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Non-dipping and arterial hypertension depend on clinical factors rather than on genetic variability of ACE and RGS2 genes in patients with type 1 diabetes
The aim of our study was to characterize the association of clinical and genetic risk factors such as: ACE genotype (rs17997552, rs1800764, rs4459609) and RGS2 (rs2746071) with the development of hypertension (HT) and non-dipping phenomenon in patients with type 1 diabetes mellitus (T1DM). A total o...
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Published in: | Acta diabetologica 2014-08, Vol.51 (4), p.633-640 |
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creator | Deja, G. Borowiec, M. Fendler, W. Pietrzak, I. Szadkowska, A. Machnica, L. Polanska, J. Mlynarski, W. Jarosz-Chobot, P. |
description | The aim of our study was to characterize the association of clinical and genetic risk factors such as:
ACE
genotype (rs17997552, rs1800764, rs4459609) and
RGS2
(rs2746071) with the development of hypertension (HT) and non-dipping phenomenon in patients with type 1 diabetes mellitus (T1DM). A total of 238 adolescents and young adults with T1DM—103 females and 135 males, aged 8–30 years (mean 17.35 ± 5.2) with diabetes duration 1–26 years (mean 7.72 ± 6.2), with mean HbA1c (IFCC) 58 ± 15 mmol/mmol—were subjected to 24-h ambulatory blood pressure measurements (ABPM). The results of the ABPM were analyzed in association with the polymorphisms of
ACE
and
RGS2
genes and clinical data of patients. HT was recognized in 65 (27 %) and non-dipping in 111 (46.63 %) patients. In the multivariate analysis of factors predisposing to HT, the variables that remained significant were the following: male sex (OR 1.62; 95 % CI 1.171–2.250), non-dipping (OR 1.40; 95 % CI 1.03–1.90) and total cholesterol level (OR 1.01; 95 % CI 1.005–1.021). The only factor influencing non-dipping was the duration of diabetes—OR 1.09 (95 % CI 1.04–1.14). The patients displaying non-dipping have a twice increased risk of development of HT (OR 2.17; 95 % CI 1.21–3.89). There was no association between disturbances of blood pressure (BP) and genotypes of
ACE
: rs17997552, rs1800764, rs4459609 and
RGS2
: rs2746071. Clinical rather than genetic risk factors seem to be connected with BP disturbances in young patients with T1DM. Although we have identified representative groups of HT versus non-HT and dipping versus non-dipping subjects, the effect of genetic predisposition to the development of higher BP is too weak to be statistically significant. |
doi_str_mv | 10.1007/s00592-014-0568-0 |
format | article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4127442</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1687664166</sourcerecordid><originalsourceid>FETCH-LOGICAL-c573t-5c00dfe080d5a78d5b30555715c8619e61068a323b69d94d9b8ebcc55fce3cf3</originalsourceid><addsrcrecordid>eNqFktFqFDEUhgdR7Lb6AN5IwBtvRk8ySSZzI5SlrUJR0N6HTObMbspsMibZyr6KT2t2t5YqiFc58H_nz8nJX1WvKLyjAO37BCA6VgPlNQipanhSLShvWC1Y0zytFtBxqAVn3Ul1mtItAGVto55XJ4wLWRCxqH5-Dr4e3Dw7vyLGD8TEjNGZiax3M5baJxc8GXDGIpbKTs47W_TR2BxiItHkNUaS18bv9RV6zM6SO1Nceje5vCNhJOfLi4P916tv7MAk4jyZTXbocyI_XF6TXG4klAylDzOmF9Wz0UwJX96fZ9XN5cXN8mN9_eXq0_L8uraibXItLMAwIigYhGnVIPoGhBAtFVZJ2qGkIJVpWNPLbuj40PUKe2uFGC02dmzOqg9H23nbb3CwZZ5oJj1HtzFxp4Nx-k_Fu7VehTvNyzY5Z8Xg7b1BDN-3mLLeuGRxmozHsE2aStVKyamU_0eFYAqUVHvXN3-ht2EbfVnEgSqfRyUvFD1SNoaUIo4Pc1PQ-4zoY0Z0yYjeZ0RD6Xn9-MEPHb9DUQB2BFKR_Arjo6v_6foLw1XIuA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1552335164</pqid></control><display><type>article</type><title>Non-dipping and arterial hypertension depend on clinical factors rather than on genetic variability of ACE and RGS2 genes in patients with type 1 diabetes</title><source>Springer Link</source><creator>Deja, G. ; Borowiec, M. ; Fendler, W. ; Pietrzak, I. ; Szadkowska, A. ; Machnica, L. ; Polanska, J. ; Mlynarski, W. ; Jarosz-Chobot, P.</creator><creatorcontrib>Deja, G. ; Borowiec, M. ; Fendler, W. ; Pietrzak, I. ; Szadkowska, A. ; Machnica, L. ; Polanska, J. ; Mlynarski, W. ; Jarosz-Chobot, P.</creatorcontrib><description>The aim of our study was to characterize the association of clinical and genetic risk factors such as:
ACE
genotype (rs17997552, rs1800764, rs4459609) and
RGS2
