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HYPERTENSION IN ESRD
Oleh : Muhammad Haris
Stase Nefrologi Pediatric
PPDS Ilmu Penyakit Jantung dan Kedokteran Vaskuler
FK UGM
INTRODUCTION
 Pediatric hypertension  widely observed. Major cause of morbidity and
mortality in United States and other countries
 The true incidence of hypertension in children is not known
 Standart of Blood Pressure for Children was made by NHLBI by using 11 surveys of
more than 83.000 infants and children
 Last, widely used The Fourth Report
 Category :
 Pre hypertension : above 9oth percentile & below 95th percentile
 Stage 1 hypertension : above 95th percentile & below 95th percentile plus 5 mmHg
 Stage 2 hypertension : above 95th percentile plus 5 mmHg
 CKD stage 1  65 % affected hypertension
 CKD stage 4 & 5  80 %
 And more than 50 % children with ESRD have uncontrolled hypertension
WORK UP
 Laboratory studies : CBC (anemia  Chronic Renal Disease), Creatinine (Renal
Disease), Hypokalemia (Hyperaldosteronism), Blood hormone (high plasma renin
 renal vascular hypertension), Urine dipstick (+proteinuria  problem in renal)
 Echocardiography : LVH from chronic hypertension  start for therapy (usually
concentric morphology
 Abdominal USG may reveal tumors or structural anomalies of kidneys or renal
vasculare
 Angiography  to reveal the structure of renal vessels
PATTERN OF HYPERTENSION IN ESRD
 Very common in all stages of CKD
 Generally :
 Fluid overload
 Activation of renin-angiotensin system
 Symphatetic activation
 Endhotelial dysfunction
 Chronic hyperparathyroidism
 Therapy :
 ACE inhibitor
 ARB
 DIuretics
PATHOFISIOLOGY
 Mechanisme of muscle sympathomimetic in elevated BP still unclear
 Maybe connected with afferent afferent signal, dopaminergic abnormalities &
accumulation of leptin in CKD
 Another postules about renal ischemia
 Renalase (amino oxidase expressed in kidney)  activity usually reduced in
patients with ESRD. Lower blood pressure and heart rate
 In uremic patients, reduced NO stimulation leads to reduced agonist
endhotelium-dependent vasodilatation
 Corelated with higher concentration of ADMA
(Hadstein, 2007)
DRUG ASSOCIATED WITH HT
 Erythropoietin cause elevated BP for several weeks
 Related with arterial wall remodeling causing vascular resistance (Schiffl H et al
1998) and voltage independent calcium channel in smooth muscle activity 
sensitivity NO decreased (Vaziri et al, 1999)
 Glucocoticoid lead to fluid retention by their mineralocorticoid effect
 Cyclosporine A causes vasoconstriction of glomerular afferent arterioles and
hyperplasia of juxtaglomerular apparatus
MANAGEMENT
PHARMACOTHERAPY
 Based on epidemiology : 75% children with CKD stages 2-4 can reduces blood
pressure (<95th percentile) with monotheraphy oh antihypertensive
 More aggressive therapy needed if targetted <50th percentile
 Start with single dose and titrate upward
 ACE inhibitorand ARB is the most useful drug  not only reduce BP but also slow
down the progession of renal failure
 Mechanism :
 Reduced proteinuria
 Lower intaglomerular pressure
 Anti inflamatory
 Anti fibrotic
PHARMACOTHERAPY (2)
 Diurretics used when hypervolemia
 Thiazides are a popular first line therapy in mild to moderate CKD but less efective when
GFR falls below 60 ml/min per 1.73 m2 body surface area
 Not efective when below 30 ml/min . Shoul used furosemide when the status is ESRD
 CCB  very potent vasodilators and do not have cardiac side effect (have side effect
proteinuria and increase intaglomerular pressure)
 Beta Blocker can be used as a second line therapy for renal hypertension in children.
Contraindications in asthma and can cause fatigue.
