Chronic Kidney Disease (CKD)

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3/10/2020

CHRONIC KIDNEY DISEASE

Candra Wibowo

DEFINITION & CLASSIFICATION


KDOQI Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, Classification and Stratification
http:/www.kidney.org/professionals/KDOQI/guidelines_ckd/p4_class_g1.htm, accessed Oct 10, 2007

• Definition (KDOQI 2002)


– Kidney damage ≥ 3 mo as defined by structural or
functional abnormalities w/o GFR, manifest by either :
– Pathological abnormalities or
– Markers of kidney damage, including abnormalities in the
composition of blood or urine, or abnormalities in imaging tests
– GFR < 60 mL/min/1.73 m2 for ≥ 3 mo, w/o kidney
damage
• Classification
– Stages of CKD is based on GFR

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DEFINING KIDNEY DAMAGE


• Pathologic Abnormalities?
– By Radiology (USG, CT, MR, etc)  e.g.
• Multiple cysts consistent with PKD
• Extensive scarring
• Small kidneys  but be careful of the term
“medical renal disease”.
• REMEMBER: Renal masses or cysts that are not
simple should be referred to a Urologist
– By Histology  ie, renal biopsy

DEFINING KIDNEY DAMAGE


• Markers of Kidney Damage?
– Proteinuria
– Microalbuminuria
– Hematuria (especially when seen with
proteinuria)
• Isolated hematuria has a long differential:
infection, stone, malignancy, etc.
– Casts (especially with cellular elements)

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CLASSIFICATION & STAGES OF CKD


KDOQI Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, Classification and Stratification
http:/www.kidney.org/professionals/KDOQI/guidelines_ckd/p4_class_g1.htm, accessed Oct 10, 2007

GFR With Kidney Damage Without Kidney Damage


(mL/min/1.73 m2) With HBP Without HBP With HBP Without HBP

≥ 90 1 1 HBP NORMAL
60 – 89 2 2 HBP with   GFR@
GFR
30 – 59 3 3 3 3

15 – 29 4 4 4 4
< 15 5 5 5 5
(or dialysis)

HBP : high blood pressure as defined as ≥ 140/90 mmHg K/DOQI – NKF, 2002
@ : may be normal in the elderly or infants

AJKD 2009; vol 20 (XX)

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KDIGO Controversies Conference:


Definition, Classification and Prognosis in
CKD, London, October 2009

ACR (mg/g)
<30 (A1) 30-299 (A2) ≥300 (A3)
Normal or
1 >90
increased

2 mild 60-89
GFR
Stages, mild-
Descrip- 3a 45-59
moderate
tion and
Range moderate-
3b 30-44
(mL/min/ severe
1.73m2)
4 severe 15-29

kidney
5 <15
failure

The known pts with ESRD


0,2%

Many pts with CKD 1-4


11-16%

ICEBERG PHENOMENONE

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Prevalence of GFR Categories in the USA


Stage Description GFR Prevalence Prevalence
(mL/min/1.73m2)
1 Kidney damage with > 90 5.9 million 3.3%
normal or  GFR
2 Mild  GFR 60-89 5.3 million 3.0%

3 Moderate  GFR 30-59 7.6 million 4.3%

4 Severe  GFR 15-29 400,000 0.2%

5 Kidney Failure < 15 or dialysis 300,000 0.2%

Coresh, et al, Am J Kidney Dis. 2003; 41: 1-12

The Patient with Early Stage CKD is


5 to 10 times MORE LIKELY to die
from a cardiovascular event than
progress to ESRD.

Foley RN, Murray AM, Li S, Herzog CA, McBean AM, Eggers PW, Collins AJ.
Chronic kidney disease and the risk for cardiovascular disease, renal
replacement, and death in the United States Medicare population, 1998 to 1999.
J Am Soc Nephrol 2005; 16:489-95.

