The Influence of G-Protein β3-Subunit Gene and Endothelial Nitric Oxide Synthase Gene in Exon 7 Polymorphisms on Progression of Autosomal Dominant Polycystic Kidney Disease
Background: A significant phenotypical variability is observed in autosomal dominant polycystic kidney disease (ADPKD). The variability cannot be fully explained by the genetic heterogeneity of the disease. We examined the influence of G-protein β3-subunit C825T polymorphism and endothelial nitric o...
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| Veröffentlicht in: | Renal failure 2004, Vol.26 (2), p.119-125 |
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| creator | Reiterová, J. Miroslav, M. Stekrová, J. Kohoutová, M. Tesar, V. Kmentová, D. Hubá ek, J. A. Viklický, O. |
| description | Background: A significant phenotypical variability is observed in autosomal dominant polycystic kidney disease (ADPKD). The variability cannot be fully explained by the genetic heterogeneity of the disease. We examined the influence of G-protein β3-subunit C825T polymorphism and endothelial nitric oxide synthase Glu298Asp polymorphism on the progression of ADPKD towards end stage renal failure (ESRF). Methods: 306 ADPKD patients (pts) were analyzed; 261 pts (136 males, 125 females) with ESRF, with subgroup of 73 pts (44 males, 29 females) with ESRF before 45 years (rapid progressors), 46 pts (20 males, 26 females) with ESRF later than in 63 years (slow progressors) and 45 ADPKD pts (17 males, 28 females) in mean age 51 years with serum creatinine under 110 µmol L (slow progressors) and 100 genetically unrelated healthy Czech subjects. DNA samples from collected blood were genotyped for G-protein β3-subunit C825T genotype in exon 10 and for endothelial nitric oxide synthase Glu298Asp genotype in exon 7. Results: The G-protein β3-subunit C825T genotype exhibited no significant differences among the groups of slow progressors (6.6% (6 91) TT, 54.9% (50 91) CT, 38.8% (35 91) CC), rapid progressors (9.6% (7 73) TT, 46.6% (34 73) CT, 43.8% (32 73) CC), ADPKD group with ESRF between 40-63 years (9.2% (13 142) TT, 50% (71 142) CT, 40.8% (58 142) CC) and control group (12% TT, 44% CT, 44% CC). When comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages: males TT-51.7 ± 8.8 years, CT-51.9 ± 10.3 years, CC-49.7 ± 10.2 years and females TT-56 ± 9.9 years, CT-53.2 ± 8.5 years, CC-53.9 ± 8.7 years. The endothelial nitric oxide synthase Glu298Asp and Asp29Asp genotypes were significantly more frequent in rapid progressors (9.6% (7 73) Asp Asp, 39.7% (29 73) Asp Glu, 50.7% (37 73) Glu Glu) and in ADPKD group with ESRF between 40-63 years (11.3% (16 142) Asp Asp, 41.5% (59 142) Asp Glu, 47.2% (67 142) Glu Glu) in comparison with slow progressors (8.8% (8 91) Asp Asp, 24.2% (22 91) Asp Glu, 67.0% (61 91) Glu Glu) and with control group (8% Asp Asp, 32% Asp Glu, 60% Glu Glu) (Chi-square test, p < 0.05). Comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages in males with Asp Asp-54.9 ± 10.4 years, Asp Glu-50.2 ± 9.4 years, Glu Glu-51.0 ± 10.4 years. We found out in homozygous Asp Asp females significantly earlier onset of ESRF (49.2 ± 5.6 years) in comparison with heterozygo |
| doi_str_mv | 10.1081/JDI-120038485 |
| format | Article |
| fullrecord | <record><control><sourceid>informahealthcare_pasca</sourceid><recordid>TN_cdi_informahealthcare_journals_10_1081_JDI_120038485</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>10_1081_JDI_120038485</sourcerecordid><originalsourceid>FETCH-LOGICAL-i2345-2ab9adb3745df024dd85e94ca36e17e4795a7b907a4a3103b644f92f3f53cef53</originalsourceid><addsrcrecordid>eNptkctu1DAUhiMEEkNhyd4blgHHl1yWVWcYBipaqUViF53Ex8SVY49sR20eig0PwjNhGEBCYmNb1v99R0d_Ubys6OuKttWb99tDWTFKeSta-ajYVJLJsqaie1xsaNvWJWXs89PiWYx3lFaybdim-Ho7ITk4bRd0IxKvyb68Dj6hceT7N17eLMPiTCJ7dEjAKbJzyqcJrQFLPpoUzEiuHoxCcrO6NEHEUzTjuwfvSEOuvV1nH46TiXMk-SvrvwSM0eR3nne-JB_9nHVbPxsHLv1CxjWm7P5glMOVbE3E7H5ePNFgI774fZ8Vn97ubi_elZdX-8PF-WVpGBeyZDB0oAbeCKk0ZUKpVmInRuA1Vg2KppPQDB1tQACvKB9qIXTHNNeSj5iPs-LVyXuEOILVAdxoYn8MZoaw9pXseM14m3PtKWec9mGGex-s6hOs1oc_UB7Q_6ynz_X0f-vJaPMPOiHYNI0QsL_zS3B5vf7_5A-ggZhj</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>The