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Содержание мочевой кислоты и ее роль на ранних стадиях гипертонической болезни
Содержание мочевой кислоты и ее роль на ранних стадиях гипертонической болезни
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Аннотация
Цель: изучение взаимоотношений уровня мочевой кислоты сыворотки крови и мочи с показателями неспецифичного воспаления и клинической характеристикой больных ГБ.
Материалы и методы: Обследовано 67 больных с ГБ (48 мужчин и 19 женщин), в возрасте от 30 до 65 лет, (в среднем 44 ± 2 г.), из них: 37 больных с I и 30–II степенью АГ умеренного и высокого риска ССО. Контрольная группа состояла из 14 здоровых добровольцев: (6 мужчин, 8 женщин) в возрасте 45,5 ± 2,1 лет с нормальным уровнем АД. Определение концентрации СРБ проведено высокочувствительным методом турбидиметрии на биохимическом автоанализаторе “HITACHI” 912, фирмы Хофман Ла Рош, Швейцария. За нормальное содержание СРБ принималась величина менее 3 мг/л. Определение мочевой кислоты сыворотки крови (МКСК) и мочи (МКМ) у больных ГБ, проведено УФ методом на биохимическом автоанализаторе “HITACHI” 912 фирмы Хофман лa Рош, Швейцария (норма МКСК- 202,3-416,5 мкмоль/л; норма МКМ 1,48-4,43 ммоль/сут). Скорость клубочковой фильтрации рассчитывалась по формуле Кокрофта-Гаулта.
Результаты: установлено достоверно большее содержание С-реактивного белка, МКСК и МКМ у больных ГБ, чем у здоровых добровольцев с нормотензией. Более высокие значения МКСК и МКМ обнаружены уже на ранних стадиях ГБ - I ст, умеренный риск ССО. При сопоставлении уровня МКСК с клинической характеристикой больных ГБ выявлено ее большее содержание у больных ГБ с ожирением и нарушениями липидного обмена. У больных ГБ с клубочковой гиперфильтрацией выявлено достоверно большее содержание МКМ и МКСК, чем у больных с нормальной скоростью клубочковой фильтрации.
Заключение: У больных гипертонической болезнью уже на ранних стадиях заболевания наблюдаются достоверно более высокие уровни мочевой кислоты в сыворотке крови и мочи, чем у здоровых лиц с нормотензией и ее позитивная ассоциация с нарушениями липидного обмена.
Ключевые слова: гипертоническая болезнь, мочевая кислота сыворотки крови и мочи, неспецифичное воспаление
Methods: 67 patients with EH (48 men) 30-65 years age (44±2) with stage 1 EH (n=37) and 2 (n=30) with moderate or high cardiovascular (CV) risk. The control group - 14 healthy peoples: (6 men) 45,5±2,1 years age with normal blood pressure (BP). The normal level of С-reactive protein (CRP) is less 3 mg/l. The normal level of UA in blood is 202,3-416,5 mkmol/l, and in urine is 1,48-4,43 mmol/24 hour. The estimates of creatinine clearance by the Cockroft-Gault formula.
Results: the patients with EH have bigger level CRP, UA in blood and urine than healthy peoples with normal BP. Higher levels UA in blood and urine have patients even with early stages EH and moderate CV risk. The bigger level of UA in blood has EH patients with obesity and dyslipidaemia. The level of UA in blood and urine is higher at EH patients with hyperfiltration vs patients with normal creatinine clearance.
Conclusion: the patients with early stage of EH have higher level of UA in blood and urine than healthy peoples with normal BP. The level of UA in blood and urine is correlated with dyslipidaemia.