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CKD Patients Are More Likely to Die


than to Progress to ESRD
5 year follow-up
GFR 15-29 N=27998

GFR 30-59 Died


RRT
Event Free
GFR 60-89; + Proteinuria Disenrolled

GFR 60-89, No
Proteinuria

0% 20 40 60 80 100
% % % % %
Keith, et al, Arch Int Med; 2004; 164:659-663

COSTS OF ESRD

• Depending on stage (compared to controls) pts


with CKD
– Had 1.9 to 2.5 times more prescriptions
– Had 1.3 to 1.9 times more outpatient visits
– were 1.6 to 2.2 times more likely to have had an
inpatient stay
– Had 1.8 to 3.1 more stays than did controls
• CKD pts had approximately double the costs of
control pts in this study
Smith DH, et al. J Am Soc Nephrol. 2004; 15: 1300-1306

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MORBIDITY & MORTALITY

• More than 50% of all death in ESRD pts are due


to CVD
• CKD is independently associated with an
increased rate of death from CVD
• The presence of CKD is associated with worse
outcomes after ACS & PCI

Go AS, et al. New Engl J Med. 2004; 351 (13): 1296-1305


Muntner P, et al. J Am Soc Nephrol. 2002; 13(3): 745-753
Wright RS, et al. Ann Intern Med. 2002; 137(7): 563-570
Best PJ, et al. J Am Coll Cardiol. 2002; 39(7): 1113-1119

MORBIDITY & MORTALITY

Go AS, et al. New Engl J Med 2004; 351 (13): 1296-1305

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CAUSE OF DEATH ON DIALYSIS

QUALITY OF LIFE
• Out of working day
– 2-3 x/week for going to HD center
– 3 x 1 x 5 hrs/day for exchanging dialysate
– 1-2 x/month for visiting doctor
– 3-6 x/year as an inpatient due to ESRD’s complications
• Associated with ESRD’s complications
– Anemia
– Ca-P disorders
– Hypertension
– Volume overload
– Infection on immunocompromised state
– CVD/CHF
– CVA
– Others

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PRIMARY PREVENTION OF CKD

EARLY DETECTION
• Screening for CKD risk factors
• Determine traditional & CKD-related
CVD risk factors
• Reduce CKD risk factors

PRIMARY PREVENTION OF CKD


• Adverse outcomes of CKD can often be prevented or
delayed through early detection and treatment.
• Earlier stages of CKD can be detected through routine
laboratory measurements.
• The presence of CKD should be established, based on
presence of kidney damage and level of kidney function
(GFR), also stage of CKD, irrespective of diagnosis;
according to the K/DOQI CKD classification

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EARLY DETECTION :
SCREENING & LOOKING FOR CAUSE OF CKD

• Who should be screened for CKD ?


• Why should we care?
• How do screen for CKD ?
• When do evaluate screening for CKD ?

Who should be screened for CKD ?

1. Everyone who gets  40 yrs old


2. Everyone who has CKD risk factors
• Traditional risk factors
• CKD-related CVD risk factors
• Risk factors of CVD
3. Everyone who gets CKD causes

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Who should be screened for CKD ?


Potential Risk Factors for Susceptibility to and Initiation of CKD
Clinical Factors Sociodemographic Factors
Diabetes mellitus Older age
Hypertension Ethnic : Afro-america, Indian, Hispanic,
Autoimmune diseases Asian/Pacific Islander
Urinary tract infections Exposure to certain chemical/ environmental
Urinary stones conditions
Lover urinary tract obstruction Low income / education
Neoplasia
Family history of CKD
Recovery from AKF
Reduction in kidney mass
Exposure to certain drugs
Obesity
Low birth weight

TRADITIONAL & CKD-RELATED FACTOR POTENTIALLY


RELATED TO AN INCREASED RISK FOR CVD

Traditional CVD risk factors CKD-related CVD risk factors


Older age Type of CVD
Male gender GFR 
White race Proteinuria
Hypertension RAA system activity
Diabetes Mellitus ECF volume overload
Tobacco user Abnormal Ca, P metabolism
LDL-C  Uremic, dyslipidemia
Physical inactivity Anemia
Menopause Malnutrition
Psychosocial stress Infection
Family history of CVD Thrombogenic factors
Hyperhomocysteinemia
K/DOQI – NKF, 2002 Oxidative stress
Chronic inflammatory state
Uremic toxin

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CAUSES OF CKD
• DM
• GNC
• Hypertension
• Glomerulonephritis primer
• Chronic UTI
• Obstruction (stones, malignancy, vesicouretero valve impaired
metastasis, cicatrix, iatrogenic, etc)
• Tubulointerstitial disease
• Polycystic disease
• Autoimmune disease (APS, lupus, etc)
• Chronic poisoning (lead Pb/Cd/Hg, drugs, antibiotic, traditional
medicine, chemotherapeutic, contrast, cell lysis syndrome, etc)
• Gout / hyperuricaemia
• NSAID
• Pre/eclamptia
• OTHERS

Cause of Chronic Kidney Disease


%

RSU Prof.Dr. R.D Kandou Manado Candra et al, Medika 2007


2002-2004
New pts with CKD
>13 yr old
N = 192
M= 126 (65.62%)
F = 66 (34.38%)

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WHY SHOULD WE CARE?

