Antihipertensivos en Insuficiencia Renal Cronica
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antihipertensivos en irc. expo en el Almanzor 2006

antihipertensivos en irc. expo en el Almanzor 2006

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Antihipertensivos en Insuficiencia Renal Cronica Presentation Transcript

  • 1. USO DE ANTIHIPERTENSIVOS EN IRC MC EDILBERTO IBAÑEZ BURGOS SERVICIO DE NEFROLOGIA HNAAA CHICLAYO-PERU
  • 2.  
  • 3.  
  • 4. Adapted from JNC VII or >100 >160 Stage 2 hypertension or 90-99 140-159 Stage 1 hypertension or 80-89 120-139 Prehypertension and <80 <120 Normal Diastolic BP, mm Hg Systolic BP, mm Hg    Classification of Blood Pressure (JNC VII)
  • 5. DASH = Dietary Approaches to Stop Hypertension Adapted from JNC VII 2-4 mm Hg Limit consumption to no more than 2 drinks per day in most men and no more than 1 drink per day in women and in lighter weight persons. Moderation of alcohol consumption 4-9 mm Hg (at least 30 minutes/day, most days of the week) Physical activity 2-8 mm Hg (2.4 g sodium or 6 g sodium chloride) Dietary sodium reduction 8-14 mm Hg fruits, vegetables, and dairy products with a reduced content of saturated and total fat (K,Ca) Adopt DASH eating plan 5-20 mm Hg/ 10 kg weight loss IMC:18.4-24.9 kg/m 2 Weight reduction Approximate SBP Reduction Range Recommendation Modification LIFESTYLE MODIFICATIONS TO MANAGE HYPERTENSION *†
  • 6. PROGRESS          X    X RECURRENT STROKE PREVENTION NKF GUIDELINE, CAPTOPRIL TRIAL, RENAAL, IDNT, REIN, AASK       X X       CHRONIC KIDNEY DISEASE NKF-ADA Guideline, UKPDS, ALLHAT    X X X X X DIABETES ALLHAT, HOPE, ANBP2, LIFE, CONVINCE    X    X X X HIGH CORONARY DISEASE RISK ACC/AHA Post-MI Guideline, BHAT, SAVE, Capricorn, EPHESUS X       X X    POSTMYOCARDIAL INFARCTION ACC/AHA Heart Failure Guideline, MERIT-HF, COPERNICUS, CIBIS, SOLVD, AIRE, TRACE, ValHEFT, RALES X    X X X X HEART FAILURE AANT BCC ARA IECA BB D Clinical Trial Basis ‡ Recommended Drugs † Compelling Indication* Clinical Trial and Guideline Basis for Compelling Indications for Individual Drug Classes
  • 7.  
  • 8.
    • K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease
    • GUIDELINE 7: PHARMACOLOGICAL THERAPY: USE OF ANTIHYPERTENSIVE AGENTS IN CKD
  • 9.
    • All antihypertensive agents can be used to lower blood pressure in CKD. Multidrug regimens will be necessary in most patients with CKD to achieve therapeutic goals. Patients with specific causes of kidney disease and CVD will benefit from specific classes of agents.
  • 10.
    • 7.1 Patients with CKD should be considered in the &quot;highest-risk&quot; group for CVD for implementing recommendations for pharmacological therapy, irrespective of cause of CKD (A).
  • 11.
    • 7.2 Target blood pressure for CVD risk reduction in CKD should be <130/80 mm Hg (B).
  • 12.
    • 7.3 Antihypertensive agents should be prescribed as follows, when possible:
    • 7.3.a Preferred agents for CKD should be used first (A)
  • 13.
    • 7.3 Antihypertensive agents should be prescribed as follows, when possible:
    • 7.3.b Diuretics should be included in the antihypertensive regimen in most patients (A).
  • 14.