Key words: essential hypertension, uric acid, non specific inflammation
Материалы и методы: Обследовано 67 больных с ГБ (48 мужчин и 19 женщин), в возрасте от 30 до 65 лет, (в среднем 44 ± 2 г.), из них: 37 больных с I и 30–II степенью АГ умеренного и высокого риска ССО. Контрольная группа состояла из 14 здоровых добровольцев: (6 мужчин, 8 женщин) в возрасте 45,5 ± 2,1 лет с нормальным уровнем АД. Определение концентрации СРБ проведено высокочувствительным методом турбидиметрии на биохимическом автоанализаторе “HITACHI” 912, фирмы Хофман Ла Рош, Швейцария. За нормальное содержание СРБ принималась величина менее 3 мг/л. Определение мочевой кислоты сыворотки крови (МКСК) и мочи (МКМ) у больных ГБ, проведено УФ методом на биохимическом автоанализаторе “HITACHI” 912 фирмы Хофман лa Рош, Швейцария (норма МКСК- 202,3-416,5 мкмоль/л; норма МКМ 1,48-4,43 ммоль/сут). Скорость клубочковой фильтрации рассчитывалась по формуле Кокрофта-Гаулта.
Результаты: установлено достоверно большее содержание С-реактивного белка, МКСК и МКМ у больных ГБ, чем у здоровых добровольцев с нормотензией. Более высокие значения МКСК и МКМ обнаружены уже на ранних стадиях ГБ - I ст, умеренный риск ССО. При сопоставлении уровня МКСК с клинической характеристикой больных ГБ выявлено ее большее содержание у больных ГБ с ожирением и нарушениями липидного обмена. У больных ГБ с клубочковой гиперфильтрацией выявлено достоверно большее содержание МКМ и МКСК, чем у больных с нормальной скоростью клубочковой фильтрации.
Заключение: У больных гипертонической болезнью уже на ранних стадиях заболевания наблюдаются достоверно более высокие уровни мочевой кислоты в сыворотке крови и мочи, чем у здоровых лиц с нормотензией и ее позитивная ассоциация с нарушениями липидного обмена.
Ключевые слова: гипертоническая болезнь, мочевая кислота сыворотки крови и мочи, неспецифичное воспаление
________________________________________________
Methods: 67 patients with EH (48 men) 30-65 years age (44±2) with stage 1 EH (n=37) and 2 (n=30) with moderate or high cardiovascular (CV) risk. The control group - 14 healthy peoples: (6 men) 45,5±2,1 years age with normal blood pressure (BP). The normal level of С-reactive protein (CRP) is less 3 mg/l. The normal level of UA in blood is 202,3-416,5 mkmol/l, and in urine is 1,48-4,43 mmol/24 hour. The estimates of creatinine clearance by the Cockroft-Gault formula.
Results: the patients with EH have bigger level CRP, UA in blood and urine than healthy peoples with normal BP. Higher levels UA in blood and urine have patients even with early stages EH and moderate CV risk. The bigger level of UA in blood has EH patients with obesity and dyslipidaemia. The level of UA in blood and urine is higher at EH patients with hyperfiltration vs patients with normal creatinine clearance.
Conclusion: the patients with early stage of EH have higher level of UA in blood and urine than healthy peoples with normal BP. The level of UA in blood and urine is correlated with dyslipidaemia.
Key words: essential hypertension, uric acid, non specific inflammation
Полный текст
Список литературы
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15. Church WH, Rappolt G. Nigrostriatal catecholamine metabolism in guinea pigs is altered by purine enzyme inhibition. Exp Brain Res 1999; 127: 147–50.
16. Challet E, Le Macho Y, Robin JP et al. Involvement of corticosterone in the fasting-induced rise in pritein utilization and locomotor activity. Pharmacol Biochem Behav 1995; 50: 405–12.
17. Hink HU, Santanam N, Dikalov S et al. Peroxidase properties of extracellular superoxidedismutase: role of uric acid in modulating in vivo activity. Arteriosclerosis Thrombosis and Vascular Biology 2002; 22: 1402–8.
18. Tan S, RadI r, Gaudier F et al. Physiologic levels of uric acid inhibit xanthine oxidase in human plasma. Pediatr Res 1993; 34: 303–7.
