各种原因引起的肾脏损害,是一种进行性恶化、肾实质不可逆转的损伤,也是各种肾脏疾病进展的终末结局[1-3]。目前,临床以消化道为首发症状的CRF患者日渐增多,胃泌素(GAS)、胃动素(MOT)是消化道疾病的常见检测指标,而肾脏又是GAS、MOT灭活和消除的主要场所,它们是一种连锁反应关系[4-5],目前临床对CRF的研究报道较多,但是对于CRF患者血浆GAS、MOT测定的相关性分析报道较少,本研究通过回顾本院一年来收治的CRF患者的血浆GAS、MOT变化水平并行相关性分析,以探讨慢性肾衰竭与血浆GAS、MOT的相关性。

1 资料与方法

1.1 一般资料

选取本院2013年1~12月末本院收治的90例以消化道为首发症状的CRF的患者(非透析)与9例正常健康者作为研究对象,90例CRF患者均未透析,病史1~4年,平均(2.04±0.63)年;其中男性56例,女性34例;年龄36~71岁,平均(44.16±2.32)岁;原发性疾病:慢性肾小球肾炎33例,慢性肾盂肾炎14例,慢性间质性肾炎13例,肾病综合征8例,高血压肾病17例,紫癜性肾炎1例,肾髓质囊性病2例,遗传性肾炎1例,尿毒症性海绵肾1例。9例正常健康者,男性6例,女性3例,年龄31~58岁,平均(39.05±0.10)岁,均无肝肾及内分泌疾病,未服用任何药物。

1.2 分组方法

以临床入院时所查肾小球滤过率(glomerular filtration rate,GFR)为标准划分,GFR≥90 ml/min为GFR1组;60 ml/min≤GFR<90 ml/min为GFR2组;30 ml/min ≤GFR<60 ml/min为GFR3组;15 ml/min≤GFR<30 ml/min为GFR4组;GFR<15 ml/min为GFR5组;正常健康者为对照组。

1.3 检测方法

受检者均于清晨空腹采血2 ml,注入预先准备的试管中,摇匀后,以3000 r/min离心10 min,取血浆作GAS、MOT酶联免疫法的测定,阴性、阳性对照,1 h孵育后,进行洗板,加相应底物,避光0.5 h进行反应,加终止液完成反应进程,读取数值。试剂盒选用上海抚生生物科技发展有限公司生产的试剂盒(CAS:FS2011)。

1.4 统计学处理

所得数据采用SPSS 17.0软件进行统计学处理,计量资料采用均数±标准差表示,采用t检验,关系测定采用相关回归分析法,以P<0.05为差异有统计学意义。

2 结果

2.1 不同GFR分组与对照组患者GAS 、MOT的比较

CRF组的血浆GAS、MOT均高于对照组;CRF中5组与对照组的GAS差异有统计学意义(P<0.01);除了GFR3、GFR4组的MOT与对照组比较差异有统计学意义(P<0.01),其余3组均差异无统计学意义(P>0.05)(表1)。

表1 不同GFR分组与对照组GAS 、MOT的比较(pg/ml,x±s)

与对照组比较,*P<0.01

2.2 各组GFR与血浆GAS、MOT的相关性

GFR1组的GAS、MOT均与GFR呈正相关(图1);GFR2组的GAS、MOT均与GFR呈正相关(图2);GFR3组的GAS与GFR呈正相关,MOT与GFR呈负相关(图3);GFR4组的GAS与GFR呈正相关,MOT与GFR呈负相关(图4);GFR5组的GAS、MOT均与GFR呈正相关(图5)。

图1 GFR≥90 ml/min腺素的相关性分析

3 讨论

对于CRF的患者来说,消化系统症状是最早和最突出的表现,由于体内大量代谢产物的堆积,酸碱平衡失调,电解质紊乱,都会引起不同程度的消化道症状,胃肠道症状主要原因为胃肠道排尿素增多,经尿素酶分解产生氨刺激胃肠道黏膜引起,此外,也与胃肠道多肽激素代谢障碍引起的黏膜屏障机制紊乱和胃肠道转移性钙化因素有关[6-8]。