    • 7.3 Antihypertensive agents should be prescribed as follows, when possible:
    • 7.3.c Choose additional agents based on cardiovascular disease-specific indications to achieve therapeutic and preventive targets and to avoid side-effects and interactions (B).
  • 15.  
  • 16.
    • 7.4 The antihypertensive regimen should be simplified as much as possible (B).
    • 7.4.a Long-acting (once-daily agents) should be used when possible (B).
  • 17.
    • 7.4 The antihypertensive regimen should be simplified as much as possible (B).
    • 7.4.b Two agents, either as separate prescriptions or as a fixed-dose combination containing preferred agents, may be considered as initial therapy for SBP >20 mm Hg above goal according to the stage of CKD and CVD risk (C).
  • 18.
    • 7.4 The antihypertensive regimen should be simplified as much as possible (B).
    • 7.4.c Fixed-dose combinations may be used for maintenance therapy after the antihypertensive regimen has been established (B).
  • 19.  
  • 20.  
  • 21.  
  • 22.  
  • 23. &quot;Preferred agents&quot;
    • “ Son agentes antihipertensivos que tienen efectos benéficos sobre la progresión de la CKD o en la reducción del riesgo de CVD, además de su efecto antihipertensivo, tales como reducción de la proteinuria, enlentecimiento de la declinación de la GFR e inhibición de otros mecanismos patogenéticos de progresión de enfermedad renal y CVD”
  • 24.
    • USE OF ANTIHYPERTENSIVE AGENTS IN CKD
  • 25.  
  • 26.
    • ß-Adrenergic Blockers
  • 27. ß-Adrenergic Blockers:
    • Mecanismo de acción:
      • Inhibición de receptores B1 en el aparato yuxtaglomerular, con descenso en la liberación de renina.
      • Inhibición de receptor B2 en la pared vascular, disminuyendoi la resisitencia periferica.
      • Disminución del SN simpático a nivel central.
  • 28.  
  • 29. ß-Adrenergic Blockers: * Medications are listed is alphabetical, not preferential order. carvedilol, labetalol Nonselective ß- and α- antagonists acebutolol ß 1 -selective with partial agonist activity atenolol, betaxolol, bisoprolol, metoprolol ß 1 -selective carteolol, penbutolol, pindolol Nonselective with partial agonist activity nadolol, propranolol, timolol Nonselective ß-adrenergic blockers Medication* Drug Class ß-Adrenergic Blockers
  • 30. ß-Adrenergic Blockers:
    • Nonselective ß-Adrenergic Blockers Timolol, nadolol, y propranolol son metabolizados preferentemente en el hígado. Sólo nadolol tiene un metabolismo hepático mímo y 75% de lo absorbido es excretado por vía renal. Es necesario una reducción en la dosis para pacientes con CKD.
  • 31. ß-Adrenergic Blockers:
    • Nonselective with Partial Agonist Activity Carteolol, penbutolol, and pindolol son representativos de esta categoría. Requieren ajuste de dosis en CKD avanzada.
  • 32. ß-Adrenergic Blockers:
    • ß1-Selective Incluye atenolol, metoprolol, betaxolol y bisoprolol.
    • Atenolol es eliminado principalmente por la orina, con escaso metabolismo hepático. Pacientes con CKD requeriran reducción de la dosis. Probablemente no sea una elección optima para terapia inicial en esta pob.
    • Metoprolol, on the other hand, has an extensive first-pass metabolism, and is cleared by biotransformation. Hence, a dose adjustment is not necessary with decreased renal function.
    • Betaxolol is metabolized primarily by the liver; however a prolonged half-life has been observed in patients with CKD because a small percentage of the active drug and all its metabolites are excreted by the kidney. Dose adjustment is necessary.
    • Bisoprolol has a low first-pass metabolism and is eliminated equally by renal and nonrenal mechanisms. One-half of the drug is eliminated unchanged in the urine. Decreased renal function prolongs its half-life, requiring dose adjustment.