19. Corry DB, Eslami P, Yamamoto K et al. Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin-angiotensin system. J Hypertension 2008; 26 (2): 269–75.
20. Sautin YY, Nakagawa T, Zharikov S et al. Adverse effects of the ckassical antioxidant uric acid in adypocites: NAD-PH oxidase-mediated oxidative/nitrosative stress. Am J Physiol Cell Physiol 2007; 293: 584–96.
21. Kang DK, Park SK, Lee IK et al. Uric acid-induced C-reactive protein expression: implication on cell proliferation and nitric oxid production of human vascular cells. J Am Soc Nephrology 2005; 16: 3553–62.
22. Khosla UM, Zharikov S, Finch JL et al. Hyperuricemia induces endothelial dysfunction. Kidney Int 2005; 67: 1739–42.
23. Watanabe S, Kang DH, Feng L et al. Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity. Hypertension 2002; 40 (3): 355–60.
24. Carnethon MR, Fortman SP, Palaniappan L et al. Risk factors for progression to incident hyperinsulinemia: the atherosclerosis risk in communiteies study 1987–1998. Am J Epidemiol 2003; 158: 1058–67.
25. Ridker PM, Danielson E, Rifai N et al. Valsartan, Blood pressure reduction and C-reactive protein. Hypertension 2006; 48: 1–7.
26. Paulleto P, Rattazzi M. Inflammation and hypertension: the search for link. Nephrol Dial Transplant 2006; 21: 850–3.
27. Kim Chul Sung, Jung Yul Suh, Bum Soo Kim et al. High Sensitivity C-reactive protein an independent risk factor for essential hypertension. Am J Hyperten 2003; 16: 429–33.
28. Ощепкова Е.В., Дмитриев В.А, Титов В.Н и др. Показатели неспецифичного воспаления у больных гипертонической болезнью. Тер. архив. 2007; 79 (12): 18–25.
29. Национальные рекомендации по профилактике диагностике и лечению артериальной гипертонии. ВНОК 2004 г., 2-й пересмотр.
30. Чазова И.Е., Ощепкова Е.В., Чихладзе Н.М. Артериальная гипертония. Принципы диагностики и лечения (пособие для врачей). М., 2005.
31. Pearson TA, Mensah GA, Wayne Alexander R et al. Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499–511.
32. Cockcroft DW, Gault MN. Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16: 31–41.
33. Conen D, Wietlisbach V, Bovet P et al. Prevalence of hyperuricemia and relation of serum uric acid with cardiovascular risk factors in a developing country. BMC Public Health 2004; 4: 9.
34. Culleton BF, Larson MG, Kannel WB et al. Serum uric acid and risk for cardiovascular disease and death: The Framingham Heart Study. Ann Int Med 1999; 131: 7–13.
35. Krishnan E, Kwoh CK, Schumacher HR et al. Hyperuricemia and incidence of hypertension among men without metabolic syndrome. Hypertension 2007; 49 (2): 298–303.
36. Niemirska A, Sladowska J, Antoniewicz J et al. Uric acid concentration, metabolic syndrome components and target organ damage in adolescents and adults with essential hypertension. J of Hypertension 2006; 25 (Suppl. 2): s346.
37. Johnson RJ, Sautin Y, Oliver WJ et al. Lessons from comparative physiology:could uric acid represent a physiologic alarm signal gone awry in western society? J Comp Physiol B.
38. McCord JM, Roy RS, Schaffer SW. Free radicals and myocardial ischemia. The role xanthine oxidase. Adv Myocardial 1985; 5: 183–9.
39. Johnson RJ, Duk-Hee Kang, Feig D et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension 2003; 41: 1183–90.
40. Niskanen LK, Laaksonen DE, Nyyssonen K et al. Uric acid level as a risk factor for cardiovascular and all-cause mortality in middle-aged men. Arch Int Med 2004; 164: 1546–51.