GAS和MOT为胃肠多肽激素,MOT主要由空肠的EC细胞分泌,分子量约为2700,具有调节胃动力和胃排空的作用;GAS主要由胃窦G细胞分泌,分子量约为2000,具有促进胃酸分泌的作用[9]。由于肾脏是GAS、MOT代谢和排泄的主要场所,当肾功能受损时,血清GAS和MOT可在机体内蓄积,导致高GAS血症和高MOT血症而引起不同程度的消化道症状[10-12]。

本研究结果显示,CRF患者的血浆GAS、MOT的指标均高于正常对照组,且与对照组差异有统计学意义;有文献报道[13],随着病情加重,MOT和GAS升高更明显,但本研究通过血浆GAS及MOT的测定比较发现,并非随着病情的严重程度,MOT和GAS一定会升高。而不同分期的CRF患者由于病情轻重不一,个体差异不同,表现的消化道症状程度也并非完全一致,所以测定的GAS和MOT数值也不一定是随着病情的严重程度而升高。本研究结果显示,CRF中5组与对照组的GAS差异有统计学意义;除了GFR3、GFR4组的MOT与对照组比较差异有统计学意义,其余3组均差异无统计学意义,说明存在个体差异。本研究结果显示,GFR1组的GAS、MOT均与GFR呈正相关;GFR2组的GAS、MOT均与GFR呈正相关;GFR3组的GAS与GFR呈正相关;GFR4组的GAS与GFR呈正相关,GFR5组的GAS、MOT均与GFR呈正相关,说明随着肾脏损害严重程度的增加,GAS随之不断升高;GFR3、GFR4组MOT与GFR呈负相关,其余组别呈正相关,可能GFR3、GFR4组患者的肾脏损害较轻,消化道症状不明显或者个体肾脏功能修复,EC细胞分泌MOT不足所致。

从基础理论上分析,本研究中CRF患者的GAS和MOT明显高于正常人,且大部分患者的GAS和MOT均与GFR呈正相关。其原因可能为:①大多数CRF患者有恶心、呕吐、腹泻、腹胀等肠道反应,而导致迷走神经兴奋、张力增高,所以会引起GAS和MOT升高;②肾衰竭时,肾脏损害严重,可使GAS和MOT的排泄减少,体内蓄积,导致GAS和MOT明显升高;③CRF患者常有胃酸分泌功能降低,这种低酸度反映了胃液中不断增多的氨而引起的中和作用或由于胃黏膜屏障功能的丧失而引起的胃炎,导致氢离子逆弥散入黏膜内所致,胃酸过低可能会刺激GAS释放,血清GAS含量增高[14-16]。肾脏损害可能会导致GAS和MOT升高,但是并不能证明GAS和MOT的升高就是肾脏损害的严重征兆。

总之,CRF是一种临床常见的多发病,可累及多个系统,临床表现多样性,部分患者起病隐匿,尤其早期缺少特征性的临床表现,易出现误诊和漏诊[17-19]。大多数CRF患者以消化道为首发症状就诊,GAS和MOT是消化道疾病的检测指标,可以衡量消化系统功能的损害程度[20],虽然它们的分泌与肾脏损害有一定程度的相关性,但不能单纯用GAS与MOT来衡量肾脏实质的损伤,因为患者个体存在差异,肾脏实质有一定损害时,GAS和MOT的水平未必会反映现实,因此延误诊治而导致病情恶化。

[参考文献]

[1]Marc J,Robet T.Role of CCK/gastrin receptors in gastrointestinal/metabolic diseases and results of human studies using gastrin/CCKreceptor agonists/antagonists in these diseases[J].Curr Top Med Chem,2007,7(12):1211-1231.