  • 33. ß-Adrenergic Blockers:
    • ß1-Selective with Partial Agonist Activity Acebutolol es el unico representante de esta clase. Tiene un importante metabolismo hepático. Necesita ajuste de dosis en CKD.
  • 34. ß-Adrenergic Blockers:
    • Nonselective ß- and α -Antagonists Labetalol y carvedilol tienen un extenso first-pass metabolism, con menos de 5% y 2% de droga excretada sin cambios en la orina, respectivamente. No necesita ajuste de dosis en CKD.
  • 35. ß-Adrenergic Blockers:
    • EFECTOS ADVERSOS:
    • Pueden causar hipercalemia, siendo los BB selectivos los que causan menos hiperkalemia que los no selectivos.
    • Elevan niveles de glicemia, triglicéridos, resistencia a la insulina.
    • Disminuyen niveles de HDL colesterol.
  • 36. ß-Adrenergic Blockers:
    • Pueden enmascarar algunos síntomas tempranos de hipoglicemia.
    • Su retiro brusco puede producir no solo hipertensión de rebote, sino también empeoramiento de angina, IMA y hasta muerte.
  • 37.
    • Calcium Channel Blockers
  • 38. Calcium Channel Blockers:
    • Es un grupo heterogeneo que comparte sus mecanismo de acción, pero difiere en sus efectos farmacológicos.
    • Se liga a los canales L dependientes de voltage y bloquean el ingreso de calcio en las células de músculo liso de las arteriolas de resistencia
  • 39. Calcium Channel Blockers:
  • 40. Calcium Channel Blockers:
    • Existen 3 clases de BCC: dihidropiridinas (nifedipine, amlodipine, isradipine, felodipine, nicardipine, and nisoldipine); fenilalkylaminas (verapamil); and benzothiazepinas (diltiazem).
    • Debido a sus diferentes efectos farmacológicos, los BCC pueden ser usados en diferentes situaciones clínicas.
  • 41. Calcium Channel Blockers:
    • .
    • Pueden ser usados con seguridad en pacientes con CKD.
    • Causan vasodilatación de la arteriola aferente produciendo un incremento agudo en la GFR, un efecto que desaparece con el uso crónico.
  • 42. Calcium Channel Blockers:
    • .
    • Todos tiene excelente absorción oral de 80% a 90%.
    • Todos alcanzan niveles pico rápidamente.
    • No se necesita ajuste de dosis en CKD
  • 43. Calcium Channel Blockers:
    • Hay diferentes efectos de los CCB en el nivel de proteinuria.
    • Los dihydropyridine CCBs y no los nondihydropyridines CCBs incrementan la tasa de excreción proteica.
    • Sin embargo, las consecuencias clínicas de este efecto aun no estan claras.
  • 44. Calcium Channel Blockers
  • 45. Calcium Channel Blockers
      • La combinación de dosis reducidas de un IECA (LISINOPRIL) y un BCC (VERAPAMIL) disminuyen tanto la albuminuria como la tasa de declinación de la TFG.
      • Treatment of arterial hypertension in diabetic humans: importance of therapeutic selection. Bakris GL , Barnhill BW , Sadler R . Kidney Int. 1992 Apr;41(4):912-9.
  • 46. Calcium Channel Blockers
    • Parece que los BCC dihidropiridinicos, en asociación con un diurético, son efectivos en disminuir PA y reducir el riesgo de CVD, pero son menos efectivos en ausencia del diurético
  • 47.
    • Angiotensin-Converting Enzyme Inhibitors
  • 48.  
  • 49.  
  • 50. Angiotensin-Converting Enzyme Inhibitors
    • In addition to lowering angiotensin II, a potent vasoconstrictor, the antihypertensive effects are also mediated by the lowering of postsynaptic norepinephrine release, inhibition of the RAAS at the vasomotor center in the medulla oblongata, and accumulation of bradykinin, a vascular vasodilator. &quot;angiotensin escape.&quot;
  • 51. Angiotensin-Converting Enzyme Inhibitors
    • El efecto neto es la disminución de la resistencia periférica total sin cambios significativos en FC o GC.