41. Squadrito GL, Cueto R, Splenser AE et al. Reaction of uric acid with peroxyntrite and implications for the mechanism of neuroprotection by uric acid. Arch Biochem Biophys 2000; 376: 333–7.
42. Ames BN, Cathcart R, Schwiers E et al. Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis. Proc Natl Acad Sci USA 1981; 78 (11): 6858–62.
43. de Ferranti S, Rifai N. C-reactive protein and cardiovascular disease: a review of risk prediction and interventions. Clinica Chemica Acta 2002; 317: 1–15.
44. Zoccali C, Maio R, Mallamaci F et al. Uric acid and endothelial dysfunction in essential hypertension. J Am Soc Nephrol 2006; 17: 1466–71.
45. Warning WS, Webb DJ, Maxwell SRJ. Uric acid as a risk factor for cardiovascular disease. QJM 2000; 93: 707–13.
46. Viazzi F, Parodi D, Leoncini G et al. Serum Uric Acid and Target Organ Damage in Primary Hypertension. Hypertension 2005; 45: 991–6.
47. Martinon F, Burns K, Tschopp J. The inflamasomme: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta. Moll Cell 2002; 10 (2): 417–26.
48. Mazzali M, Hughes J, Kim Yoon-Goo et al. Elevated uric acid increases bloods pressure in the rat by a novel crystal-independent mechanism. Hypertension 2001; 38: 1101–6.
49. Johnson RJ, Rodriguez-Iturbe B, Duk-Hee Kang et al. A unifying pathway for essential hypertension. Am J Hypertens 2005; 18: 431–40.
50. Yasunari K, Maeda K, Nakamura M et al. Oxidative stress in leukocytes is a possible link between blood pressure, blood glucose and C-reactive protein. Hypertension 2002; 39: 777–89.
51. Ruggiero C, Cherubini A, Ble A et al. Uric acid and inflammatory markers. Eur Heart J 2006; 27: 1171-81.
52. Coutinho TA, Turner ST, Peyser PA et al. Associations of serum uric acid with markers of inflammation, metabolic syndrome, and subclinical coronary atherosclerosis. Am J Hypertens 2007; 20 (1): 83-9.
53. Feig DI, Duk Hee Kang, Johnson R. Uric acid and cardiovascular risk. NEJM 2008; 359: 1811-21.
2. Gertler MM, Garn SM, Levine SA. Serum uric acid in relation to age and physique in health and coronary heart disease. Ann Intern Med 1951; 34: 1421–31.
3. Brand FN, McGee DL, Kannel WB et al. Hyperuricemia as a risk factor of coronary heart disease: the Framingham study. Am J Epidemiol 1985; 121: 11–8.
4. Freedman DS, Williamson DF, Gunter EW et al. Relation of serum uric acid to mortality and ischemic heart disease. The NHANES I Epidemiologic Follow-Up study. Am J Epidemiol 1985; 141: 637–44.
5. Bengtsson C, Lapidus L, Stendahl C et al. Hyperuricaemia and risk of cardiovascular disease and overall. A 12-year follow-up of participants in the population study of women in Gotheburg, Sweden. Acta Med Scand 1988; 224: 549–55.
6. Reunanen A, Takkunen H, Knekt P et al. Hyperuricemia as a risk factor for cardiovascular mortality 1982; 668: 49–59.
7. Alderman MH. Podagra, uric acid, and cardiovascular disease. Circulation 2007; 116: 880–3.
8. Sundstro..m J, Sulliva L, D`Agostino RB et al. Relations of serum uric acid to longitudinal blood pressure tracking and hypertension incidence. Hypertension 2005; 45: 28–33.
9. Perlstein TS, Gumeniak O, Williams GH et al. Uric Acid and the development of hypertension. The Normative Ageing Study. Hypertension 2006; 48: 1031–6.
