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Клинико-генетические факторы риска развития микроальбуминурии при артериальной гипертензии
Клинико-генетические факторы риска развития микроальбуминурии при артериальной гипертензии
Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Аннотация
Цель: Анализ влияния клинических и генетических факторов риска на возникновение микроальбуминурии (МАУ) при артериальной гипертензии (АГ).
Материалы и методы. Обследован 371 пациент с АГ, 65% мужчин, средний возраст 51,7±8,3 года. Группу контроля составили 184 человека, 83% мужчин, средний возраст 37±14 лет. Обследование: липидный спектр, гликемия, креатинин, анализ мочи, определение МАУ (тест-полоски Micral-test), положительный результат при повторном выявлении более 20 мг/л. Генотипирование по однонуклеотидным заменам Glu298Asp гена эндотелиальной NO-синтазы (eNOS), С242Т гена субъединицы p22phox NADPH-оксидазы, А1166С гена ATR 1 проводили методом полимеразной цепной реакции (ПЦР) с анализом полиморфизма длины рестрикционных фрагментов, а по заменам М235Т, G(-6)A гена AGT с помощью аллель-специфичной ПЦР «в реальном времени». Достоверность различий определяли с использованием χ2, рассчитывали показатели относительного риска (ОР) и отношения шансов (ОШ).
Результаты. МАУ выявлена у 10,5%. Достоверно повышали ее риск курение (ОШ 2,2; р=0,017), сахарный диабет (ОШ 2,7; р=0,009) и III степень АГ (ОШ 3,2; р=0,009), влияние отягощенной наследственности, пола, ожирения, дислипидемии, давности АГ недостоверно. В целом по группе не получено влияния изучаемых полиморфизмов на развитие МАУ. При делении на подгруппы по возрасту больных и возрасту установления АГ получена достоверность отличий и показано участие полиморфизмов Glu298Asp гена eNOS, G(-6)A гена AGT и А1166С гена ATR1.
Выводы. Риск МАУ повышается у больных АГ при наличии курения, сахарного диабета, III степени АГ. У лиц до 50 лет МАУ ассоциировалась с аллелем G полиморфизма G(-6)A гена AGT (ОШ 2,6; р=0,02); при установлении АГ в возрасте до 35 лет риск МАУ ассоциировался с аллелем А полиморфизма Glu298Asp гена eNOS (ОШ 3,6; р=0,02) и аллелем С полиморфизма А1166С гена ATR1 (ОШ 2,6; р=0,034).
Ключевые слова: микроальбуминурия, генетический полиморфизм, факторы риска.
Materials and methods: 371 patient AH, 65% of men, age 51,7±8,3, control group – 184 people, age 37±14 years, 83% of men was tested (surveyed).
Examination. Lipidic spectrum, glycemia, kreatine, the urine analysis, MAU definition (test strip Micral-test), positive result at repeated revealing >20 mg/l. The genetic typing on single nucleotides replacements Glu298Asp of a eNOS gene, the С242Т of a gene subunit p22phox NADPH oxydase, А1166С of a ATR 1 gene was performed by the PTSR method with the length of restriction fragment polymorphism analysis, and on the М235Т, G (-6) A gene AGT replacements by means of allele-specific PTSR «in real time». The accuracy of diversity was defined with the use of ?2, figuring out the relative risk factor and the ratio chances (OR).
Results. MAU was revealed in 10,5%. The risk of MAU was increased by smoking (OR 2,2, р=0,017), diabetes (OR 2,7, р=0,009) and third stage AH (OR 3,2, р=0,009), the influence of the burdened heredity, sex, obesity, dislipidemii, prescription AH is doubtful. The influence of polymorphism under test on the MAU development is not obtained for the group on the whole. The significance of difference for subgroups on age and age of AH reliability establishment was acquired and the involvement of polymorphisms Glu298Asp of eNOS gene, G (-6) A gene AGT and А1166С gene ATR1 was shown.