• The outcomes of pts with reduced GFR are uniformly


poor
• Pts with CKD are more likely to die than go onto dialysis
• Early recognition of CKD permits intervention to alter the
Natural History of the disease :
– Nephroprotection
– Cardio-vascular protection

Mortality Increase Exponentially as GFR Decrease

Go et al. NEJM 2004; 351: 1296-1305

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Patients with CKD are More Likely to Die than Go onto Dialysis

US Renal Data System. Am J Kidney Dis 2007; 49 (suppl I): S20

Nephroprotective Treatment :
more effective when started earlier

Paul E de Jong, Netherlands 2007

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How do screen for CKD?

• Blood pressure
• Urinalysis
• Dipstick for proteinuria, or microalbuminuria
• Kidney function test (creatinin, ureum, cystatin C, CCT)
• Kidney imaging (USG, IVP, CT, MRI, Renal study)
• Kidney biopsy

How do screen for CKD?


All Patients
Measurement of BP
SCr to eGFR
Protein-to-creatinine ratio or alb-to-creatinine ratio in a first-morning or random
untimed ”spot” urine specimen

Selected Patients, Depending on Risk Factors


USG : in pts with symptoms of urinary tract obstruction, infection or stone, or
family history of PKD
Serum electrolytes : Na, K, Cl, HCO3
Urinary concentration or dilution (SG or Osm)
Urinary acidification (pH)

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BLOOD PRESSURE
• Pts should be seated with their backs supported, arms bared & at
heart level
• Refrain from smoking or ingesting caffeine 30’ preceding the
measurement
• Start after at least 5’ of rest
• Appropriate cuff size: the bladder within the cuff should encircle at
least 80% of the arm
• Taken preferably with a mercury sphygmomanometer or
calibrated aneroid manometer or validated electronic device
• The 1st appearance of sound (phase 1) is used to define for SBP
& the disappearance of sound (phase 5) is used to define DBP
• 2 or more readings separated by 2 min should be averaged. If the
1st readings differ by more than 5 mm Hg; additional readings
should be obtained and averaged
• OR : 1st is discarded to ensure that pts is relaxed, & the mean of
2nd – 3rd readings is calculated

AMBULATORY BP MONITORING
• Useful in pts with apparent drug resistance, hypotensive
symptoms with antihypertensive drugs, episodic
hypertension.
• Seldom required & should not be used to delay appropriate
therapy
• BP tends to be higher in clinic than outside of the office
(white-coat hypertension)
• Ambulatory results are an average of 10/5 mm Hg lower
than office BP
• No agreement on upper limit of normal home BP; but
reading of 135/85 or greater should be considered elevated.
Definition HTN 140/90 or greater.
• Awake < 135/85 mm Hg and asleep 125/75 mm Hg.
majority; BP falls 10-20% during the night

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BLOOD PRESSURE

• In mild hypertension : reassessment 3 months later


• In moderate hypertension : reassessment 3-4 weeks
later
• In severe hypertension (>180/110 mm Hg) :
reassessment 2 weeks later and treatment started if this
level is sustained
• Immediate treatment is required in accelerated
hypertension (papilloedema, retinal haemorrhages and
exudates, acute cardiac complication (aortic dissection)

URINALYSIS
• Recommended collection of urine sampling :
– Mid stream urine
– Fresh urine (within 3 h)
– At the morning 30-60 min after the 1st mixture
• Examination
– Macroscopic : - Chemist reaction :
• Colour pH
• Smell protein/albumin
• Bubble glucose
• SG nitrite
– Microscopic :
• Cylinder/cast : hyalin, erythrocyte, leukocyte, epithel, broad
• Bacteria
• Crystals : cystine, tyrosine, leucin, sulfa
• Epithel
• Erythrocyte/leukocyte

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DEFINITION OF PROTEINURIA & ALBUMINURIA


KDOQI Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, Classification and Stratification
http:/www.kidney.org/professionals/KDOQI/guidelines_ckd/p4_class_g1.htm, accessed Oct 10, 2007