10. Mellen PB, Bleyer AJ, Erlinger TP et al. Serum uric acid predicts incident hypertension in a biethnic cohort. The atherosclerosis risk in communities study. Hypertension 2006; 48: 1037–42.
11. Johnson RJ, Feig DI, Herera-Acosta J et al. Resurrection of uric acid as a causal risk factor in essential hypertension. Hypertension 2005; 45: 18–20.
12. Forman JP, Choi H, Curhan GC. Plasma uric acid level and risk for incident hypertension among man. J Am Soc Nephrol 2007; 18: 287–92.
13. Мухин Н.А., Балкаров И.М., Шоничев Д.Г. и др. Формирование артериальной гипертонии при уратном тубулоинтерстициальном поражении почек. Тер. архив. 1999; 6: 23–7.
14. Feig DI, Nakagawa T, Karumanchi SA et al. Hypothesis: Uric acid, nephron number and the pathogenesis of essential hypertension. Kidney Int 2004; 66 (1): 281–7.
15. Church WH, Rappolt G. Nigrostriatal catecholamine metabolism in guinea pigs is altered by purine enzyme inhibition. Exp Brain Res 1999; 127: 147–50.
16. Challet E, Le Macho Y, Robin JP et al. Involvement of corticosterone in the fasting-induced rise in pritein utilization and locomotor activity. Pharmacol Biochem Behav 1995; 50: 405–12.
17. Hink HU, Santanam N, Dikalov S et al. Peroxidase properties of extracellular superoxidedismutase: role of uric acid in modulating in vivo activity. Arteriosclerosis Thrombosis and Vascular Biology 2002; 22: 1402–8.
18. Tan S, RadI r, Gaudier F et al. Physiologic levels of uric acid inhibit xanthine oxidase in human plasma. Pediatr Res 1993; 34: 303–7.
19. Corry DB, Eslami P, Yamamoto K et al. Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin-angiotensin system. J Hypertension 2008; 26 (2): 269–75.
20. Sautin YY, Nakagawa T, Zharikov S et al. Adverse effects of the ckassical antioxidant uric acid in adypocites: NAD-PH oxidase-mediated oxidative/nitrosative stress. Am J Physiol Cell Physiol 2007; 293: 584–96.
21. Kang DK, Park SK, Lee IK et al. Uric acid-induced C-reactive protein expression: implication on cell proliferation and nitric oxid production of human vascular cells. J Am Soc Nephrology 2005; 16: 3553–62.
22. Khosla UM, Zharikov S, Finch JL et al. Hyperuricemia induces endothelial dysfunction. Kidney Int 2005; 67: 1739–42.
23. Watanabe S, Kang DH, Feng L et al. Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity. Hypertension 2002; 40 (3): 355–60.
24. Carnethon MR, Fortman SP, Palaniappan L et al. Risk factors for progression to incident hyperinsulinemia: the atherosclerosis risk in communiteies study 1987–1998. Am J Epidemiol 2003; 158: 1058–67.
25. Ridker PM, Danielson E, Rifai N et al. Valsartan, Blood pressure reduction and C-reactive protein. Hypertension 2006; 48: 1–7.
26. Paulleto P, Rattazzi M. Inflammation and hypertension: the search for link. Nephrol Dial Transplant 2006; 21: 850–3.
27. Kim Chul Sung, Jung Yul Suh, Bum Soo Kim et al. High Sensitivity C-reactive protein an independent risk factor for essential hypertension. Am J Hyperten 2003; 16: 429–33.
28. Ощепкова Е.В., Дмитриев В.А, Титов В.Н и др. Показатели неспецифичного воспаления у больных гипертонической болезнью. Тер. архив. 2007; 79 (12): 18–25.
29. Национальные рекомендации по профилактике диагностике и лечению артериальной гипертонии. ВНОК 2004 г., 2-й пересмотр.
30. Чазова И.Е., Ощепкова Е.В., Чихладзе Н.М. Артериальная гипертония. Принципы диагностики и лечения (пособие для врачей). М., 2005.