(rs2746071) with the development of hypertension (HT) and non-dipping phenomenon in patients with type 1 diabetes mellitus (T1DM). A total of 238 adolescents and young adults with T1DM—103 females and 135 males, aged 8–30 years (mean 17.35 ± 5.2) with diabetes duration 1–26 years (mean 7.72 ± 6.2), with mean HbA1c (IFCC) 58 ± 15 mmol/mmol—were subjected to 24-h ambulatory blood pressure measurements (ABPM). The results of the ABPM were analyzed in association with the polymorphisms of
ACE
and
RGS2
genes and clinical data of patients. HT was recognized in 65 (27 %) and non-dipping in 111 (46.63 %) patients. In the multivariate analysis of factors predisposing to HT, the variables that remained significant were the following: male sex (OR 1.62; 95 % CI 1.171–2.250), non-dipping (OR 1.40; 95 % CI 1.03–1.90) and total cholesterol level (OR 1.01; 95 % CI 1.005–1.021). The only factor influencing non-dipping was the duration of diabetes—OR 1.09 (95 % CI 1.04–1.14). The patients displaying non-dipping have a twice increased risk of development of HT (OR 2.17; 95 % CI 1.21–3.89). There was no association between disturbances of blood pressure (BP) and genotypes of
ACE
: rs17997552, rs1800764, rs4459609 and
RGS2
: rs2746071. Clinical rather than genetic risk factors seem to be connected with BP disturbances in young patients with T1DM. Although we have identified representative groups of HT versus non-HT and dipping versus non-dipping subjects, the effect of genetic predisposition to the development of higher BP is too weak to be statistically significant.</description><identifier>ISSN: 0940-5429</identifier><identifier>EISSN: 1432-5233</identifier><identifier>DOI: 10.1007/s00592-014-0568-0</identifier><identifier>PMID: 24562335</identifier><identifier>CODEN: ACDAEZ</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Adolescent ; Adult ; Blood Pressure ; Child ; Clinical trials ; Diabetes ; Diabetes Mellitus, Type 1 - complications ; Diabetes Mellitus, Type 1 - enzymology ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - metabolism ; Female ; Genetic Variation ; Genetics ; Humans ; Hypertension ; Hypertension - enzymology ; Hypertension - etiology ; Hypertension - genetics ; Hypertension - physiopathology ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Original ; Original Article ; Patients ; Peptidyl-Dipeptidase A - genetics ; Peptidyl-Dipeptidase A - metabolism ; Polymorphism, Single Nucleotide ; RGS Proteins - genetics ; RGS Proteins - metabolism ; Young Adult</subject><ispartof>Acta diabetologica, 2014-08, Vol.51 (4), p.633-640</ispartof><rights>The Author(s) 2014</rights><rights>Springer-Verlag Italia 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c573t-5c00dfe080d5a78d5b30555715c8619e61068a323b69d94d9b8ebcc55fce3cf3</citedby><cites>FETCH-LOGICAL-c573t-5c00dfe080d5a78d5b30555715c8619e61068a323b69d94d9b8ebcc55fce3cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24562335$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deja, G.</creatorcontrib><creatorcontrib>Borowiec, M.</creatorcontrib><creatorcontrib>Fendler, W.</creatorcontrib><creatorcontrib>Pietrzak, I.</creatorcontrib><creatorcontrib>Szadkowska, A.</creatorcontrib><creatorcontrib>Machnica, L.</creatorcontrib><creatorcontrib>Polanska, J.</creatorcontrib><creatorcontrib>Mlynarski, W.</creatorcontrib><creatorcontrib>Jarosz-Chobot, P.</creatorcontrib><title>Non-dipping and arterial hypertension depend on clinical factors rather than on genetic variability of ACE and RGS2 genes in patients with type 1 diabetes</title><title>Acta diabetologica</title><addtitle>Acta Diabetol</addtitle><addtitle>Acta Diabetol</addtitle><description>The aim of our study was to characterize the association of clinical and genetic risk factors such as:
ACE
genotype (rs17997552, rs1800764, rs4459609) and
RGS2
(rs2746071) with the development of hypertension (HT) and non-dipping phenomenon in patients with type 1 diabetes mellitus (T1DM). A total of 238 adolescents and young adults with T1DM—103 females and 135 males, aged 8–30 years (mean 17.35 ± 5.2) with diabetes duration 1–26 years (mean 7.72 ± 6.2), with mean HbA1c (IFCC) 58 ± 15 mmol/mmol—were subjected to 24-h ambulatory blood pressure measurements (ABPM). The results of the ABPM were analyzed in association with the polymorphisms of
ACE
and
RGS2