  • 52. Angiotensin-Converting Enzyme Inhibitors
    • Existen 3 categorías químicas: sulfhydril, carboxyl, and phosphinyl , de acuerdo a la unión de su ión zinc.
  • 53. Angiotensin-Converting Enzyme Inhibitors
    • El sulfhydril ACE inhibitor (captopril) tiene la más larga biodisponibilidad pero la vida media más corta.
  • 54. Angiotensin-Converting Enzyme Inhibitors
    • Los carboxyl ACE inhibitors (benazepril, enalapril, lisinopril, moexipril, quinapril, ramipril, trandolapril) como grupo tiene un avida media más larga, haciéndolos efectivos en una sola o 2 dosis diarias. Todas, excepto el lisinopril, son prodrogas que requieren hidrólisis hepática.
  • 55. Angiotensin-Converting Enzyme Inhibitors
    • El unico representante de phosphinyl group, fosinopril , es activado x hidrólisis en la mucosa GI e hígado también tiene una vida media larga.
  • 56. Angiotensin-Converting Enzyme Inhibitors
    • La mayoría requerirá ajuste de dosis en CKD. La excepción es el fosinopril, cuya eliminación hepática se incrementa en cuanto la función renal declina.
  • 57. Angiotensin-Converting Enzyme Inhibitors
    • Pueden causar un incremento en la TFG, manifestado como incremento de la creatinina sérica. Se ve en estados como hipovolemia, estenosis de la arteria renal, ICC o CKD.
  • 58. Angiotensin-Converting Enzyme Inhibitors
    • LA hipercalemia es otra complicación de la terapia con IECA.
    • Estan en riesgo los pacientes con DM, o quienes usan diuréticos ahorradores de potasio.
    • Creatinina sérica y potasio deben ser monitorizados en 1 semana de iniciar la terapia con IECA.
  • 59. Angiotensin-Converting Enzyme Inhibitors
  • 60.
    • Angiotensin II Receptor Blockers
  • 61.  
  • 62. Angiotensin II Receptor Blockers
  • 63. Angiotensin II Receptor Blockers
    • Angiotensin II receptor blockers (ARBs) lower blood pressure by lowering total peripheral resistance. They block the distal effects of angiotensin II by binding to one of its receptors, AT1 (Figure 1) . Blockade of the AT1 receptor prevents angiotensin II-induced vasoconstriction
  • 64. Angiotensin II Receptor Blockers
    • ARBs also decrease aldosterone production and therefore sodium retention. Some other putative effects include inhibition of the brain RAAS, inhibition of the central or peripheral sympathetic nervous system by antagonizing angiotensin II, and regression of vascular remodeling.
  • 65. Angiotensin II Receptor Blockers
    • Quimicamente, los ARBs están divididos en 3 diferentes categorías:
    • biphenyl tetrazoles (eg, candesartan, irbesartan, losartan, and olmesartan);
    • nonbiphenyl tetrazoles (telmisartan); and the
    • nonhetererocyclic compounds (valsartan).
  • 66. Angiotensin II Receptor Blockers
    • Todos son componentes no peptídicos.
    • Como grupo alcanzan rápidamente un nivel pico en sangre.
    • El metabolismo hepático de Losartan produce un metabolito farmacológicamente activo, el E3174.
  • 67. Angiotensin II Receptor Blockers
    • Telmisartan tiene la vida media más larga (24 horas).
    • Se recomienda la dosis más baja para pacientes con CKD sólo con Candesartan .
  • 68.
    • Central α2-Agonists
  • 69.  