[2]Basile DP,Anderson MD,Sutton TA.Pathophy siology of Acute Kidney Injury[J].Comper Physiol Apr,2012,2(2):1303-1353.

[3]Dreisbach AW,Lertora JL.The effect of chronic renal failure on drug metabolism and transport[J].Expert Opin Drug Metab Toxicol,2008,4(8):1065-1074.

[4]Mitsushige S,Yoshio Y.Review of Helicobacter pylori infection and chronic renal failure[J].Ther Apher Dial,2011, 15(1):1-9.

[5]Sirinek KR,Odorisio TM,Gaskill HV,et al.Chronic renal failure:effect of hemodialysis on gastrointestinal hormones[J].Am J Surg,1984,148(6):732-735.

[6]Kao WH,Klag MJ,Meoni LA,et al.Family Investigation of Nephropathy and Diabetes Research Group. MYH9 is associated with nondiabetic end-stage renal disease in African Americans[J].Nat Genet,2008,40(1):1185-1192.

[7]Freedman BI,Hicks PJ,Bostrom MA,et al.Polymorphisms in the non-muscle myosin heavy chain 9 gene (MYH9)are strongly associated with end-stage renal disease historically attributed to hypertension in African Americans[J].Kidney Int,2009,75(1):736-745.

[8]Genovese G,Friedman DJ,Ross MD,et al.Association of trypanolytic ApoL1 variants with kidney disease in African Americans[J].Science,2010,13,(329):841-845.

[9]Furgala A,Blauk-Kadzielska U,Stojakowska M,et al.Gasttic dysfunction in dialysed patients with chronic renal failure[J].Folia Med Cracov,2012,52(1):39-55.

[10]Donadio C.Effect of glomerular filtration rate impairment on diagnostic performance of neutrophil gelatinase-associated lipocalin and B-type natriuretic peptide as markers of acute cardiac and renal failure in chronic kidney disease patients[J].Crit Care,2014,18(1):39.

[11]Meijers BK,Van Kerckhoven S,Verbeke K,et al.The uremic retention solute p-cresyl sulfate and markers of endothelial damage[J].Am J Kidney Dis,2009,54(1):891-901.

[12]Lin CJ,Wu CJ,Pan CF,et al.Serum protein-bound uraemic toxins and clinical outcomes in haemodialysis patients[J].Nephrol Dial Transplant,2010;25(1):3693-3700.

[13]Harmar AJ.Clinical endocrinology and metabolism. Receptors for gut peptides[J].Clin Endocrinol Metab,2004, 18(4):463-475.

[14]Lin CJ,Pan CF,Chuang CK,et al.Gastrointestinal-related uremic toxins in peritoneal dialysis: a pilot study with a 5-year follow-up[J].Arch Med Res,2013,44(7):535-541.

[15]Lin CJ,Pan CF,Liu HL,et al.The role of protein-bound uremic toxins on peripheral artery disease and vascular access failure in patients on hemodialysis[J].Atherosclerosis,2012,225(1):173-179.

[16]Lin CJ,Liu HL,Pan CF,et al.Indoxyl sulfate predicts cardiovascular disease and renal function deterioration in advanced chronic kidney disease[J].Arch Med Res,2012, 43(1):451-456.

[17]Kobori H,Nangaku M,Navar GL,et al.The Intrarenal Renin-Angiotensin System: from physiology to the pathobiology of hypertension and kidney disease[J].Pharmacol Rev, 2007,59(3):251-287.

[18]José M López-Novoa,Ana B Rodríguez-Pe?觡a,Alberto Ortiz,et al.Etiopathology of chronic tubular,glomerular and renovascular nephropathies:clinical implications[J].J Transl Med,2011,9(1):13.

[19]Bellomo G,Venanzi S,Verdura C,et al.Association of uric acid with change in kidney function in healthy normotensive individuals[J].Am J Kidney Dis,2010,56(1):264-272.