Influence of G-Protein β3-Subunit Gene and Endothelial Nitric Oxide Synthase Gene in Exon 7 Polymorphisms on Progression of Autosomal Dominant Polycystic Kidney Disease</title><source>Taylor & Francis Journals Complete</source><source>Alma/SFX Local Collection</source><creator>Reiterová, J. ; Miroslav, M. ; Stekrová, J. ; Kohoutová, M. ; Tesar, V. ; Kmentová, D. ; Hubá ek, J. A. ; Viklický, O.</creator><creatorcontrib>Reiterová, J. ; Miroslav, M. ; Stekrová, J. ; Kohoutová, M. ; Tesar, V. ; Kmentová, D. ; Hubá ek, J. A. ; Viklický, O.</creatorcontrib><description>Background: A significant phenotypical variability is observed in autosomal dominant polycystic kidney disease (ADPKD). The variability cannot be fully explained by the genetic heterogeneity of the disease. We examined the influence of G-protein β3-subunit C825T polymorphism and endothelial nitric oxide synthase Glu298Asp polymorphism on the progression of ADPKD towards end stage renal failure (ESRF). Methods: 306 ADPKD patients (pts) were analyzed; 261 pts (136 males, 125 females) with ESRF, with subgroup of 73 pts (44 males, 29 females) with ESRF before 45 years (rapid progressors), 46 pts (20 males, 26 females) with ESRF later than in 63 years (slow progressors) and 45 ADPKD pts (17 males, 28 females) in mean age 51 years with serum creatinine under 110 µmol L (slow progressors) and 100 genetically unrelated healthy Czech subjects. DNA samples from collected blood were genotyped for G-protein β3-subunit C825T genotype in exon 10 and for endothelial nitric oxide synthase Glu298Asp genotype in exon 7. Results: The G-protein β3-subunit C825T genotype exhibited no significant differences among the groups of slow progressors (6.6% (6 91) TT, 54.9% (50 91) CT, 38.8% (35 91) CC), rapid progressors (9.6% (7 73) TT, 46.6% (34 73) CT, 43.8% (32 73) CC), ADPKD group with ESRF between 40-63 years (9.2% (13 142) TT, 50% (71 142) CT, 40.8% (58 142) CC) and control group (12% TT, 44% CT, 44% CC). When comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages: males TT-51.7 ± 8.8 years, CT-51.9 ± 10.3 years, CC-49.7 ± 10.2 years and females TT-56 ± 9.9 years, CT-53.2 ± 8.5 years, CC-53.9 ± 8.7 years. The endothelial nitric oxide synthase Glu298Asp and Asp29Asp genotypes were significantly more frequent in rapid progressors (9.6% (7 73) Asp Asp, 39.7% (29 73) Asp Glu, 50.7% (37 73) Glu Glu) and in ADPKD group with ESRF between 40-63 years (11.3% (16 142) Asp Asp, 41.5% (59 142) Asp Glu, 47.2% (67 142) Glu Glu) in comparison with slow progressors (8.8% (8 91) Asp Asp, 24.2% (22 91) Asp Glu, 67.0% (61 91) Glu Glu) and with control group (8% Asp Asp, 32% Asp Glu, 60% Glu Glu) (Chi-square test, p < 0.05). Comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages in males with Asp Asp-54.9 ± 10.4 years, Asp Glu-50.2 ± 9.4 years, Glu Glu-51.0 ± 10.4 years. We found out in homozygous Asp Asp females significantly earlier onset of ESRF (49.2 ± 5.6 years) in comparison with heterozygous females (53.3 ± 7.2 years) and with Glu Glu homozygous females (54.8 ± 9.7 years) (t-test, p < 0.05). Conclusion: We excluded the significance of G-protein β3-subunit C825T polymorphism on the progression of ADPKD. We established the negative prognostic value of the carriers of Asp variant of eNOS polymorphism. Finding of new modifiers could have in future clinical consequences for ADPKD patients.