Angiotensin-converting enzyme polymorphism gene and evolution of nephropathy to end-stage renal disease
Genetic polymorphisms of the renin‐angiotensin system (RAS) have been implicated in the pathogenesis of nephropathy and end‐stage renal disease (ESRD). The association between angiotensin‐converting enzyme (ACE) gene polymorphism and nephropathy evolution was studied. A random sample of 161 subjects...
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| Veröffentlicht in: | Nephrology (Carlton, Vic.) Vic.), 2003-08, Vol.8 (4), p.171-176 |
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| creator | ORTIZ, M Angels DE PRADO, Anna DOÑATE, Teresa GALLART, Lluis CLARAMUNT, Helena HERNÁNDEZ, Marta MARTÍNEZ, Joaquin MARTÍNEZ, Esther POU, Jose M |
| description | Genetic polymorphisms of the renin‐angiotensin system (RAS) have been implicated in the pathogenesis of nephropathy and end‐stage renal disease (ESRD). The association between angiotensin‐converting enzyme (ACE) gene polymorphism and nephropathy evolution was studied. A random sample of 161 subjects from the Nephrology Department (of Hospital de Sant Pau) were divided into two groups: (i) 117 with end‐stage renal disease; (ii) 44 with established nephropathy; and (iii) control groups of 129 subjects. The ACE gene polymorphism was performed by using polymerase chain reaction. High DD genotype presentation was observed in the two groups of subjects with nephropathy (46.12 and 61.37%, respectively vs 35.66% in controls; P |
| doi_str_mv | 10.1046/j.1440-1797.2003.00165.x |
| format | Article |
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The association between angiotensin‐converting enzyme (ACE) gene polymorphism and nephropathy evolution was studied. A random sample of 161 subjects from the Nephrology Department (of Hospital de Sant Pau) were divided into two groups: (i) 117 with end‐stage renal disease; (ii) 44 with established nephropathy; and (iii) control groups of 129 subjects. The ACE gene polymorphism was performed by using polymerase chain reaction. High DD genotype presentation was observed in the two groups of subjects with nephropathy (46.12 and 61.37%, respectively vs 35.66% in controls; P < 0.0482), and also, a decrease was observed in the II genotype (6.4 and 4.54%, respectively vs 13.17% in controls, P < 0.0404). Glomerular filtration rate (GFR) was evaulated after 44 months of follow up. An important decrease of GFR was observed in patients with DD polymorphism versus other genotypes (initial, 32.3 ± 7.9 and at 44 months, 18.35 ± 3.3 mL/min vs 31.4 ± 11.9 and 11.7 ± 3.2 mL/min; P < 0.039). In a non‐longitudinal study of patients in ESRD, patients with an ACE‐DD genotype had a lower period of time between diagnosis of nephropathy and ESRD than patients with other genotypes (10.45 ± 9.32 vs 19.5 ± 8.4 years; P < 0.034). In conclusion, the ACE gene that controls RAS response may influence the development and progression of nephropathy to ESRD. Patients who develop several types of nephropathy have a higher risk of severe evolution if they have a profile of ACE‐DD genotype.</description><identifier>ISSN: 1320-5358</identifier><identifier>EISSN: 1440-1797</identifier><identifier>DOI: 10.1046/j.1440-1797.2003.00165.x</identifier><identifier>PMID: 15012717</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Science Pty</publisher><subject>DD and II genotype ; Disease Progression ; end-stage renal disease ; Female ; genetic markers ; Humans ; Kidney Diseases - complications ; Kidney Diseases - genetics ; Kidney Failure, Chronic - etiology ; Kidney Failure, Chronic - genetics ; Male ; Middle Aged ; nephropathy evolution ; Peptidyl-Dipeptidase A - genetics ; Polymorphism, Genetic ; renin-angiotensin system</subject><ispartof>Nephrology (Carlton, Vic.), 2003-08, Vol.8 (4), p.171-176</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4335-6c25a44d315d5ef20bda59973c154e8a13bcca03891be8d7da085136298cbd793</citedby><cites>FETCH-LOGICAL-c4335-6c25a44d315d5ef20bda59973c154e8a13bcca03891be8d7da085136298cbd793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1440-1797.2003.00165.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1440-1797.2003.00165.