genes and clinical data of patients. HT was recognized in 65 (27 %) and non-dipping in 111 (46.63 %) patients. In the multivariate analysis of factors predisposing to HT, the variables that remained significant were the following: male sex (OR 1.62; 95 % CI 1.171–2.250), non-dipping (OR 1.40; 95 % CI 1.03–1.90) and total cholesterol level (OR 1.01; 95 % CI 1.005–1.021). The only factor influencing non-dipping was the duration of diabetes—OR 1.09 (95 % CI 1.04–1.14). The patients displaying non-dipping have a twice increased risk of development of HT (OR 2.17; 95 % CI 1.21–3.89). There was no association between disturbances of blood pressure (BP) and genotypes of
ACE
: rs17997552, rs1800764, rs4459609 and
RGS2
: rs2746071. Clinical rather than genetic risk factors seem to be connected with BP disturbances in young patients with T1DM. Although we have identified representative groups of HT versus non-HT and dipping versus non-dipping subjects, the effect of genetic predisposition to the development of higher BP is too weak to be statistically significant.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Blood Pressure</subject><subject>Child</subject><subject>Clinical trials</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - complications</subject><subject>Diabetes Mellitus, Type 1 - enzymology</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Female</subject><subject>Genetic Variation</subject><subject>Genetics</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - enzymology</subject><subject>Hypertension - etiology</subject><subject>Hypertension - genetics</subject><subject>Hypertension - physiopathology</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Original</subject><subject>Original Article</subject><subject>Patients</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Peptidyl-Dipeptidase A - metabolism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>RGS Proteins - genetics</subject><subject>RGS Proteins - metabolism</subject><subject>Young Adult</subject><issn>0940-5429</issn><issn>1432-5233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNqFktFqFDEUhgdR7Lb6AN5IwBtvRk8ySSZzI5SlrUJR0N6HTObMbspsMibZyr6KT2t2t5YqiFc58H_nz8nJX1WvKLyjAO37BCA6VgPlNQipanhSLShvWC1Y0zytFtBxqAVn3Ul1mtItAGVto55XJ4wLWRCxqH5-Dr4e3Dw7vyLGD8TEjNGZiax3M5baJxc8GXDGIpbKTs47W_TR2BxiItHkNUaS18bv9RV6zM6SO1Nceje5vCNhJOfLi4P916tv7MAk4jyZTXbocyI_XF6TXG4klAylDzOmF9Wz0UwJX96fZ9XN5cXN8mN9_eXq0_L8uraibXItLMAwIigYhGnVIPoGhBAtFVZJ2qGkIJVpWNPLbuj40PUKe2uFGC02dmzOqg9H23nbb3CwZZ5oJj1HtzFxp4Nx-k_Fu7VehTvNyzY5Z8Xg7b1BDN-3mLLeuGRxmozHsE2aStVKyamU_0eFYAqUVHvXN3-ht2EbfVnEgSqfRyUvFD1SNoaUIo4Pc1PQ-4zoY0Z0yYjeZ0RD6Xn9-MEPHb9DUQB2BFKR_Arjo6v_6foLw1XIuA</recordid><startdate>20140801</startdate><enddate>20140801</enddate><creator>Deja, G.</creator><creator>Borowiec, M.</creator><creator>Fendler, W.</creator><creator>Pietrzak, I.</creator><creator>Szadkowska, A.</creator><creator>Machnica, L.</creator><creator>Polanska, J.</creator><creator>Mlynarski, W.</creator><creator>Jarosz-Chobot, P.</creator><general>Springer Milan</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20140801</creationdate><title>Non-dipping and arterial hypertension depend on clinical factors rather than on genetic variability of ACE and RGS2 genes in patients with type 1 diabetes</title><author>Deja, G. ; Borowiec, M. ; Fendler, W. ; Pietrzak, I. ; Szadkowska, A. ; Machnica, L. ; Polanska, J. ; Mlynarski, W. ; Jarosz-Chobot, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c573t-5c00dfe080d5a78d5b30555715c8619e61068a323b69d94d9b8ebcc55fce3cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Blood Pressure</topic><topic>Child</topic><topic>Clinical trials</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - complications</topic><topic>Diabetes Mellitus, Type 1 - enzymology</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Female</topic><topic>Genetic Variation</topic><topic>Genetics</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - enzymology</topic><topic>Hypertension - etiology</topic><topic>Hypertension - genetics</topic><topic>Hypertension - physiopathology</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Original</topic><topic>Original Article</topic><topic>Patients</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Peptidyl-Dipeptidase A - metabolism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>RGS Proteins - genetics</topic><topic>RGS Proteins - metabolism</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deja, G.