Conclusions. The MAU risk rises in AH patients with the habit of smoking, in patients with diabetes, 3 stage AH. In patients under the age of 50 MAU was associated with allele G of polymorphism G (-6) A gene AGT (OR 2,6, р=0,02); at AH determination before the age of 35 the risk of MAU is associated with allele A of polymorphism Glu298Asp of a gene eNOS (OR 3,6, р=0,02) and with allele C of polymorphism А1166С of gene ATR1 (OR 2,6, р=0,034).
Keywords: microalbuminuria, genetic polymorphism, risk factors.
Материалы и методы. Обследован 371 пациент с АГ, 65% мужчин, средний возраст 51,7±8,3 года. Группу контроля составили 184 человека, 83% мужчин, средний возраст 37±14 лет. Обследование: липидный спектр, гликемия, креатинин, анализ мочи, определение МАУ (тест-полоски Micral-test), положительный результат при повторном выявлении более 20 мг/л. Генотипирование по однонуклеотидным заменам Glu298Asp гена эндотелиальной NO-синтазы (eNOS), С242Т гена субъединицы p22phox NADPH-оксидазы, А1166С гена ATR 1 проводили методом полимеразной цепной реакции (ПЦР) с анализом полиморфизма длины рестрикционных фрагментов, а по заменам М235Т, G(-6)A гена AGT с помощью аллель-специфичной ПЦР «в реальном времени». Достоверность различий определяли с использованием χ2, рассчитывали показатели относительного риска (ОР) и отношения шансов (ОШ).
Результаты. МАУ выявлена у 10,5%. Достоверно повышали ее риск курение (ОШ 2,2; р=0,017), сахарный диабет (ОШ 2,7; р=0,009) и III степень АГ (ОШ 3,2; р=0,009), влияние отягощенной наследственности, пола, ожирения, дислипидемии, давности АГ недостоверно. В целом по группе не получено влияния изучаемых полиморфизмов на развитие МАУ. При делении на подгруппы по возрасту больных и возрасту установления АГ получена достоверность отличий и показано участие полиморфизмов Glu298Asp гена eNOS, G(-6)A гена AGT и А1166С гена ATR1.
Выводы. Риск МАУ повышается у больных АГ при наличии курения, сахарного диабета, III степени АГ. У лиц до 50 лет МАУ ассоциировалась с аллелем G полиморфизма G(-6)A гена AGT (ОШ 2,6; р=0,02); при установлении АГ в возрасте до 35 лет риск МАУ ассоциировался с аллелем А полиморфизма Glu298Asp гена eNOS (ОШ 3,6; р=0,02) и аллелем С полиморфизма А1166С гена ATR1 (ОШ 2,6; р=0,034).
Ключевые слова: микроальбуминурия, генетический полиморфизм, факторы риска.
________________________________________________
Materials and methods: 371 patient AH, 65% of men, age 51,7±8,3, control group – 184 people, age 37±14 years, 83% of men was tested (surveyed).
Examination. Lipidic spectrum, glycemia, kreatine, the urine analysis, MAU definition (test strip Micral-test), positive result at repeated revealing >20 mg/l. The genetic typing on single nucleotides replacements Glu298Asp of a eNOS gene, the С242Т of a gene subunit p22phox NADPH oxydase, А1166С of a ATR 1 gene was performed by the PTSR method with the length of restriction fragment polymorphism analysis, and on the М235Т, G (-6) A gene AGT replacements by means of allele-specific PTSR «in real time». The accuracy of diversity was defined with the use of ?2, figuring out the relative risk factor and the ratio chances (OR).
Results. MAU was revealed in 10,5%. The risk of MAU was increased by smoking (OR 2,2, р=0,017), diabetes (OR 2,7, р=0,009) and third stage AH (OR 3,2, р=0,009), the influence of the burdened heredity, sex, obesity, dislipidemii, prescription AH is doubtful. The influence of polymorphism under test on the MAU development is not obtained for the group on the whole. The significance of difference for subgroups on age and age of AH reliability establishment was acquired and the involvement of polymorphisms Glu298Asp of eNOS gene, G (-6) A gene AGT and А1166С gene ATR1 was shown.