  • 70. Central α2-Agonists
    • The mechanism of action for this class of drugs is characterized by a direct effect on presynaptic and postsynaptic α2-adrenergic receptors in the vasomotor center in the brain stem
  • 71. Central α2-Agonists
    • Stimulation of the central α2-adrenergic receptors decreases the sympathetic outflow and increases vagal activity.
    • El efecto neto es una reducción en la liberación de norepinefrina.
  • 72. Central α2-Agonists
    • En general, estas drogas causan una disminución en la resistencia periférica total y un enlentecimiento de la frecuencia cardiaca.
  • 73. Central α2-Agonists
    • The most commonly used drug in this class is clonidine . It reaches its peak plasma concentration in 3 to 5 hours, making it an effective drug for the treatment of hypertensive urgencies .
  • 74. Central α2-Agonists
    • A reduced dose should be used for patients with CKD. Forty to sixty percent is excreted unchanged in the urine, and its normal long half-life of 12 to 15 hours can be extended to more than 40 hours
  • 75. Central α2-Agonists
    • El resto de las drogas en esta clase son raramente usadas en la práctica actual debido a su débil efecto antihipertensivo y su perfil de efectos colaterales adversos.
    • De estos, sólo metildopa necesita ser ajustado para pacientes con CKD.
  • 76. Central α2-Agonists
    • Tienen efectos benéficos en el metabolismo de lípidos y mejora la sensibilidad a la insulina.
  • 77. Central α2-Agonists
  • 78.
    • Peripheral α1-Adrenergic Blockers
  • 79. Peripheral α1-Adrenergic Blockers
    • The antihypertensive mechanism of this class of drugs is mediated by inhibition of the postjunctional α1-adrenergic receptors. This provokes dilation of the arterial and venous vessels. 19 The net effect is a decrease in total peripheral resistance without an increase in renin, cardiac output, or reflex tachycardia
  • 80. Peripheral α1-Adrenergic Blockers
    • At the renal level, these agents have little effect on renal hemodynamics. However, a decrease in the fractional excretion of sodium has been noted, with expansion of the extracellular volume
  • 81. Peripheral α1-Adrenergic Blockers
    • The members of this group include doxazosin, prazosin, and terazosin . None requires adjustment in patients with CKD. The premature termination of the doxazosin arm of the recently published ALLHAT trial 7 suggests that these medications should not be used as first-line therapy.
  • 82.
    • Direct Vasodilators
  • 83. Direct Vasodilators
    • The exact antihypertensive mechanism of this class of drugs is also not well understood. They have a direct effect on the vascular smooth muscle cell, dilating the arterial and venous system , primarily the arterial system. 20 It is thought that they alter intracellular calcium metabolism.
  • 84. Direct Vasodilators
    • The net effect is a decrease in total peripheral resistance associated with an increase in heart rate and cardiac output. This occurs by sympathetic activation that increases renin release and therefore activation of the RAAS system.
  • 85. Direct Vasodilators
    • The net effect is a decrease in total peripheral resistance associated with an increase in heart rate and cardiac output. This occurs by sympathetic activation that increases renin release and therefore activation of the RAAS system.
  • 86. Direct Vasodilators
    • Minoxidil , a more potent vasodilator, has a rapid onset of action. It is metabolized mainly by the liver and does not require dose adjustment.
  • 87.
    • CONCLUSION
  • 88. CONCLUSION
    • La mayoría de loa antihipertensivos pueden ser usados en el manejo de HTA en CKD.
    • Son necesarios estimar la TFG y adecuar la dosis para alcanzar mejores resultados y evitar efectos colaterales innecesarios y morbilidad.
  • 89. CONCLUSION
    • Hay pocos estudios en el tto de HTA en CKD.
    • La mayoría de las recomendaciones de la 7º guía de la KDOQUI son extrapoladas de estudios clínicos realizados en la población general.
    • Estudios clínicos adicionales son necesarios en el tto de HTA en pacientes con CKD.
  • 90. GRACIAS