</description><identifier>ISSN: 0886-022X</identifier><identifier>EISSN: 1525-6049</identifier><identifier>DOI: 10.1081/JDI-120038485</identifier><identifier>CODEN: REFAE8</identifier><language>eng</language><publisher>Colchester: Informa UK Ltd</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Autosomal dominant polycystic kidney disease ; Biological and medical sciences ; Endothelial nitric oxide synthase Glu298Asp polymorphism ; G-protein β ; Kidneys ; Malformations of the urinary system ; Medical sciences ; Nephrology. Urinary tract diseases ; Progression ; subunit C825T polymorphism</subject><ispartof>Renal failure, 2004, Vol.26 (2), p.119-125</ispartof><rights>2004 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2004</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1081/JDI-120038485$$EPDF$$P50$$Ginformaworld$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1081/JDI-120038485$$EHTML$$P50$$Ginformaworld$$H</linktohtml><link.rule.ids>314,776,780,4010,27900,27901,27902,59620,60409,61194,61375</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15936238$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Reiterová, J.</creatorcontrib><creatorcontrib>Miroslav, M.</creatorcontrib><creatorcontrib>Stekrová, J.</creatorcontrib><creatorcontrib>Kohoutová, M.</creatorcontrib><creatorcontrib>Tesar, V.</creatorcontrib><creatorcontrib>Kmentová, D.</creatorcontrib><creatorcontrib>Hubá ek, J. A.</creatorcontrib><creatorcontrib>Viklický, O.</creatorcontrib><title>The Influence of G-Protein β3-Subunit Gene and Endothelial Nitric Oxide Synthase Gene in Exon 7 Polymorphisms on Progression of Autosomal Dominant Polycystic Kidney Disease</title><title>Renal failure</title><description>Background: A significant phenotypical variability is observed in autosomal dominant polycystic kidney disease (ADPKD). The variability cannot be fully explained by the genetic heterogeneity of the disease. We examined the influence of G-protein β3-subunit C825T polymorphism and endothelial nitric oxide synthase Glu298Asp polymorphism on the progression of ADPKD towards end stage renal failure (ESRF). Methods: 306 ADPKD patients (pts) were analyzed; 261 pts (136 males, 125 females) with ESRF, with subgroup of 73 pts (44 males, 29 females) with ESRF before 45 years (rapid progressors), 46 pts (20 males, 26 females) with ESRF later than in 63 years (slow progressors) and 45 ADPKD pts (17 males, 28 females) in mean age 51 years with serum creatinine under 110 µmol L (slow progressors) and 100 genetically unrelated healthy Czech subjects. DNA samples from collected blood were genotyped for G-protein β3-subunit C825T genotype in exon 10 and for endothelial nitric oxide synthase Glu298Asp genotype in exon 7. Results: The G-protein β3-subunit C825T genotype exhibited no significant differences among the groups of slow progressors (6.6% (6 91) TT, 54.9% (50 91) CT, 38.8% (35 91) CC), rapid progressors (9.6% (7 73) TT, 46.6% (34 73) CT, 43.8% (32 73) CC), ADPKD group with ESRF between 40-63 years (9.2% (13 142) TT, 50% (71 142) CT, 40.8% (58 142) CC) and control group (12% TT, 44% CT, 44% CC). When comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages: males TT-51.7 ± 8.8 years, CT-51.9 ± 10.3 years, CC-49.7 ± 10.2 years and females TT-56 ± 9.9 years, CT-53.2 ± 8.5 years, CC-53.9 ± 8.7 years. The endothelial nitric oxide synthase Glu298Asp and Asp29Asp genotypes were significantly more frequent in rapid progressors (9.6% (7 73) Asp Asp, 39.7% (29 73) Asp Glu, 50.7% (37 73) Glu Glu) and in ADPKD group with ESRF between 40-63 years (11.3% (16 142) Asp Asp, 41.5% (59 142) Asp Glu, 47.2% (67 142) Glu Glu) in comparison with slow progressors (8.8% (8 91) Asp Asp, 24.2% (22 91) Asp Glu, 67.0% (61 91) Glu Glu) and with control group (8% Asp Asp, 32% Asp Glu, 60% Glu Glu) (Chi-square test, p < 0.05). Comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages in males with Asp Asp-54.9 ± 