Conclusions. The MAU risk rises in AH patients with the habit of smoking, in patients with diabetes, 3 stage AH. In patients under the age of 50 MAU was associated with allele G of polymorphism G (-6) A gene AGT (OR 2,6, р=0,02); at AH determination before the age of 35 the risk of MAU is associated with allele A of polymorphism Glu298Asp of a gene eNOS (OR 3,6, р=0,02) and with allele C of polymorphism А1166С of gene ATR1 (OR 2,6, р=0,034).
Keywords: microalbuminuria, genetic polymorphism, risk factors.
Полный текст
Список литературы
1. Арутюнов Г.П., Чернявская Т.К. Проблема нефропротекции у пациентов с артериальной гипертонией. Значение показателя микроальбуминурии для врача общей практики. Качество жизни. Медицина. 2005; 3 (10): 22–7.
2. Мухин Н.А., Моисеев В.С., Фомин В.В. Микроальбуминурия – интегральный маркер кардиоренальных взаимоотношений. Сердеч. недостаточность. 2007; 8 (6): 301–5.
3. Мухин Н.А., Фомин В.В., Моисеев С.В., Нанчиева М.Л. Микроальбуминурия – универсальный маркер неблагоприятного прогноза. Сердеч. недостаточность. 2008; 9 (2): 79–82.
4. Dinneen SF, Gerstein HC. The association of microalbuminuria and mortality in non-insulin-dependent diabetes mellitus. A systematic overview of the literature. Arch Internal Med 1997; 157: 1413–8.
5. Kannel WB, Stampfer MJ, Castelli WP, Verter J. The prognostic significance of proteinuria: The Framingham study. Am Heart J 1984; 108: 1347–52.
6. Borch-Johnsen K, Feldt-Rasmussen B, Strandgaard S et al. Urinary albumin excretion. An independent predictor of ischemic heart disease. Arterioscleros Thrombos Vascular Biol 1999; 19: 1992–7.
7. Hillege HL, Fidler V, Diercks GF et al. Prevention of Renal and Vascular End Stage Disease (PREVEND) Study Group: Urinary albumin excretion predicts cardiovascular and noncardiovascular mortality in the general population. Circulation 2002; 106: 1777–82.
8. Romundstad S, Holmen J, Kvenild K. Microalbuminuria and all-cause mortality in 2,089 apparently healthy individuals: A 4.4-year follow-up study. The Nord-Trondelag Health Study (HUNT), Norway. Am J Kidney Dis 2003; 42: 466–73.
9. Yuyun MF, Khaw KT, Luben R et al. European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) Population Study: Microalbuminuria independently predicts all-cause and cardiovascular mortality in a British population: The European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) population study. Internat J Epidemiol 2004; 33: 189–98.
10. Pontremoli R, Leoncini G, Viazzi F et al. Evaluation of subclinical organ damage for risk assessment and treatment in the hypertensive patient: role of microalbuminuria. J Am Soc Nephrol JASN 2006; 17 (4), Suppl 2: S112–4
11. Schrader J, Lиders S, Kulschewski A et al. Microalbuminuria and tubular proteinuria as risk predictors of cardiovascular morbidity and mortality in essential hypertension: final results of a prospective long-term study (MARPLE Study). J Hypertens 2006; 24 (3): 541–8.
12. de Zeeuw D, Parving HH, Henning RH. Microalbuminuria as an early marker for cardiovascular disease. J Am Soc Nephrol JASN 2006; 17 (8): 2100–5.
13. Leoncini G, Ratto E, Viazzi F et al. Improving cardiovascular risk stratification: the case for redefining microalbuminuria. J Nephrol 2007; 20 (Suppl. 12): S51–5.
14. Palatini P. Microalbuminuria in hypertension. Cur Hypertens Rep 2003; 5 (3): 208–14.
15. Hitha B, Pappachan JM, Pillai HB et al. Microalbuminuria in patients with essential hypertension and its relationship to target organ damage: an Indian experience. Saudi journal of kidney diseases and transplantation: an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia 2008; 19 (3): 411–9.
16. Jones CA, Francis ME, Eberhardt MS et al. Microalbumiuria I the US population: third National Health and Nutrition Examination Survey. Am J Kidney Dis 2002; 39 (3): 445–59.