[20]Zeisberg M,Duffield JS.Resolved:EMT produces fibroblasts in the kidney[J].J Am Soc Nephrol,2010,21(1):1247-1253.

(收稿日期:2014-03-17本文编辑:林利利)

[作者简介] 刘永明(1980-),男,硕士,主管技师,研究方向:消化内科

▲通讯作者:许翠萍,女,教授

[5]Sirinek KR,Odorisio TM,Gaskill HV,et al.Chronic renal failure:effect of hemodialysis on gastrointestinal hormones[J].Am J Surg,1984,148(6):732-735.

[6]Kao WH,Klag MJ,Meoni LA,et al.Family Investigation of Nephropathy and Diabetes Research Group. MYH9 is associated with nondiabetic end-stage renal disease in African Americans[J].Nat Genet,2008,40(1):1185-1192.

[7]Freedman BI,Hicks PJ,Bostrom MA,et al.Polymorphisms in the non-muscle myosin heavy chain 9 gene (MYH9)are strongly associated with end-stage renal disease historically attributed to hypertension in African Americans[J].Kidney Int,2009,75(1):736-745.

[8]Genovese G,Friedman DJ,Ross MD,et al.Association of trypanolytic ApoL1 variants with kidney disease in African Americans[J].Science,2010,13,(329):841-845.

[9]Furgala A,Blauk-Kadzielska U,Stojakowska M,et al.Gasttic dysfunction in dialysed patients with chronic renal failure[J].Folia Med Cracov,2012,52(1):39-55.

[10]Donadio C.Effect of glomerular filtration rate impairment on diagnostic performance of neutrophil gelatinase-associated lipocalin and B-type natriuretic peptide as markers of acute cardiac and renal failure in chronic kidney disease patients[J].Crit Care,2014,18(1):39.

[11]Meijers BK,Van Kerckhoven S,Verbeke K,et al.The uremic retention solute p-cresyl sulfate and markers of endothelial damage[J].Am J Kidney Dis,2009,54(1):891-901.

[12]Lin CJ,Wu CJ,Pan CF,et al.Serum protein-bound uraemic toxins and clinical outcomes in haemodialysis patients[J].Nephrol Dial Transplant,2010;25(1):3693-3700.

[13]Harmar AJ.Clinical endocrinology and metabolism. Receptors for gut peptides[J].Clin Endocrinol Metab,2004, 18(4):463-475.

[14]Lin CJ,Pan CF,Chuang CK,et al.Gastrointestinal-related uremic toxins in peritoneal dialysis: a pilot study with a 5-year follow-up[J].Arch Med Res,2013,44(7):535-541.

[15]Lin CJ,Pan CF,Liu HL,et al.The role of protein-bound uremic toxins on peripheral artery disease and vascular access failure in patients on hemodialysis[J].Atherosclerosis,2012,225(1):173-179.

[16]Lin CJ,Liu HL,Pan CF,et al.Indoxyl sulfate predicts cardiovascular disease and renal function deterioration in advanced chronic kidney disease[J].Arch Med Res,2012, 43(1):451-456.

[17]Kobori H,Nangaku M,Navar GL,et al.The Intrarenal Renin-Angiotensin System: from physiology to the pathobiology of hypertension and kidney disease[J].Pharmacol Rev, 2007,59(3):251-287.

[18]José M López-Novoa,Ana B Rodríguez-Pe?觡a,Alberto Ortiz,et al.Etiopathology of chronic tubular,glomerular and renovascular nephropathies:clinical implications[J].J Transl Med,2011,9(1):13.

[19]Bellomo G,Venanzi S,Verdura C,et al.Association of uric acid with change in kidney function in healthy normotensive individuals[J].Am J Kidney Dis,2010,56(1):264-272.

[20]Zeisberg M,Duffield JS.Resolved:EMT produces fibroblasts in the kidney[J].J Am Soc Nephrol,2010,21(1):1247-1253.