31. Pearson TA, Mensah GA, Wayne Alexander R et al. Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499–511.
32. Cockcroft DW, Gault MN. Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16: 31–41.
33. Conen D, Wietlisbach V, Bovet P et al. Prevalence of hyperuricemia and relation of serum uric acid with cardiovascular risk factors in a developing country. BMC Public Health 2004; 4: 9.
34. Culleton BF, Larson MG, Kannel WB et al. Serum uric acid and risk for cardiovascular disease and death: The Framingham Heart Study. Ann Int Med 1999; 131: 7–13.
35. Krishnan E, Kwoh CK, Schumacher HR et al. Hyperuricemia and incidence of hypertension among men without metabolic syndrome. Hypertension 2007; 49 (2): 298–303.
36. Niemirska A, Sladowska J, Antoniewicz J et al. Uric acid concentration, metabolic syndrome components and target organ damage in adolescents and adults with essential hypertension. J of Hypertension 2006; 25 (Suppl. 2): s346.
37. Johnson RJ, Sautin Y, Oliver WJ et al. Lessons from comparative physiology:could uric acid represent a physiologic alarm signal gone awry in western society? J Comp Physiol B.
38. McCord JM, Roy RS, Schaffer SW. Free radicals and myocardial ischemia. The role xanthine oxidase. Adv Myocardial 1985; 5: 183–9.
39. Johnson RJ, Duk-Hee Kang, Feig D et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension 2003; 41: 1183–90.
40. Niskanen LK, Laaksonen DE, Nyyssonen K et al. Uric acid level as a risk factor for cardiovascular and all-cause mortality in middle-aged men. Arch Int Med 2004; 164: 1546–51.
41. Squadrito GL, Cueto R, Splenser AE et al. Reaction of uric acid with peroxyntrite and implications for the mechanism of neuroprotection by uric acid. Arch Biochem Biophys 2000; 376: 333–7.
42. Ames BN, Cathcart R, Schwiers E et al. Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis. Proc Natl Acad Sci USA 1981; 78 (11): 6858–62.
43. de Ferranti S, Rifai N. C-reactive protein and cardiovascular disease: a review of risk prediction and interventions. Clinica Chemica Acta 2002; 317: 1–15.
44. Zoccali C, Maio R, Mallamaci F et al. Uric acid and endothelial dysfunction in essential hypertension. J Am Soc Nephrol 2006; 17: 1466–71.
45. Warning WS, Webb DJ, Maxwell SRJ. Uric acid as a risk factor for cardiovascular disease. QJM 2000; 93: 707–13.
46. Viazzi F, Parodi D, Leoncini G et al. Serum Uric Acid and Target Organ Damage in Primary Hypertension. Hypertension 2005; 45: 991–6.
47. Martinon F, Burns K, Tschopp J. The inflamasomme: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta. Moll Cell 2002; 10 (2): 417–26.
48. Mazzali M, Hughes J, Kim Yoon-Goo et al. Elevated uric acid increases bloods pressure in the rat by a novel crystal-independent mechanism. Hypertension 2001; 38: 1101–6.
49. Johnson RJ, Rodriguez-Iturbe B, Duk-Hee Kang et al. A unifying pathway for essential hypertension. Am J Hypertens 2005; 18: 431–40.
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Авторы
Е.В.Ощепкова*, В.А.Дмитриев, О.В.Половиткина, В.Н.Титов
ФГУ РКНПК Федерального агентства по высокотехнологичной медицинской помощи, Москва
НИИ кардиологии им. А.Л.Мясникова, Москва
*arthyplab@list.ru
*arthyplab@list.ru
ФГУ РКНПК Федерального агентства по высокотехнологичной медицинской помощи, Москва
НИИ кардиологии им. А.Л.Мясникова, Москва
*arthyplab@list.ru
________________________________________________
*arthyplab@list.ru
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