17. Tedesco MA, Natale F, Mocerino RJ et al. Renal resistive index and cardiovascular organ damage in a large population of hypertensive patients. J Hum Hypertens 2007; 21 (4): 291–6.
18. Leoncini G, Sacchi G, Ravera M. Microalbuminuria is an integrated marker of subclinical organ damage in primary hypertension. J Hum Hypertens 2002; 16: 399–404.
19. Thomas GN, Critchley JA, Tomlinson B et al. Albuminuria and the renin-angiotensin system gene polymorphisms in type-2-diabetic and in normoglycemic hypertensive Chinese. Clin Nephrol 2001; 55 (1): 7–15.
20. Viazzi F, Leoncini G, Ratto E et al. Microalbuminuria, blood pressure load, and systemic vascular permeability in primary hypertension. Am J Hypertens 2006; 19 (11): 1183–9.
21. Cirillo V, Stellato D, Laurenzi M et al. Pulse pressure and isolated systolic hypertension: association with microalbuminuria. The GUBIO Study Collaborative Research group. Kidney International 2000; 58 (3): 1211–8.
22. Reboldi G, Gentile G, Angeli F, Verdecchia P. Microalbuminuria and hypertension. Minerva Medica 2005; 96 (4): 261–75.
23. Bonnet F, Marre M, Halimi JM et al. Waist circumference and the metabolic syndrome predict the development of elevated albuminuria in non-diabetic subjects: the DESIR study. J Hypertens 2006; 24 (6): 1157–63.
24. Falqui V, Viazzi F, Leoncini G et al. Blood pressure load, vascular permeability and target organ damage in primary hypertension. J Nephrol 2007; 20 (Suppl. 12): S63–7.
25. Liese AD, Hense HW, Broun AA et al. Microalbuminuria, central adiposity and hypertension in non-diabetic urban population of the MONICA Augsburg survey1994/95. J Hum Hypertens 2001; 15 (11): 799–804.
26. Redon J, Liao Y, Lozano JV et al. Factors related to the presence of microalbuminuria in essential hypertension. Am J Hypertens 1994; 7 (9), Pt 1: 801–7.
27. Metclaf P, Bekker J, Scott A et al. Albuminuria in people at least 40 years old: effect of obesity, hypertension and hyperlipidemia. Clin Chem 1992; 38 (9): 1802–8.
28. Diercks GF, Janssen WM, van Boven AJ et al. Rationale, desighn and baseline characteristics of a trial of prevention of cardiovascular and renal disease with fosinopril and pravastatin in nonhypertensive, nonhypercholesterolemic subjects with microalbuminuria (the Prevention of REnal and Vascular ENdstage Desease Intervention Trial (PREVEND IT). Am J Cardiol 2000; 86 (6): 635–8.
29. Orth SR. Smoking – a renal risk factor. Nephron 2000; 86 (1): 12–26.
30. Pinto-Sietsma SJ, Mulder J, Janssen WM et al. Smoking is related to albuminuria and abnormal renal function in non-diabetic persons. Ann Internal Med 2000; 133 (8): 585–91.
31. Buraczynskа M, Ksiazek P, ?opaty?ski J et al. Association of the renin-angiotensin system gene polymorphism with nephropathy in type II diabetes. Polskie archiwum medycyny wewnetrznej 2002; 108 (2): 725–30.
32. Fabris B, Bortoletto M, Candido R et al. Genetic polymorphisms of the renin-angiotensin-aldosterone system and renal insufficiency in essential hypertension. J Hypertens 2005; 23 (2): 309–16.
33. Marin P, Julve R, Chaves FJ et al. Polymorphisms of the angiotensinogen gene and the outcome of microalbuminuria in essential hypertension: a 3-year follow-up study. J Hum Hypertens 2004; 18 (1): 25–31.
34. Wong TY, Chan JC, Poon E, Li PK. Lack of association of angiotensin-converting enzyme (DD/II) and angiotensinogen M235T gene polymorphism with renal function among Chinese patients with type II diabetes. Am J Kidney Dis 1999; 33 (6): 1064–70.
35. Young RP, Chan JC, Critchley JA et al. Angiotensinogen T235 and ACE insertion/deletion polymorphisms associated with albuminuria in Chinese type 2 diabetic patients. Diabet Care 1998; 21 (3): 431–7.