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,778,782,1414,27911,27912,45561,45562</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15012717$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ORTIZ, M Angels</creatorcontrib><creatorcontrib>DE PRADO, Anna</creatorcontrib><creatorcontrib>DOÑATE, Teresa</creatorcontrib><creatorcontrib>GALLART, Lluis</creatorcontrib><creatorcontrib>CLARAMUNT, Helena</creatorcontrib><creatorcontrib>HERNÁNDEZ, Marta</creatorcontrib><creatorcontrib>MARTÍNEZ, Joaquin</creatorcontrib><creatorcontrib>MARTÍNEZ, Esther</creatorcontrib><creatorcontrib>POU, Jose M</creatorcontrib><title>Angiotensin-converting enzyme polymorphism gene and evolution of nephropathy to end-stage renal disease</title><title>Nephrology (Carlton, Vic.)</title><addtitle>Nephrology (Carlton)</addtitle><description>Genetic polymorphisms of the renin‐angiotensin system (RAS) have been implicated in the pathogenesis of nephropathy and end‐stage renal disease (ESRD). The association between angiotensin‐converting enzyme (ACE) gene polymorphism and nephropathy evolution was studied. A random sample of 161 subjects from the Nephrology Department (of Hospital de Sant Pau) were divided into two groups: (i) 117 with end‐stage renal disease; (ii) 44 with established nephropathy; and (iii) control groups of 129 subjects. The ACE gene polymorphism was performed by using polymerase chain reaction. High DD genotype presentation was observed in the two groups of subjects with nephropathy (46.12 and 61.37%, respectively vs 35.66% in controls; P < 0.0482), and also, a decrease was observed in the II genotype (6.4 and 4.54%, respectively vs 13.17% in controls, P < 0.0404). Glomerular filtration rate (GFR) was evaulated after 44 months of follow up. An important decrease of GFR was observed in patients with DD polymorphism versus other genotypes (initial, 32.3 ± 7.9 and at 44 months, 18.35 ± 3.3 mL/min vs 31.4 ± 11.9 and 11.7 ± 3.2 mL/min; P < 0.039). In a non‐longitudinal study of patients in ESRD, patients with an ACE‐DD genotype had a lower period of time between diagnosis of nephropathy and ESRD than patients with other genotypes (10.45 ± 9.32 vs 19.5 ± 8.4 years; P < 0.034). In conclusion, the ACE gene that controls RAS response may influence the development and progression of nephropathy to ESRD. Patients who develop several types of nephropathy have a higher risk of severe evolution if they have a profile of ACE‐DD genotype.</description><subject>DD and II genotype</subject><subject>Disease Progression</subject><subject>end-stage renal disease</subject><subject>Female</subject><subject>genetic markers</subject><subject>Humans</subject><subject>Kidney Diseases - complications</subject><subject>Kidney Diseases - genetics</subject><subject>Kidney Failure, Chronic - etiology</subject><subject>Kidney Failure, Chronic - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>nephropathy evolution</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Polymorphism, Genetic</subject><subject>renin-angiotensin system</subject><issn>1320-5358</issn><issn>1440-1797</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhiNERT_gLyCfuCX1xHGcSFyqqpRCWTgAPVpOPJv1ktipnW03_Hq87Ko9wskj-XlmpPdNEgI0A1qU5-sMioKmIGqR5ZSyjFIoebZ9kZw8fbyMM8tpyhmvjpPTENYREnkJr5Jj4BRyAeIk6S5sZ9yENhibts4-oJ-M7Qja3_OAZHT9PDg_rkwYSIcWibKa4IPrN5NxlrglsTiuvBvVtJrJ5KKo0zCpDolHq3qiTUAV8HVytFR9wDeH9yz58eHq--XH9Pbr9c3lxW3aFozxtGxzropCM-Ca4zKnjVa8rgVrgRdYKWBN2yrKqhoarLTQilYcWJnXVdtoUbOz5N1-7-jd_QbDJAcTWux7ZdFtghTAS1aw8p9gDhDvQhXBag-23oXgcSlHbwblZwlU7tqQa7kLXe5Cl7s25N825Daqbw83Ns2A-lk8xB-B93vg0fQ4__diubj6Foeop3vdhAm3T7ryv2QpmODybnEt2c9PvL77vJBf2B_Zn6ke</recordid><startdate>200308</startdate><enddate>200308</enddate><creator>ORTIZ, M Angels</creator><creator>DE PRADO, Anna</creator><creator>DOÑATE, Teresa</creator><creator>GALLART, Lluis</creator><creator>CLARAMUNT, Helena</creator><creator>HERNÁNDEZ, Marta</creator><creator>MARTÍNEZ, Joaquin</creator><creator>MARTÍNEZ, Esther</creator><creator>POU, Jose M</creator><general>Blackwell Science Pty</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200308</creationdate><title>Angiotensin-converting enzyme polymorphism gene and evolution of nephropathy to end-stage renal disease</title><author>ORTIZ, M Angels ; DE PRADO, Anna ; DOÑATE, Teresa ; GALLART, Lluis ; CLARAMUNT, Helena ; HERNÁNDEZ, Marta ; MARTÍNEZ, Joaquin ; MARTÍNEZ, Esther ; POU, Jose