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INTERRELACION ENTRE HIPERTROFIA VENTRICULAR IZQUIERDA Y NEFROPATIA DIABETICA

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La hipertrofia ventricular izquierda (HVI) en pacientes con nefropatía diabética (ND) se asocia con un aumento del riesgo de enfermedad cardiovascular y progresión de la ND. El tratamiento intensivo debe dirigirse a producir la regresión de la HVI y el enlentecimiento de la ND.
boner9.jpg Autor:
Geoffrey Boner
Columnista Experto de SIIC
Artículos publicados por Geoffrey Boner
Aprobación
23 de Mayo, 2007 		Primera edición
15 de Junio, 2007 		Segunda edición, ampliada y corregida
7 de Junio, 2021

INTERRELACION ENTRE HIPERTROFIA VENTRICULAR IZQUIERDA Y NEFROPATIA DIABETICA

Resumen
La diabetes mellitus (DM) y sus muchas complicaciones son causas importantes de morbimortalidad. El propósito de esta revisión es examinar las relaciones entre hipertrofia ventricular izquierda (HVI) y nefropatía diabética (ND). La HVI es un componente del síndrome de resistencia a la insulina aun en ausencia de hipertensión. La DM es un fuerte factor de predicción de enfermedad cardiovascular y puede asociarse con HVI incluso en ausencia de hipertensión. En un estudio de gran tamaño de sujetos hipertensos con HVI se observó un aumento del riesgo de microalbuminuria y proteinuria franca. Esto también se puso en evidencia en personas con DM. En los pacientes con ND existe una asociación positiva entre HVI y albuminuria. Un nuevo análisis de los datos del estudio Reduction of Endpoints in NIDDM with Angiotensin II Antagonist (RENAAL) mostró que en los pacientes con ND, la presencia de HVI era un factor de riesgo importante para enfermedad cardiovascular y mortalidad y para la progresión de la ND. El tratamiento antihipertensivo con diferentes agentes produjo regresión de la HVI. Además, en el estudio RENAAL el tratamiento con un bloqueante del receptor de angiotensina se asoció con una disminución importante del riesgo, tanto cardíaco como renal. Por lo tanto, la presencia de ND e HVI se asocia con un aumento del riesgo de enfermedad cardiovascular y renal, que puede reducirse con el tratamiento apropiado.

Palabras clave
hipertorfia ventricular izquierda, nefropatía diabética, bloqueante del receptor de angiotensina, progresión de la enfermedad renal, RENAAL


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THE INTERRELATIONSHIPS BETWEEN LEFT VENTRICULAR HYPERTROPHY AND PROGRESSION OF RENAL DISEASE IN DIABETIC NEPHROPATHY

Abstract
Diabetes mellitus (DM) and its many complications are major causes of morbidity and mortality. The purpose of this review is to examine the relationships between left ventricular hypertrophy (LVH) and diabetic nephropathy (DN). LVH is a component of the insulin resistance syndrome even in the absence of hypertension. DM is a strong predictor of cardiovascular (CV) disease and may be associated with LVH even in the absence of hypertension. In a large study of hypertensive subjects with LVH there was an increased risk for microalbuminuria and overt proteinuria. This was also evident in those subjects with DM. In patients with DN there is a positive association between LVH and albuminuria. A new analysis of data from the Reduction of Endpoints in MIDDM with Angiotensin II Antagonist (RENAAL) study has shown that in patients with DN the presence of LVH was a significant risk factor for CV and mortality and for the progression of DN. Antihypertensive therapy with different agents has caused a regression in LVH. Moreover, in the RENAAL study treatment with a angiotensin receptor blocker was associated with a significant improvement in both the cardiac and renal risk. The presence of DN and LVH is thus associated with an increased risk for both CV and renal disease, which can be reduced by appropriate treatment.

Key words
LVH, diabetic nephropathy, angiotensin receptor blocker, progression of renal disease, RENAAL


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Especialidades
Principal: Cardiología, Nefrología y Medio Interno
Relacionadas: Bioquímica, Diagnóstico por Imágenes, Diagnóstico por Laboratorio, Medicina Interna