TERIMA KASIH & MOHON ASUPAN

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Hypertension in ESRD

  • 1. HYPERTENSION IN ESRD Oleh : Muhammad Haris Stase Nefrologi Pediatric PPDS Ilmu Penyakit Jantung dan Kedokteran Vaskuler FK UGM
  • 2. INTRODUCTION  Pediatric hypertension  widely observed. Major cause of morbidity and mortality in United States and other countries  The true incidence of hypertension in children is not known  Standart of Blood Pressure for Children was made by NHLBI by using 11 surveys of more than 83.000 infants and children  Last, widely used The Fourth Report  Category :  Pre hypertension : above 9oth percentile & below 95th percentile  Stage 1 hypertension : above 95th percentile & below 95th percentile plus 5 mmHg  Stage 2 hypertension : above 95th percentile plus 5 mmHg
  • 3.  CKD stage 1  65 % affected hypertension  CKD stage 4 & 5  80 %  And more than 50 % children with ESRD have uncontrolled hypertension
  • 4. WORK UP  Laboratory studies : CBC (anemia  Chronic Renal Disease), Creatinine (Renal Disease), Hypokalemia (Hyperaldosteronism), Blood hormone (high plasma renin  renal vascular hypertension), Urine dipstick (+proteinuria  problem in renal)  Echocardiography : LVH from chronic hypertension  start for therapy (usually concentric morphology  Abdominal USG may reveal tumors or structural anomalies of kidneys or renal vasculare  Angiography  to reveal the structure of renal vessels
  • 5. PATTERN OF HYPERTENSION IN ESRD  Very common in all stages of CKD  Generally :  Fluid overload  Activation of renin-angiotensin system  Symphatetic activation  Endhotelial dysfunction  Chronic hyperparathyroidism  Therapy :  ACE inhibitor  ARB  DIuretics
  • 6. PATHOFISIOLOGY  Mechanisme of muscle sympathomimetic in elevated BP still unclear  Maybe connected with afferent afferent signal, dopaminergic abnormalities & accumulation of leptin in CKD  Another postules about renal ischemia  Renalase (amino oxidase expressed in kidney)  activity usually reduced in patients with ESRD. Lower blood pressure and heart rate  In uremic patients, reduced NO stimulation leads to reduced agonist endhotelium-dependent vasodilatation  Corelated with higher concentration of ADMA
  • 8. DRUG ASSOCIATED WITH HT  Erythropoietin cause elevated BP for several weeks  Related with arterial wall remodeling causing vascular resistance (Schiffl H et al 1998) and voltage independent calcium channel in smooth muscle activity  sensitivity NO decreased (Vaziri et al, 1999)  Glucocoticoid lead to fluid retention by their mineralocorticoid effect  Cyclosporine A causes vasoconstriction of glomerular afferent arterioles and hyperplasia of juxtaglomerular apparatus
  • 10. PHARMACOTHERAPY  Based on epidemiology : 75% children with CKD stages 2-4 can reduces blood pressure (<95th percentile) with monotheraphy oh antihypertensive  More aggressive therapy needed if targetted <50th percentile  Start with single dose and titrate upward  ACE inhibitorand ARB is the most useful drug  not only reduce BP but also slow down the progession of renal failure  Mechanism :  Reduced proteinuria  Lower intaglomerular pressure  Anti inflamatory  Anti fibrotic
  • 11. PHARMACOTHERAPY (2)  Diurretics used when hypervolemia  Thiazides are a popular first line therapy in mild to moderate CKD but less efective when GFR falls below 60 ml/min per 1.73 m2 body surface area  Not efective when below 30 ml/min . Shoul used furosemide when the status is ESRD  CCB  very potent vasodilators and do not have cardiac side effect (have side effect proteinuria and increase intaglomerular pressure)  Beta Blocker can be used as a second line therapy for renal hypertension in children. Contraindications in asthma and can cause fatigue.
  • 12. TERIMA KASIH & MOHON ASUPAN