36. Dell'Omo G, Penno G, Pucci L et al. Lack of association between endothelial nitric oxide synthase gene polymorphisms, microalbuminuria and endothelial dysfunction in hypertensive men. J Hypertens 2007; 25 (7): 1389–95.
37. Castejon AM, Bracero J, Hoffmann IS et al. NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics. J Hum Hypertens 2006; 20 (10): 772–9.
38. Hodgkinson AD, Millward BA, Demaine AG. Association of the p22phox component of NAD(P)H oxidase with susceptibility to diabetic nephropathy in patients with type 1 diabetes. Diabet Care 2003; 26 (11): 3111–5.
39. Matsunaga-Irie S, Maruyama T, Yamamoto Y et al. Relation Between Development of Nephropathy and the p22phox C242T and Receptor for Advanced Glycation End Product G1704T Gene Polymorphisms in Type 2 Diabetic Patients. Diabet Care 2004; 27: 303–7.
40. Профилактика, диагностика и лечение артериальной гипертензии. Российские рекомендации (3-й пересмотр). Кардиоваскул. тер. и профилак. 2008; 7 (Прил. 2): 5–16.
41. Knight EL, Kramer HM, Curhan GC et al. High-normal blood pressure and microalbuminuria. Am J Kidney Dis 2003; 41 (3): 588–95.
42. Tsakiris A, Doumas M, Lagatouras D et al. Microalbuminuria is determined by systolic and pulse pressure over a 12-year period and related to periphery artery disease in normotensive and hypertensive subjects: the Three Arias Study in Greece (TAS-GR). Angiology 2006; 57 (3): 313–20.
2. Мухин Н.А., Моисеев В.С., Фомин В.В. Микроальбуминурия – интегральный маркер кардиоренальных взаимоотношений. Сердеч. недостаточность. 2007; 8 (6): 301–5.
3. Мухин Н.А., Фомин В.В., Моисеев С.В., Нанчиева М.Л. Микроальбуминурия – универсальный маркер неблагоприятного прогноза. Сердеч. недостаточность. 2008; 9 (2): 79–82.
4. Dinneen SF, Gerstein HC. The association of microalbuminuria and mortality in non-insulin-dependent diabetes mellitus. A systematic overview of the literature. Arch Internal Med 1997; 157: 1413–8.
5. Kannel WB, Stampfer MJ, Castelli WP, Verter J. The prognostic significance of proteinuria: The Framingham study. Am Heart J 1984; 108: 1347–52.
6. Borch-Johnsen K, Feldt-Rasmussen B, Strandgaard S et al. Urinary albumin excretion. An independent predictor of ischemic heart disease. Arterioscleros Thrombos Vascular Biol 1999; 19: 1992–7.
7. Hillege HL, Fidler V, Diercks GF et al. Prevention of Renal and Vascular End Stage Disease (PREVEND) Study Group: Urinary albumin excretion predicts cardiovascular and noncardiovascular mortality in the general population. Circulation 2002; 106: 1777–82.
8. Romundstad S, Holmen J, Kvenild K. Microalbuminuria and all-cause mortality in 2,089 apparently healthy individuals: A 4.4-year follow-up study. The Nord-Trondelag Health Study (HUNT), Norway. Am J Kidney Dis 2003; 42: 466–73.
9. Yuyun MF, Khaw KT, Luben R et al. European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) Population Study: Microalbuminuria independently predicts all-cause and cardiovascular mortality in a British population: The European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) population study. Internat J Epidemiol 2004; 33: 189–98.
10. Pontremoli R, Leoncini G, Viazzi F et al. Evaluation of subclinical organ damage for risk assessment and treatment in the hypertensive patient: role of microalbuminuria. J Am Soc Nephrol JASN 2006; 17 (4), Suppl 2: S112–4
11. Schrader J, Lиders S, Kulschewski A et al. Microalbuminuria and tubular proteinuria as risk predictors of cardiovascular morbidity and mortality in essential hypertension: final results of a prospective long-term study (MARPLE Study). J Hypertens 2006; 24 (3): 541–8.