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Enviar correspondencia a:
Geoffrey Boner, Sackler Medical Faculty, Tel Aviv University , 40295, 81 Kochav Hayam, Tel Aviv, Israel
Patrocinio y reconocimiento:
Agradecimiento: Al Profesor Mark E. Cooper, del Baker Research Institute, Melbourne, Australia, quien me inspiró y ayudó en la investigación de la asociación entre hipertrofia ventricular izquierda y nefropatía diabética. La investigación inicial y la revisión de la bibliografía se realizaron durante un año sabático en su departamento.
Bibliografía del artículo
1. Haffner SM, Lehto S, Ronnemaa T, Pyorala K, Lasko M. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med 339(4):229-234, 1998.
2. Hypertension in Diabetes Study (HDS): I. Prevalence of hypertension in newly presenting type 2 diabetic patients and the association with risk factors for cardiovascular and diabetic complications. J Hypertens 11(3):309-317, 1993.
3. Hypertension in Diabetes Study (HDS): II. Increased risk of cardiovascular complications in hypertensive type 2 diabetic patients. J Hypertens 11(3): 319-325, 1993.
4. Butler R, MacDonald TM, Struthers AD, Morris AD. The clinical implications of diabetic heart disease. Eur Heart J 19(11):1617-1627, 1998.
5. Struthers AD, Morris AD. Screening for and treating left-ventricular abnormalities in diabetes mellitus: a new way of reducing cardiac deaths. Lancet 359(9315):1430-1432, 2002.
6. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 322(22):1561-1566, 1990.
7. Valensi P, Sachs RN, Lormeau B, et al. Silent myocardial ischaemia and left ventricle hypertrophy in diabetic patients. Diabetes Metab 23(5):409-416, 1997.
8. Rutter MK, McComb JM, Forster J, Brady S, Marshall SN. Increased left ventricular mass index and nocturnal systolic blood pressure in patients with Type 2 diabetes mellitus and microalbuminuria. Diabet Med 17(4):321-325, 2000.
9. Gatzka CD, Reid CM, Lux A, Dart AM, Jennings GL. Left ventricular mass and microalbuminuria: relation to ambulatory blood pressure. Hypertension Diagnostic Service Investigators. Clin Exp Pharmacol Physiol 26(7):514-516, 1999.
10. De Simone G, Palmieri V, Bella JN, et al. Association of left ventricular hypertrophy with metabolic risk factors: the HyperGEN study. J Hypertens 20(2):323-331, 2002.
11. Davis CL, Kapuku G, Snieder H, Kumar M, Treiber FA. Insulin resistance syndrome and left ventricular mass in healthy young people. Am J Med Sci 324(2):72-75, 2002.
12. Paternostro G, Pagano D, Gnecchi-Ruscone T, Bonser RS, Camici PG. Insulin resistance in patients with cardiac hypertrophy. Cardiovasc Res 42(1):246-253, 1999.
13. Phillips RA, Krakoff LR, Dunaif A, Finegood DT, Gorlin R, Shimabukuro S. Relation among left ventricular mass, insulin resistance, and blood pressure in nonobese subjects. J Clin Endocrinol Metab 83(12):4284-4288, 1998.
14. Andersson PE, Lind L, Andren B, et al. Regression of left ventricular wall thickness during ACE-inhibitor treatment of essential hypertension is associated with an increase in insulin mediated skeletal muscle blood flow. Blood Press 7(2):118-126, 1998.
15. El-Atat FA, Stas SN, McFarlane SI, Sowers JR. The relationship between hyperinsulinemia, hypertension and progressive renal disease. J Am Soc Nephrol 15(11):2816-2827, 2004.
16. Lind L, Berne C, Andren B, Lithell H. Relationship between diastolic hypertension and myocardial morphology and function in elderly males with diabetes mellitus. Diabetologia 39(12):1603-1606, 1996.
17. Grossman E, Rosenthal T. Hypertensive heart disease and the diabetic patient. Current Opinion in Cardiology 10(5):458-465, 1995.
18. Grossman E, Shemesh J, Shamiss A, Thaler M, Carroll J, Rosenthal T. Left ventricular mass in diabetes-hypertension. Arch Intern Med 152(5):1001-1004, 1992.
19 Sachs RN, Valensi P, Lormeau B, et al. Determinants of echocardiographically measured left ventricular mass in diabetic patients with or without silent myocardial ischaemia. Diabetes Metab 25(2):128-136, 1999.
20. Bella JN, Devereux RB, Roman MJ, et al. Separate and joint effects of systemic hypertension and diabetes mellitus on left ventricular structure and function in American Indians (the Strong Heart Study). Am J Cardiol 87(11):1260-1265, 2001.
21. Devereux RB, Roman MJ, Paranicas M, et al. Impact of diabetes on cardiac structure and function: the strong heart study. Circulation 101(19):2271-2276, 2000.
22. De Kreutzenberg SV, Avogaro A, Tiengo A, Del Prato S. Left ventricular mass in type 2 diabetes mellitus. A study employing a simple ECG index: the Cornell voltage. J Endocrinol Invest 23(3):139-144, 2000.
23. Fang ZY, Yuda S, Anderson V, Short L, Case C, Marwick TH. Echocardiographic detection of early diabetic myocardial disease. J Am Coll Cardiol 41(4):611-617, 2003.