10.4 years, Asp Glu-50.2 ± 9.4 years, Glu Glu-51.0 ± 10.4 years. We found out in homozygous Asp Asp females significantly earlier onset of ESRF (49.2 ± 5.6 years) in comparison with heterozygous females (53.3 ± 7.2 years) and with Glu Glu homozygous females (54.8 ± 9.7 years) (t-test, p < 0.05). Conclusion: We excluded the significance of G-protein β3-subunit C825T polymorphism on the progression of ADPKD. We established the negative prognostic value of the carriers of Asp variant of eNOS polymorphism. Finding of new modifiers could have in future clinical consequences for ADPKD patients.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Autosomal dominant polycystic kidney disease</subject><subject>Biological and medical sciences</subject><subject>Endothelial nitric oxide synthase Glu298Asp polymorphism</subject><subject>G-protein β</subject><subject>Kidneys</subject><subject>Malformations of the urinary system</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Progression</subject><subject>subunit C825T polymorphism</subject><issn>0886-022X</issn><issn>1525-6049</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNptkctu1DAUhiMEEkNhyd4blgHHl1yWVWcYBipaqUViF53Ex8SVY49sR20eig0PwjNhGEBCYmNb1v99R0d_Ubys6OuKttWb99tDWTFKeSta-ajYVJLJsqaie1xsaNvWJWXs89PiWYx3lFaybdim-Ho7ITk4bRd0IxKvyb68Dj6hceT7N17eLMPiTCJ7dEjAKbJzyqcJrQFLPpoUzEiuHoxCcrO6NEHEUzTjuwfvSEOuvV1nH46TiXMk-SvrvwSM0eR3nne-JB_9nHVbPxsHLv1CxjWm7P5glMOVbE3E7H5ePNFgI774fZ8Vn97ubi_elZdX-8PF-WVpGBeyZDB0oAbeCKk0ZUKpVmInRuA1Vg2KppPQDB1tQACvKB9qIXTHNNeSj5iPs-LVyXuEOILVAdxoYn8MZoaw9pXseM14m3PtKWec9mGGex-s6hOs1oc_UB7Q_6ynz_X0f-vJaPMPOiHYNI0QsL_zS3B5vf7_5A-ggZhj</recordid><startdate>2004</startdate><enddate>2004</enddate><creator>Reiterová, J.</creator><creator>Miroslav, M.</creator><creator>Stekrová, J.</creator><creator>Kohoutová, M.</creator><creator>Tesar, V.</creator><creator>Kmentová, D.</creator><creator>Hubá ek, J. A.</creator><creator>Viklický, O.</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><scope>IQODW</scope></search><sort><creationdate>2004</creationdate><title>The Influence of G-Protein β3-Subunit Gene and Endothelial Nitric Oxide Synthase Gene in Exon 7 Polymorphisms on Progression of Autosomal Dominant Polycystic Kidney Disease</title><author>Reiterová, J. ; Miroslav, M. ; Stekrová, J. ; Kohoutová, M. ; Tesar, V. ; Kmentová, D. ; Hubá ek, J. A. ; Viklický, O.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i2345-2ab9adb3745df024dd85e94ca36e17e4795a7b907a4a3103b644f92f3f53cef53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Autosomal dominant polycystic kidney disease</topic><topic>Biological and medical sciences</topic><topic>Endothelial nitric oxide synthase Glu298Asp polymorphism</topic><topic>G-protein β</topic><topic>Kidneys</topic><topic>Malformations of the urinary system</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Progression</topic><topic>subunit C825T polymorphism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reiterová, J.</creatorcontrib><creatorcontrib>Miroslav, M.</creatorcontrib><creatorcontrib>Stekrová, J.</creatorcontrib><creatorcontrib>Kohoutová, M.</creatorcontrib><creatorcontrib>Tesar, V.</creatorcontrib><creatorcontrib>Kmentová, D.</creatorcontrib><creatorcontrib>Hubá ek, J. A.</creatorcontrib><creatorcontrib>Viklický, O.</creatorcontrib><collection>Pascal-Francis</collection><jtitle>Renal failure</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reiterová, J.</au><au>Miroslav, M.</au><au>Stekrová, J.</au><au>Kohoutová, M.</au><au>Tesar, V.</au><au>Kmentová, D.</au><au>Hubá ek, J. A.</au><au>Viklický, O.