12. de Zeeuw D, Parving HH, Henning RH. Microalbuminuria as an early marker for cardiovascular disease. J Am Soc Nephrol JASN 2006; 17 (8): 2100–5.
13. Leoncini G, Ratto E, Viazzi F et al. Improving cardiovascular risk stratification: the case for redefining microalbuminuria. J Nephrol 2007; 20 (Suppl. 12): S51–5.
14. Palatini P. Microalbuminuria in hypertension. Cur Hypertens Rep 2003; 5 (3): 208–14.
15. Hitha B, Pappachan JM, Pillai HB et al. Microalbuminuria in patients with essential hypertension and its relationship to target organ damage: an Indian experience. Saudi journal of kidney diseases and transplantation: an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia 2008; 19 (3): 411–9.
16. Jones CA, Francis ME, Eberhardt MS et al. Microalbumiuria I the US population: third National Health and Nutrition Examination Survey. Am J Kidney Dis 2002; 39 (3): 445–59.
17. Tedesco MA, Natale F, Mocerino RJ et al. Renal resistive index and cardiovascular organ damage in a large population of hypertensive patients. J Hum Hypertens 2007; 21 (4): 291–6.
18. Leoncini G, Sacchi G, Ravera M. Microalbuminuria is an integrated marker of subclinical organ damage in primary hypertension. J Hum Hypertens 2002; 16: 399–404.
19. Thomas GN, Critchley JA, Tomlinson B et al. Albuminuria and the renin-angiotensin system gene polymorphisms in type-2-diabetic and in normoglycemic hypertensive Chinese. Clin Nephrol 2001; 55 (1): 7–15.
20. Viazzi F, Leoncini G, Ratto E et al. Microalbuminuria, blood pressure load, and systemic vascular permeability in primary hypertension. Am J Hypertens 2006; 19 (11): 1183–9.
21. Cirillo V, Stellato D, Laurenzi M et al. Pulse pressure and isolated systolic hypertension: association with microalbuminuria. The GUBIO Study Collaborative Research group. Kidney International 2000; 58 (3): 1211–8.
22. Reboldi G, Gentile G, Angeli F, Verdecchia P. Microalbuminuria and hypertension. Minerva Medica 2005; 96 (4): 261–75.
23. Bonnet F, Marre M, Halimi JM et al. Waist circumference and the metabolic syndrome predict the development of elevated albuminuria in non-diabetic subjects: the DESIR study. J Hypertens 2006; 24 (6): 1157–63.
24. Falqui V, Viazzi F, Leoncini G et al. Blood pressure load, vascular permeability and target organ damage in primary hypertension. J Nephrol 2007; 20 (Suppl. 12): S63–7.
25. Liese AD, Hense HW, Broun AA et al. Microalbuminuria, central adiposity and hypertension in non-diabetic urban population of the MONICA Augsburg survey1994/95. J Hum Hypertens 2001; 15 (11): 799–804.
26. Redon J, Liao Y, Lozano JV et al. Factors related to the presence of microalbuminuria in essential hypertension. Am J Hypertens 1994; 7 (9), Pt 1: 801–7.
27. Metclaf P, Bekker J, Scott A et al. Albuminuria in people at least 40 years old: effect of obesity, hypertension and hyperlipidemia. Clin Chem 1992; 38 (9): 1802–8.
28. Diercks GF, Janssen WM, van Boven AJ et al. Rationale, desighn and baseline characteristics of a trial of prevention of cardiovascular and renal disease with fosinopril and pravastatin in nonhypertensive, nonhypercholesterolemic subjects with microalbuminuria (the Prevention of REnal and Vascular ENdstage Desease Intervention Trial (PREVEND IT). Am J Cardiol 2000; 86 (6): 635–8.
29. Orth SR. Smoking – a renal risk factor. Nephron 2000; 86 (1): 12–26.
30. Pinto-Sietsma SJ, Mulder J, Janssen WM et al. Smoking is related to albuminuria and abnormal renal function in non-diabetic persons. Ann Internal Med 2000; 133 (8): 585–91.