Urine collection Normal Micro Albuminuria or


methods albuminuria clinical proteinuria
Total 24 h excretion < 300 mg/d NA > 300 mg/d
Protein
Spot urine dipstick < 30 mg/dl NA > 30 mg/dl
Spot urine protein to < 200 mg/g NA > 200 mg/g
creat ratio
Albumin 24 h excretion < 30 mg/d 30 – 300 mg/d > 300 mg/d
Spot urine alb < 3 mg/dl > 3 mg/dl NA
specific dipstick
Spot urine alb to < 17 mg/g (m) 17 – 250 mg/g > 250 mg/g (m)
creat ratio < 25 mg/g (w) 25 – 355 mg/g > 355 mg/g (w)
Gender specific cut-off values are from a single study. Use of the same cut-off value
K/DOQI – NKF, 2002
leads to higher values of prevalence for women than men. Current recommendation from
ADA do the cut-off values for spo t urine alb-to- creat ratio for microalbuminuria and
albuminuriaas 30 and 300 mg/g respectively w/o regard to gender

DEFINITION OF PROTEINURIA & ALBUMINURIA


KDOQI Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, Classification and Stratification
http:/www.kidney.org/professionals/KDOQI/guidelines_ckd/p4_class_g1.htm, accessed Oct 10, 2007

Category Abnormal values


Normal
24-h excretion albumin < 30 mg/d
Microalbuminuria 30-300 mg/d
24-h excretion albumin/creatinine ratio > 2.5 mg/mmol cr
Clinical (overt) albuminuria > 300 mg/d
24-h excretion albumin/creatinine ratio > 3.5 mg/mmol cr
Clinical proteinuria > 300 mg/d
24-h excretion protein/creatinine ratio > 13.0 mg/mmol cr

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RENAL SURVIVAL AND PROTEINURIA

METHODS OF ESTIMATING GFR


1. Inulin/iothalamate clearance : GOLD STANDARD
2. Creatinine clearance (collect 24 h urine)
U.cr Vol. urine X 1,73
X
P.cr 1440 Koef
3. Equations base on SCr
(140 – age) x BW
1. Cockcroft-Gault :
72 x P.cr

2. MDRD : 186 x [Pcr]-1.154 x [age]-0.203


x [0.742 if female] x [1.212 if AfAm]

Note : women must be corrected by 85%


>18 yrs old uses Schwartz OR Counahan-Barratt

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SCr, CrCl & eGFR are not in PERFECT

§ Serum Creatinine alone CAN NOT be used to accurately


assess level of kidney function.
§ Serum creatinine is a function of production (muscle mass)
and excretion (both GFR and tubular secretion).
§ Age, sex, and lean body mass have to be taken into
account.
§ Estimations of eGFR (MDRD equation) and CrCl
(Cockcroft-Gault equation) were NOT developed in
subjects with normal renal function or normal health.

FACTORS AFFECTING SCr CONCENTRATION

Increase Decrease
Kidney disease Reduced muscle mass
Ketoacidosis Malnutrition
Ingestion of cooked meat Elderly age
Post trauma (mechanic, electric, thermal)
Drugs : Trimethoprim
Cimetidine
Flucytosine
PPI
Ketoconazol
Some cephalosporins

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GFR NORMALLY DECREASE WITH AGE

A significant proportion of >60 yrs old has eGFR <60 ml/min.

SCr is an Inadequate Screening Test for Renal


Failure in Elderly Patients

At what level of creatinine does a 65 yr old diabetic,


hypertensive woman with BW 50 kg have CKD?
NKDEP conducted a survey with 600 primary care providers.
77% said : creatinine > 1.5 mg/dl
GFR = 37 mL/min/1.73 m2
Ccreat= 30 mL/min

Creatinine > 1.0 mg/dl


GFR = 59 mL/min/1.73 m2

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COCKCROFT-GAULT EQUATION
TO PREDICT GFR

• Developed to predict creatinine clearance, thus an


overestimate of GFR
• Prediction based on age, gender, creatinine and ideal
body weight
• ClCr (cc/min) = [140-age] x BW/72 x SCr x [0.85 if female]

Used almost universally as the basis for drug dosing!

MDRD EQUATION TO PREDICT GFR

• Prediction based on age, gender, race and


serum creatinine. Developed to follow GFR
as part of the Modification of Diet in Renal
Disease (MDRD) study. Validated.
• GFR/1.73m2 = 186 x [Pcr]-1.154 x [age]-0.203 x
[0.742 if female] x [1.212 if AfAm]

http://www.kidney.org/professionals/KDOQI/gfr.cfm

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COCKCROFT-GAULT VS MDRD

§ The MDRD equation estimates GFR.