</creatorcontrib><creatorcontrib>Borowiec, M.</creatorcontrib><creatorcontrib>Fendler, W.</creatorcontrib><creatorcontrib>Pietrzak, I.</creatorcontrib><creatorcontrib>Szadkowska, A.</creatorcontrib><creatorcontrib>Machnica, L.</creatorcontrib><creatorcontrib>Polanska, J.</creatorcontrib><creatorcontrib>Mlynarski, W.</creatorcontrib><creatorcontrib>Jarosz-Chobot, P.</creatorcontrib><collection>SpringerOpen (Open Access)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest research library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta diabetologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deja, G.</au><au>Borowiec, M.</au><au>Fendler, W.</au><au>Pietrzak, I.</au><au>Szadkowska, A.</au><au>Machnica, L.</au><au>Polanska, J.</au><au>Mlynarski, W.</au><au>Jarosz-Chobot, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Non-dipping and arterial hypertension depend on clinical factors rather than on genetic variability of ACE and RGS2 genes in patients with type 1 diabetes</atitle><jtitle>Acta diabetologica</jtitle><stitle>Acta Diabetol</stitle><addtitle>Acta Diabetol</addtitle><date>2014-08-01</date><risdate>2014</risdate><volume>51</volume><issue>4</issue><spage>633</spage><epage>640</epage><pages>633-640</pages><issn>0940-5429</issn><eissn>1432-5233</eissn><coden>ACDAEZ</coden><abstract>The aim of our study was to characterize the association of clinical and genetic risk factors such as:
ACE
genotype (rs17997552, rs1800764, rs4459609) and
RGS2
(rs2746071) with the development of hypertension (HT) and non-dipping phenomenon in patients with type 1 diabetes mellitus (T1DM). A total of 238 adolescents and young adults with T1DM—103 females and 135 males, aged 8–30 years (mean 17.35 ± 5.2) with diabetes duration 1–26 years (mean 7.72 ± 6.2), with mean HbA1c (IFCC) 58 ± 15 mmol/mmol—were subjected to 24-h ambulatory blood pressure measurements (ABPM). The results of the ABPM were analyzed in association with the polymorphisms of
ACE
and
RGS2
genes and clinical data of patients. HT was recognized in 65 (27 %) and non-dipping in 111 (46.63 %) patients. In the multivariate analysis of factors predisposing to HT, the variables that remained significant were the following: male sex (OR 1.62; 95 % CI 1.171–2.250), non-dipping (OR 1.40; 95 % CI 1.03–1.90) and total cholesterol level (OR 1.01; 95 % CI 1.005–1.021). The only factor influencing non-dipping was the duration of diabetes—OR 1.09 (95 % CI 1.04–1.14). The patients displaying non-dipping have a twice increased risk of development of HT (OR 2.17; 95 % CI 1.21–3.89). There was no association between disturbances of blood pressure (BP) and genotypes of
ACE
: rs17997552, rs1800764, rs4459609 and
RGS2
: rs2746071. Clinical rather than genetic risk factors seem to be connected with BP disturbances in young patients with T1DM. Although we have identified representative groups of HT versus non-HT and dipping versus non-dipping subjects, the effect of genetic predisposition to the development of higher BP is too weak to be statistically significant.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>24562335</pmid><doi>10.1007/s00592-014-0568-0</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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language | eng |
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source | Springer Link |
subjects | Adolescent Adult Blood Pressure Child Clinical trials Diabetes Diabetes Mellitus, Type 1 - complications Diabetes Mellitus, Type 1 - enzymology Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - metabolism Female Genetic Variation Genetics Humans Hypertension Hypertension - enzymology Hypertension - etiology Hypertension - genetics Hypertension - physiopathology Internal Medicine Male Medicine Medicine & Public Health Metabolic Diseases Original Original Article Patients Peptidyl-Dipeptidase A - genetics Peptidyl-Dipeptidase A - metabolism Polymorphism, Single Nucleotide RGS Proteins - genetics RGS Proteins - metabolism Young Adult |
title | Non-dipping and arterial hypertension depend on clinical factors rather than on genetic variability of ACE and RGS2 genes in patients with type 1 diabetes |
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