Hypertension and The

Kidney

Introductio
Introduction
n

>1/2 the people with CKD have high BP

Hypertension increases the chance that kidney disease
get worse.
Every year, hypertension causes >25,000 new cases of
kidney failure in the US
1/3 adults in the United States has hypertension .
Higher among patients with CKD, progressively
increasing with the severity of CKD.
23.3% of individuals without CKD, and 35.8% of stage
1, 48.1% of stage 2, 59.9% of stage 3, and 84.1% of
stage 4-5 CKD patients
NKF-KDOQI
NIDDK, 2007

 Riset Kesehatan Dasar (Riskesdas)

2007
Hypertension in the population age >
18 years old : prevalence 31,7%,
only 7,2% understand that they have
hypertension and only 0,4% use
hypertension medicine.

Introduction
Hyperten
sion

Hypertension in CKD increases the risk of

important adverse outcomes:
loss of kidney function and kidney failure,
early development and accelerated progression of
CVD,
premature death
NKF-KDOQI
NIDDK

Patophysiology, Hypertension and

kidney disease
1. High blood pressure is a leading
cause of CKD.
Damage blood vessels reduce the
blood supply to the kidneys.
High BP damages glomerulus in
kidneys. The kidneys may stop
removing wastes and extra fluid
raise BP
NKF-KDOQI
NIDDK

Hypertension and kidney

disease
2. complication of CKD.
kidneys play a key role in keeping
blood pressure
Diseased kidneys are less able to
help regulate blood pressure.

Hypertension

Kidney Autoregulation of Blood

Pressure

Sympathetic nervous systems

Myogenic mechanism
Tubuloglomerular Feedback
RAAS System

Neural reflect arcs

High pressure baroreceptors in the aortic
arch and carotid sinus
Low pressure cardiopulmonary
baroreceptors in the ventricles and atria
Intrarenal baroreceptor : renin secreting
granular cells act as baroreceptors,
measuring pressure in the late afferent aa.
secretion is inversely related to arteriolar
pressure

The Role sympathetic Nervous

Systems
Increase heart rate
Direct vasoconstriction effect
Induce release of epinephrine from
adrenal medulla thus lead to
vasoconstrictor effect through and
adrenergic receptor
Induce renin release

Myogenic Mechanism, Tubuloglomerular

Feedback and RAAS Systems

 Themyogenic mechanismis howarteriesand

arteriolesreact to an increase or decrease of
blood pressureto keep the blood flow within the
blood vesselconstant.

Na-K-2Cl
cotransport
er

Adenosi
n

 Juxtaglomerular Apparatus
Def'n: = an aggregation of three cell types,
1. granular cells
differentiated smooth muscle cells of afferent arterioles
secretory vesicles contain renin
2. extraglomerular mesangial cells - continuous with
the mesangium
3. macula densa cells
terminal part of thick ascending limb LOH
probably control both renin secretion and GFR
NB: JGA has a rich sympathetic nerve supply

The Role of Angiotensin II

Constricts vascular smooth muscle

Stimulates aldosteron secretion
Potentiates sympathetic nervous system activity
Stimulates salt and water reabsorption in the
proximal tubule
Stimulate prostaglandin, nitrit oxide, and
endothelin release
Increase thirst
Growth factor activity : increase remodelling,
inflammation and vasculopaty

The Role of Aldosterone

Mediates changes in sodium
channels in distal tubular epithelium,
leading to sodium retention and
potassium excretion
Growth factor to increase sensitivity
of mineralocorticoid receptor

Comprehensive Clinical

Special Definition
Pre hypertension : lack of uniform
agreement, most usefully defined as
BP of 130 to 139/85-89 mmHg
White Coat Hypertension : BP that is
normal during usual daily activities
but is hypertensive in clinical setting
Masked Hypertension : BP that is
lower in the clinical setting compared
with ambulatory BP
Comprehensive Clinical

 Sustained Hypertension : Persistent

hypertension, in individual whose BP
levels are elevated both inside and
outside clinical setting
Pseudohypertension : condition in which
the cuff pressure is inappropiately higher
when compared to the intra-arterial
pressure because of excessive atheroma
or medial hyperthrophy in the arterial tree

 Isolated Hypertension: SBP of 140 or

higher and DBP of 90 mmHg or lower
because of increase stiffness of
artery due to arterioclerosis
Resistant Hypertension : BP that is
not achieve the treatment goal
despite optimal doses of three
antihypertensive drugs including
diuretic

 Accelerated Hypertension : severe diastolic hypertension (usually > 120 mmHg)

in the presence of grade III retinopathy
Hypertensive urgencies : Systolic 180 and diastolic 120 and asymptomatic
Hypertensive emergencies are acute, life-threatening, and usually associated
with marked increases in blood pressure (BP), generally 180/120 mmHg There
are two major clinical syndromes induced by the severe hypertension:
Malignant hypertension is marked hypertension with retinal hemorrhages,
exudates, or papilledema. There may also be renal involvement, called malignant
nephrosclerosis. Although papilledema had been thought to represent a more
severe lesion, it does not appear to connote a worse prognosis than hemorrhages
and exudates alone (so-called accelerated hypertension) [4]. Thus, treatment is
the same whether or not papilledema is present.
Hypertensive encephalopathy refers to the presence of signs of cerebral edema
caused by breakthrough hyperperfusion from severe and sudden rises in blood
pressure

Up to Date
19.3

Algorithm for Treatment of Hypertension

Lifestyle modifications
Not at goal blood pressure (<140/90 mm Hg)
(<130/80 mm Hg for those with diabetes or chronic
kidney disease)
Initial drug choices
Without compelling
indications

Stage 1 hypertension

Stage 2 hypertension

(SBP 140159 or DBP 9099 mm Hg)

Thiazide-type diuretics for most.
May consider ACEI, ARB, BB, CCB,
or combination.

(SBP >160 or DBP >100 mm

Hg)
2-drug combination for most
(usually thiazide-type diuretic
and
ACEI, or ARB, or BB, or CCB)

With compelling
indications

Drugs for the

compelling indications
Other antihypertensive drugs
(diuretics, ACEI, ARB, BB,
CCB)
as needed.

Not at goal
blood pressure
Optimize dosages or add additional drugs
until goal blood pressure is achieved.
Consider consultation with hypertension specialist
Source: The Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure

NICE, 2011

Hypertension: NICE guideline . 2011

Terima Kasih