§ eGFR is given per 1.73m2 BSA
§ The Cockcroft-Gault equation estimates
CrCl.
§ CrCl is best used for drug dosing decisions
 drug dosing is usually indexed to CrCl.

When do evaluate screening for CKD ?

• When negative : (TREAT ON RISK FACTORS)


– every 1 yrs for pts with risk factor
– every gets systemic disorders
• When positive : (MANAGEMENT ON CKD)
– Re-evaluate for several times within 1-3 months
– Make diagnosis
– Do therapeutic

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PATIENTS SUFFER FROM KIDNEY DISEASE?

Find & reduce risk factor Determine Stage of CKD


Determine underlying cause
Identify risk factors for
progression
Identify comorbidites

STAGES IN PROGESSION OF CKD AND


THERAPEUTIC STATEGIES
COMPLICATION

NORMAL  RISK DAMAGE  GFR ESRD DEATH

Screening Diag & treat, RRT by dialysis


for CKD treat comorbid, or transplant
risk factor slow progression
CKD risk Estimate
reduction, progression,
screening treat complic,
for CKD prepare for RRT

PRIMARY PREVENTION SECONDARY PREVENTION TERTIARY PREVENTION

K/DOQI – NKF, 2002

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EARLY TREATMENT ON RISK FACTORS

Interventions proven to be effective include:


1. Strict glucose control in diabetes;
2. Strict blood pressure control;
3. ACEI and ARBs

Interventions that may be effective, but studies


are inconclusive, include:
1. Dietary protein restriction;
2. Dietary callory restriction;
3. Lipid-lowering therapy;
4. Partial correction of anemia.

EARLY TREATMENT ON RISK FACTORS

Attempts should be made to prevent acute renal failure:

1. Volume depletion;
2. IV contrast;
3. Some antibiotics : aminoglycosides & amphotericin B;
4. NSAIDs, including COX 2 inhibitors;
5. Other drugs: ACEI, ARBs, calcineurin inhibitors
6. Obstruction.

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SLOWING PROGRESSION
DO EARLIER… GET BETTER

DIABETES MELLITUS

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DIABETIC EVOLUTION

STRICT GLYCEMIC CONTROL

• 80% Type I DM with microalbuminuria


develop DN in 10-15years, 50% to ESRD
– DCCT, benefit of tight control in reducing
occurrence subclinical and overt DN(40-60%)

• 20-40% Type II DM with microalbuminuria


develop DN, 20% to ESRD
– UKPDS 33, 25% reduction in microvascular
events
– Kumamoto
– Steno Type 2, 73% reduction in clinical proteinuria

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CRITERIA OF DIABETES CONTROL

Good Moderate Worse


Fasting blood glucose (mg/dL) 80 – 109 110 – 125 ≥ 126
2 h post prandial blood glucose 110 – 144 145 – 179 ≥ 180
A1C (%) < 6.5 6.5 – 8 >8
Total cholesterol (mg/dL) < 200 200 – 239 ≥ 240
LDL-C (mg/dL) < 100 100 – 129 ≥ 130
HDL-C (mg/dL) > 45
Triglyceride (mg/dL) < 150 150 – 199 ≥ 200
IMT (kg/m2) 18.5-22.9 23 – 25 > 25
Blood pressure (mmHg) < 130/80 130-140/80-90 > 140/90
Recommended : A1c < 7 ADA, 2002

H
Y
P
E
R
T
E
N
S
I
O
N

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CLASSIFICATION OF BOOD PRESSURE


FOR ADUTS AGED 18 YRS OR OLDER
Hypertension is defined as blood pressure 140/90 mmHg
JNC 6 1997, WHO-ISH 1999, ESH/ESC 2003,
ESH/ESC 2007 JNC 7 2002

Category Systolic Diastolic Systolic Diastolic Category

Optimal < 120 < 80 < 120 < 80 Normal


Normal < 130 < 85
High-normal 130 -139 85 – 89 120 - 139 80 -89 Prehypertension
Borderline hypertens 140 - 149 90 – 94 140 - 159 90 - 99 Stage I
Grade I (mild) 140 - 159 90 – 99
Grade 2 (moderate) 160 - 179 100 – 109 ≥ 160 ≥ 100 Stage II
Grade 3 (severe) ≥ 180 ≥ 110
Isolated systolic >140 < 90 >140 < 90 Isolated systolic
hypertension hypertension
Subgroup borderline > 140 < 90

2007 Guidelines for the management of


arterial hypertension

European Heart Journal (2007) 28, 1462–1536

The Task Force for the Management of Arterial


Hypertension of the European Society of
Hypertension (ESH) and of the European Society of
Cardiology (ESC)