(收稿日期:2014-03-17本文编辑:林利利)

[作者简介] 刘永明(1980-),男,硕士,主管技师,研究方向:消化内科

▲通讯作者:许翠萍,女,教授

[5]Sirinek KR,Odorisio TM,Gaskill HV,et al.Chronic renal failure:effect of hemodialysis on gastrointestinal hormones[J].Am J Surg,1984,148(6):732-735.

[6]Kao WH,Klag MJ,Meoni LA,et al.Family Investigation of Nephropathy and Diabetes Research Group. MYH9 is associated with nondiabetic end-stage renal disease in African Americans[J].Nat Genet,2008,40(1):1185-1192.

[7]Freedman BI,Hicks PJ,Bostrom MA,et al.Polymorphisms in the non-muscle myosin heavy chain 9 gene (MYH9)are strongly associated with end-stage renal disease historically attributed to hypertension in African Americans[J].Kidney Int,2009,75(1):736-745.

[8]Genovese G,Friedman DJ,Ross MD,et al.Association of trypanolytic ApoL1 variants with kidney disease in African Americans[J].Science,2010,13,(329):841-845.

[9]Furgala A,Blauk-Kadzielska U,Stojakowska M,et al.Gasttic dysfunction in dialysed patients with chronic renal failure[J].Folia Med Cracov,2012,52(1):39-55.

[10]Donadio C.Effect of glomerular filtration rate impairment on diagnostic performance of neutrophil gelatinase-associated lipocalin and B-type natriuretic peptide as markers of acute cardiac and renal failure in chronic kidney disease patients[J].Crit Care,2014,18(1):39.

[11]Meijers BK,Van Kerckhoven S,Verbeke K,et al.The uremic retention solute p-cresyl sulfate and markers of endothelial damage[J].Am J Kidney Dis,2009,54(1):891-901.

[12]Lin CJ,Wu CJ,Pan CF,et al.Serum protein-bound uraemic toxins and clinical outcomes in haemodialysis patients[J].Nephrol Dial Transplant,2010;25(1):3693-3700.

[13]Harmar AJ.Clinical endocrinology and metabolism. Receptors for gut peptides[J].Clin Endocrinol Metab,2004, 18(4):463-475.

[14]Lin CJ,Pan CF,Chuang CK,et al.Gastrointestinal-related uremic toxins in peritoneal dialysis: a pilot study with a 5-year follow-up[J].Arch Med Res,2013,44(7):535-541.

[15]Lin CJ,Pan CF,Liu HL,et al.The role of protein-bound uremic toxins on peripheral artery disease and vascular access failure in patients on hemodialysis[J].Atherosclerosis,2012,225(1):173-179.

[16]Lin CJ,Liu HL,Pan CF,et al.Indoxyl sulfate predicts cardiovascular disease and renal function deterioration in advanced chronic kidney disease[J].Arch Med Res,2012, 43(1):451-456.

[17]Kobori H,Nangaku M,Navar GL,et al.The Intrarenal Renin-Angiotensin System: from physiology to the pathobiology of hypertension and kidney disease[J].Pharmacol Rev, 2007,59(3):251-287.

[18]José M López-Novoa,Ana B Rodríguez-Pe?觡a,Alberto Ortiz,et al.Etiopathology of chronic tubular,glomerular and renovascular nephropathies:clinical implications[J].J Transl Med,2011,9(1):13.

[19]Bellomo G,Venanzi S,Verdura C,et al.Association of uric acid with change in kidney function in healthy normotensive individuals[J].Am J Kidney Dis,2010,56(1):264-272.

[20]Zeisberg M,Duffield JS.Resolved:EMT produces fibroblasts in the kidney[J].J Am Soc Nephrol,2010,21(1):1247-1253.

(收稿日期:2014-03-17本文编辑:林利利)

[作者简介] 刘永明(1980-),男,硕士,主管技师,研究方向:消化内科

▲通讯作者:许翠萍,女,教授

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