24. Dahlof B, Devereux R, De Faire U, et al. The Losartan Intervention For Endpoint reduction (LIFE) in hypertension study: rationale, design, and methods. The LIFE Study Group. Am J Hypertens 10(7 pt 1):705-713, 1997.
25. Wachtell K, Olsen MH, Dahlof B, et al. Microalbuminuria in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study. J Hypertens 20(3):405-412, 2002.
26. Lindholm LH, Ibsen H, Dahlof B, et al. Cardiovascular morbidity and mortality in patients with diabetes in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 359(9311):1004-1010, 2002.
27. Nielsen FS, Ali S, Rossing P, et al. Left ventricular hypertrophy in non-insulin-dependent diabetic patients with and without diabetic nephropathy. Diabet Med 14(7):538-546, 1997.
28. Nielsen FS, Sato A, Ali S, et al. Beneficial impact of ramipril on left ventricular hypertrophy in normotensive nonalbuminuric NIDDM patients. Diabetes Care 21(5):804-809, 1998.
29. Sato A, Tarnow L, Parving HH. Prevalence of left ventricular hypertrophy in Type I diabetic patients with diabetic nephropathy. Diabetologia 42(1):76-80, 1999.
30. Mehler PS, Jeffers BW, Estacio R, Schrier RW. Associations of hypertension and complications in non-insulin-dependent diabetes mellitus. Am J Hypertens 10(2):152-161, 1997.
31. Gerstein HC, Mann JF, Pogue J, et al. Prevalence and determinants of microalbuminuria in high-risk diabetic and nondiabetic patients in the Heart Outcomes Prevention Evaluation Study. The HOPE Study Investigators. Diabetes Care 23(Suppl 2):B35-39, 2000.
32. Suzuki K, Kato K, Hanyu O, Nakagawa O, Aizawa Y. Left ventricular mass index increases in proportion to the progression of diabetic nephropathy in Type 2 diabetic patients. Diabetes Res Clin Pract 54(3):173-180, 2001.
33. Boner G, Cooper ME, McCarroll K. Adverse effects of left ventricular hypertrophy in the reduction of endpoints in NIDDM with the angiotensin II antagonist losartan RENAAL study. Diabetologia 48(10):1980-1987, 2005.
34. Bakris GL, Weir MR, Shahinfar S, et al. Effects of blood pressure level on progression of diabetic nephropathy: results from the RENAAL study. Arch Intern Med 163(13):1555-1565, 2003.
35. Weinrauch LA, Burger A, Gleason RE, Lee AT, D'Elia J. Left ventricular mass reduction in type 1diabetic patients with nephropathy. .J Clin Hypertens 7(3):159-164, 2005.
36. Okin PM, Devereux RB, Gerdts E, et al. Impact of diabetes mellitus on regression of electrocardiographic left ventricular hypertrophy and the prediction of outcome during antihypertensive therapy: the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study. Circulation 113(12):1588-1596, 2006.
37. Dahlof B, Hansson L. Regression of left ventricular hypertrophy in previously untreated essential hypertension: different effects of enalapril and hydrochlorothiazide. J Hypertens 10(12):1513-1524, 1992.
38. Dahlof B, Pennert K, Hansson L. Reversal of left ventricular hypertrophy in hypertensive patients. A metaanalysis of 109 treatment studies. Am J Hypertens 5(2):95-110, 1992.
39. Gerritsen TA, Bak AA, Stolk RP, Jonker JJ, Grobbee DE. Effects of nitrendipine and enalapril on left ventricular mass in patients with non-insulin-dependent diabetes mellitus and hypertension. J Hypertens 16(5):689-696, 1988.
40. Scognamiglio R, Nosadini R, Marin M, et al. Evaluation of the efficacy and tolerability of nitrendipine in reducing both pressure and left ventricular mass in hypertensive type 2 diabetic patients. Diabetes Care 20(8):1290-1292, 1997.
41. Tarnow L, Sato A, Ali S, Rossing P, Nielsen FS, Parving HH. Effects of nisoldipine and lisinopril on left ventricular mass and function in diabetic nephropathy. Diabetes Care 22(3):491-494, 1999.
42. Gerdts E, Svarstad E, Aanderud S, Myking OL, Lund-Johansen P, Omvik P. Factors influencing reduction in blood pressure and left ventricular mass in hypertensive type-1 diabetic patients using captopril or doxazosin for 6 months. Am J Hypertens 11(10):1178-1187, 1998.
43. Malmqvist K, Kahan T, Edner M, et al. Regression of left ventricular hypertrophy in human hypertension with irbesartan. J Hypertens 19(6):1167-1176, 2001.
44. Malmqvist K, Kahan T, Isaksson H, Ostergren J. Regression of left ventricular mass with captopril and metoprolol, and the effects on glucose and lipid metabolism. Blood Press 10(2):101-110, 2001.
45. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy. Heart Outcomes Prevention Evaluation Study Investigators. Lancet 355(9200):253-259, 2000.
46. Dahlof B, Devereux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 359(9311):995-1003, 2002.
 
 
 
 
 
 
 
 
 
 
 
 
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