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Definitions & Classification of BP Levels


Category Systolic Diastolic
Optimal <120 and <80
Normal 120–129 and/or 80–84
High normal 130–139 and/or 85–89
Grade 1 hypertension 140–159 and/or 90–99
Grade 2 hypertension 160–179 and/or 100–109
Grade 3 hypertension >180 and/or >110
Isolated systolic hypertension >140 and <90
Isolated systolic hypertension should be graded (1 ,2,3) according to systolic blood pressurevalues in the ranges indicated,
provided that diastolic values are <90 mmHg. Grades 1 , 2and 3 correspond to classification in mild, moderate and
severe hypertension, respectively. These terms have been now omitted to avoid confusion with quantification
of total cardiovascular risk.

TARGET ON BLOOD PRESSURE LEVEL

Chobanian AV, et al. JAMA 2003; 289: 2560-2571


American Diabetes Association. Diabetes Care 2002; 25: 134-147
National Kidney Foundation. Am J Kidn Dis 2002; 39 (suppl 1): S1-S266

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Clinical Practice Guidelines for


Management of Hypertension in CKD

Type of Kidney Disease Blood Pressure Preferred Agents Other Agents


Target for CKD, with or to Reduce CVD Risk
(mm Hg) without and Reach Blood
Hypertension Pressure Target
Diabetic Kidney Disease

ACE inhibitor Diuretic preferred, then


Nondiabetic Kidney Disease or ARB BB or CCB
with Urine Total Protein-to-
Creatinine Ratio 200 mg/g
<130/80
Nondiabetic Kidney Disease Diuretic preferred, then
with Spot Urine Total Protein- ACE inhibitor, ARB, BB
to-Creatinine ratio <200 mg/g None preferred or CCB
Kidney Disease in Kidney CCB, diuretic, BB, ACE
Transplant Recipient inhibitor, ARB

TREATMENT OF HYPERTENSION
Life style modification

Not at Goal BP
(<140/90 mmHg for those with DM or CKD)

Initial drug choices

Hypertension without Hypertension with


compelling indications compelling indications

Stage 1
Stage 2
Thiazide type diuretics
2 drugs combination Drugs for compelling
Consider ACE-I, ARB,
for most indication
BB, CCB or combination

Not at Goal BP

Optimize dosages or
JNC VII. JAMA 2003;289:2560-2572
add additional drugs

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INTERVENTIONS TO DELAY PROGRESSION


OF CKD : ACE-I AND ARBs

• Mechanisms
– Lower systemic blood pressure
– Lower glomerular capillary blood pressure and
protein filtration
– Reduce AT II mediated cell proliferation and
fibrosis

Should be employed in all proteinuric kidney disease !!!

INTERVENTIONS TO DELAY PROGRESSION


OF CKD : ACE-I AND ARBs

• Diabetic Kidney Disease


– ACEI or ARB in all diabetic patients with microalbuminuria
– ACEI (alt ARB) in Type 1 Diabetics with macroalbuminuria
– ARB (alt. ACEI) in Type 2 Diabetics with macroalbuminuria

• Nondiabetic Kidney Disease


– ACEI/ARB recommended in all proteinuric (>200 mg/g Cr on spot
urine) patients with CKD
– May tolerate creatinine rise of 35% above baseline
– <130/80 is goal
– 3 or more drugs may be required! One will probably be a diuretic
(thiazide first, then loop)
– ACEI and ARB may be used in combination
KDOQI 2002, 2006
JNC 7, 2003

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SUMMARY
• As most cases with CKD even though
ESRD are not known by physicians, so…
we need active detect subjects at risk in
an early phase.
• Such screening is needed as it enables
early prevention not only of progressive
CKD; but also of progressive CVD.
• Screening for albuminuria and eGFR is
simple, cheap and important things.

SUMMARY
• Screening for albuminuria helps to detect
subjects at risk of progression CKD & CVD; but
also subjects at risk for new DM and new HTN
• Albuminuria :
– stage 1 & 2 CKD is presented in 5-6% of the general
population
– stage 3 is presented in another 4-5% of the general
population
• Screening for stage 3 CKD helps to detect
subjects at risk of CVD.

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SUMMARY
• Screening for albuminuria and early
treatment of those found positive is cost
effective to prevent CKD and also CVD.
• Lowering albuminuria helps to prevent
progressive CKD & CVD in general
population.

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