31. Buraczynskа M, Ksiazek P, ?opaty?ski J et al. Association of the renin-angiotensin system gene polymorphism with nephropathy in type II diabetes. Polskie archiwum medycyny wewnetrznej 2002; 108 (2): 725–30.
32. Fabris B, Bortoletto M, Candido R et al. Genetic polymorphisms of the renin-angiotensin-aldosterone system and renal insufficiency in essential hypertension. J Hypertens 2005; 23 (2): 309–16.
33. Marin P, Julve R, Chaves FJ et al. Polymorphisms of the angiotensinogen gene and the outcome of microalbuminuria in essential hypertension: a 3-year follow-up study. J Hum Hypertens 2004; 18 (1): 25–31.
34. Wong TY, Chan JC, Poon E, Li PK. Lack of association of angiotensin-converting enzyme (DD/II) and angiotensinogen M235T gene polymorphism with renal function among Chinese patients with type II diabetes. Am J Kidney Dis 1999; 33 (6): 1064–70.
35. Young RP, Chan JC, Critchley JA et al. Angiotensinogen T235 and ACE insertion/deletion polymorphisms associated with albuminuria in Chinese type 2 diabetic patients. Diabet Care 1998; 21 (3): 431–7.
36. Dell'Omo G, Penno G, Pucci L et al. Lack of association between endothelial nitric oxide synthase gene polymorphisms, microalbuminuria and endothelial dysfunction in hypertensive men. J Hypertens 2007; 25 (7): 1389–95.
37. Castejon AM, Bracero J, Hoffmann IS et al. NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics. J Hum Hypertens 2006; 20 (10): 772–9.
38. Hodgkinson AD, Millward BA, Demaine AG. Association of the p22phox component of NAD(P)H oxidase with susceptibility to diabetic nephropathy in patients with type 1 diabetes. Diabet Care 2003; 26 (11): 3111–5.
39. Matsunaga-Irie S, Maruyama T, Yamamoto Y et al. Relation Between Development of Nephropathy and the p22phox C242T and Receptor for Advanced Glycation End Product G1704T Gene Polymorphisms in Type 2 Diabetic Patients. Diabet Care 2004; 27: 303–7.
40. Профилактика, диагностика и лечение артериальной гипертензии. Российские рекомендации (3-й пересмотр). Кардиоваскул. тер. и профилак. 2008; 7 (Прил. 2): 5–16.
41. Knight EL, Kramer HM, Curhan GC et al. High-normal blood pressure and microalbuminuria. Am J Kidney Dis 2003; 41 (3): 588–95.
42. Tsakiris A, Doumas M, Lagatouras D et al. Microalbuminuria is determined by systolic and pulse pressure over a 12-year period and related to periphery artery disease in normotensive and hypertensive subjects: the Three Arias Study in Greece (TAS-GR). Angiology 2006; 57 (3): 313–20.
Авторы
Т.Ю.Кузнецова*1, Д.В.Гаврилов2, Л.М.Самоходская3, А.Ю.Постнов4, С.А.Бойцов4
1 ГОУ ВПО Петрозаводский государственный университет министерства образования и науки РФ,
2 Больница скорой медицинской помощи, Петрозаводск,
3 ФФМ МГУ им. М.В.Ломоносова,
4 ФГУ РКНПК МЗ и СР РФ, Москва
*eme@karelia.ru
1 GOU VPO «Petrozavodsk state university MO &N RF,
2 Clinic of emergency medicine, Petrozavodsk,
3 Laboratory of genetic and cell technology FFM MGU M.V.Lomonosov,
4 FSI RC SPC Ministry of Health
*eme@karelia.ru
1 ГОУ ВПО Петрозаводский государственный университет министерства образования и науки РФ,
2 Больница скорой медицинской помощи, Петрозаводск,
3 ФФМ МГУ им. М.В.Ломоносова,
4 ФГУ РКНПК МЗ и СР РФ, Москва
*eme@karelia.ru
________________________________________________
1 GOU VPO «Petrozavodsk state university MO &N RF,
2 Clinic of emergency medicine, Petrozavodsk,
3 Laboratory of genetic and cell technology FFM MGU M.V.Lomonosov,
4 FSI RC SPC Ministry of Health
*eme@karelia.ru
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