M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4335-6c25a44d315d5ef20bda59973c154e8a13bcca03891be8d7da085136298cbd793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>DD and II genotype</topic><topic>Disease Progression</topic><topic>end-stage renal disease</topic><topic>Female</topic><topic>genetic markers</topic><topic>Humans</topic><topic>Kidney Diseases - complications</topic><topic>Kidney Diseases - genetics</topic><topic>Kidney Failure, Chronic - etiology</topic><topic>Kidney Failure, Chronic - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>nephropathy evolution</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Polymorphism, Genetic</topic><topic>renin-angiotensin system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ORTIZ, M Angels</creatorcontrib><creatorcontrib>DE PRADO, Anna</creatorcontrib><creatorcontrib>DOÑATE, Teresa</creatorcontrib><creatorcontrib>GALLART, Lluis</creatorcontrib><creatorcontrib>CLARAMUNT, Helena</creatorcontrib><creatorcontrib>HERNÁNDEZ, Marta</creatorcontrib><creatorcontrib>MARTÍNEZ, Joaquin</creatorcontrib><creatorcontrib>MARTÍNEZ, Esther</creatorcontrib><creatorcontrib>POU, Jose M</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Nephrology (Carlton, Vic.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ORTIZ, M Angels</au><au>DE PRADO, Anna</au><au>DOÑATE, Teresa</au><au>GALLART, Lluis</au><au>CLARAMUNT, Helena</au><au>HERNÁNDEZ, Marta</au><au>MARTÍNEZ, Joaquin</au><au>MARTÍNEZ, Esther</au><au>POU, Jose M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin-converting enzyme polymorphism gene and evolution of nephropathy to end-stage renal disease</atitle><jtitle>Nephrology (Carlton, Vic.)</jtitle><addtitle>Nephrology (Carlton)</addtitle><date>2003-08</date><risdate>2003</risdate><volume>8</volume><issue>4</issue><spage>171</spage><epage>176</epage><pages>171-176</pages><issn>1320-5358</issn><eissn>1440-1797</eissn><abstract>Genetic polymorphisms of the renin‐angiotensin system (RAS) have been implicated in the pathogenesis of nephropathy and end‐stage renal disease (ESRD). The association between angiotensin‐converting enzyme (ACE) gene polymorphism and nephropathy evolution was studied. A random sample of 161 subjects from the Nephrology Department (of Hospital de Sant Pau) were divided into two groups: (i) 117 with end‐stage renal disease; (ii) 44 with established nephropathy; and (iii) control groups of 129 subjects. The ACE gene polymorphism was performed by using polymerase chain reaction. High DD genotype presentation was observed in the two groups of subjects with nephropathy (46.12 and 61.37%, respectively vs 35.66% in controls; P < 0.0482), and also, a decrease was observed in the II genotype (6.4 and 4.54%, respectively vs 13.17% in controls, P < 0.0404). Glomerular filtration rate (GFR) was evaulated after 44 months of follow up. An important decrease of GFR was observed in patients with DD polymorphism versus other genotypes (initial, 32.3 ± 7.9 and at 44 months, 18.35 ± 3.3 mL/min vs 31.4 ± 11.9 and 11.7 ± 3.2 mL/min; P < 0.039). In a non‐longitudinal study of patients in ESRD, patients with an ACE‐DD genotype had a lower period of time between diagnosis of nephropathy and ESRD than patients with other genotypes (10.45 ± 9.32 vs 19.5 ± 8.4 years; P < 0.034). In conclusion, the ACE gene that controls RAS response may influence the development and progression of nephropathy to ESRD. Patients who develop several types of nephropathy have a higher risk of severe evolution if they have a profile of ACE‐DD genotype.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Science Pty</pub><pmid>15012717</pmid><doi>10.1046/j.1440-1797.2003.00165.x</doi><tpages>6</tpages></addata></record> |
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| subjects | DD and II genotype Disease Progression end-stage renal disease Female genetic markers Humans Kidney Diseases - complications Kidney Diseases - genetics Kidney Failure, Chronic - etiology Kidney Failure, Chronic - genetics Male Middle Aged nephropathy evolution Peptidyl-Dipeptidase A - genetics Polymorphism, Genetic renin-angiotensin system |
| title | Angiotensin-converting enzyme polymorphism gene and evolution of nephropathy to end-stage renal disease |
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