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Influence of G-Protein β3-Subunit Gene and Endothelial Nitric Oxide Synthase Gene in Exon 7 Polymorphisms on Progression of Autosomal Dominant Polycystic Kidney Disease</atitle><jtitle>Renal failure</jtitle><date>2004</date><risdate>2004</risdate><volume>26</volume><issue>2</issue><spage>119</spage><epage>125</epage><pages>119-125</pages><issn>0886-022X</issn><eissn>1525-6049</eissn><coden>REFAE8</coden><abstract>Background: A significant phenotypical variability is observed in autosomal dominant polycystic kidney disease (ADPKD). The variability cannot be fully explained by the genetic heterogeneity of the disease. We examined the influence of G-protein β3-subunit C825T polymorphism and endothelial nitric oxide synthase Glu298Asp polymorphism on the progression of ADPKD towards end stage renal failure (ESRF). Methods: 306 ADPKD patients (pts) were analyzed; 261 pts (136 males, 125 females) with ESRF, with subgroup of 73 pts (44 males, 29 females) with ESRF before 45 years (rapid progressors), 46 pts (20 males, 26 females) with ESRF later than in 63 years (slow progressors) and 45 ADPKD pts (17 males, 28 females) in mean age 51 years with serum creatinine under 110 µmol L (slow progressors) and 100 genetically unrelated healthy Czech subjects. DNA samples from collected blood were genotyped for G-protein β3-subunit C825T genotype in exon 10 and for endothelial nitric oxide synthase Glu298Asp genotype in exon 7. Results: The G-protein β3-subunit C825T genotype exhibited no significant differences among the groups of slow progressors (6.6% (6 91) TT, 54.9% (50 91) CT, 38.8% (35 91) CC), rapid progressors (9.6% (7 73) TT, 46.6% (34 73) CT, 43.8% (32 73) CC), ADPKD group with ESRF between 40-63 years (9.2% (13 142) TT, 50% (71 142) CT, 40.8% (58 142) CC) and control group (12% TT, 44% CT, 44% CC). When comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages: males TT-51.7 ± 8.8 years, CT-51.9 ± 10.3 years, CC-49.7 ± 10.2 years and females TT-56 ± 9.9 years, CT-53.2 ± 8.5 years, CC-53.9 ± 8.7 years. The endothelial nitric oxide synthase Glu298Asp and Asp29Asp genotypes were significantly more frequent in rapid progressors (9.6% (7 73) Asp Asp, 39.7% (29 73) Asp Glu, 50.7% (37 73) Glu Glu) and in ADPKD group with ESRF between 40-63 years (11.3% (16 142) Asp Asp, 41.5% (59 142) Asp Glu, 47.2% (67 142) Glu Glu) in comparison with slow progressors (8.8% (8 91) Asp Asp, 24.2% (22 91) Asp Glu, 67.0% (61 91) Glu Glu) and with control group (8% Asp Asp, 32% Asp Glu, 60% Glu Glu) (Chi-square test, p < 0.05). Comparing the ages of ESRF of all patients with ESRF, we did not find significant differences in the ages in males with Asp Asp-54.9 ± 10.4 years, Asp Glu-50.2 ± 9.4 years, Glu Glu-51.0 ± 10.4 years. We found out in homozygous Asp Asp females significantly earlier onset of ESRF (49.2 ± 5.6 years) in comparison with heterozygous females (53.3 ± 7.2 years) and with Glu Glu homozygous females (54.8 ± 9.7 years) (t-test, p < 0.05). Conclusion: We excluded the significance of G-protein β3-subunit C825T polymorphism on the progression of ADPKD. We established the negative prognostic value of the carriers of Asp variant of eNOS polymorphism. Finding of new modifiers could have in future clinical consequences for ADPKD patients.</abstract><cop>Colchester</cop><pub>Informa UK Ltd</pub><doi>10.1081/JDI-120038485</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Renal failure, 2004, Vol.26 (2), p.119-125 |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Autosomal dominant polycystic kidney disease Biological and medical sciences Endothelial nitric oxide synthase Glu298Asp polymorphism G-protein β Kidneys Malformations of the urinary system Medical sciences Nephrology. Urinary tract diseases Progression subunit C825T polymorphism |
| title | The Influence of G-Protein β3-Subunit Gene and Endothelial Nitric Oxide Synthase Gene in Exon 7 Polymorphisms on Progression of Autosomal Dominant Polycystic Kidney Disease |
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