K13-Kuliah CKD

Chronic Kidney Disease
Dr H Adhi Permana, SpPD

RSMP/FK MUHAMMADIYAH
PALEMBANG
Outline
 Definition
 Screening
 Patophysiology CKD
 Equation for CKD
 Diagnosis
 Management CKD
Definition
Defining “CKD”
 Kidney damage for ≥ 3 months, defined by

structural or functional abnormalities of the
kidney, with or without decreased GFR, manifest
by either
 Pathologic abnormalities, or
 Markers of kidney damage, such as abnormalities of
the blood or urine, or in imaging tests (but NOT
HTN).
 GFR < 60 mL/min/1.73 m2 for ≥ 3 months with
or without kidney damage.
Defining “Kidney Damage”
 Pathologic Abnormalities?
 By Radiology (US, 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)
Screening
Who should we screen?
How should we screen?
Patophysiology CKD
PROGRESSIVE RENAL DAMAGE:
The Final Common Pathway
RENAL INJURY
Reduction in nephron mass
Glomerular capillary hypertension
Increased glomerular permeability

Increased BP
to macromolecules
Increased filtration of plasma proteins

Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
RENAL SCARRING
Pathogenic Mechanisms of High Blood
Pressure in CKD
 Pre-existing essential hypertension
 Extracellular fluid volume expansion
 Renin-agniotensin aldosterone system stimulation
 Increased sympathetic activity
 Alteration in endothelium-derived factors(NO/endothelin)
 Increased body weight
 Erythropoietin administration
 PTH secretion/hypercalcemia
 calcified arterial tree
 renal vascular disease and renal artery stenosis
Equation for CKD
Serum Creatinine, CrCl, and eGFR--
Nothing is Perfect!
 Serum Creatinine alone CAN NOT be used to
accurately assess level of kidney function.
 S. 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 Serum Creatinine
Concentration
Increase Decrease
 Kidney Disease  Reduced Muscle Mass
 Ketoacidosis  Malnutrition
 Ingestion of cooked meat
 Drugs:
 Trimethoprim
 Cimetidine
 Flucytosine
 Some cephalosporins
Remember….
GFR normally decreases with age!
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 IBW/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]
Get it at
http://www.kidney.org/professionals/KDOQI/gfr.cfm
TA-DA!
(Your on-line link to the MDRD GFR
calculator)
http://www.kidney.org/professionals/KDOQI/gfr.cfm
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.
American Journal of Kidney Diseases 2014 63, 713-735DOI: (10.1053/j.ajkd.2014.01.416)
Copyright © 2014 Terms and Conditions
Diagnosis
Patient meets definition of Chronic
Kidney Disease?
YES NO
Determine Stage of CKD Risk Factor Reduction

Determine underlying cause
Identify risk factors for
progression
Identify comorbidites
A Simple Laboratory Evaluation!
Simplified Classification of CKD by
Diagnosis
 Diabetic Kidney
Disease
 Nondiabetic Kidney
Disease  Glomerular disease
 autoimmune, sytemic infections,
drugs, neoplasia, idiopathic
 Vascular disease
 ischemic renal disease, hypertensive
nephrosclerosis, microangiopathy
 Tubulointerstitial disease
 UTO, stones, UTI, drug toxicity
 Cystic disease
 Post-Transplant
Differential Diagnosis of Chronic
Kidney Disease
 Everyone deserves a diagnosis!
 This is especially true for Stage 1 or 2 CKD!
 When in doubt, consult a nephrologist!
 Initial evaluation will guide further diagnostics,
decisions about renal biopsy and often decisions
about treatment and prognosis.
Management CKD
So Now What Do You Do?
(There’s a lot you can do!)
Primary Goals of CKD Care
• To prevent cardiovascular events and death
• Heart Attacks
• Congestive Heart Failure
• Sudden Cardiac Death
• Stroke
• To prevent the progression of CKD to Kidney
Failure or ESRD
• To prevent complications of CKD
• To prepare for dialysis/transplantation in a timely
manner
Management of Patients with Chronic
Kidney Disease
E a r ly D e t e c t io n o f C K D
I n t e r v e n t io n s t h a t d e la y p r o g r e s s io n P r e v e n t io n o f U r e m ic C o m p lic a t io n s M o d ifc a t io n o f C o m o r b id it y P r e p a r a t io n fo r R e n a l R e p la c e m e n t T h e r a p y
( G F R < 6 0 c c / m in / 1 . 7 3 m 2 ) ( G R F < 3 0 c c / m in / 1 . 7 3 m 2 )
A C E I n h ib it o r s A n e m ia C a r d io v a s c u la r D is e a s e E d u c a t io n
A n " E S R D C lin ic "
ARBs O s te o d y s tro p h y K id n e y T r a n s p la n t E v a lu a t io n C h o ic e o f D ia ly s is M o d a lit y
B P C o n tro l M a ln u t r it io n P r e - e m p t iv e T r a n s p la n t a t io n T im e ly D ia ly s is A c c e s s P la c e m e n t
B lo o d g lu c o s e c o n t r o l R e d u c e d F u n c t io n in g a n d W e ll- b e in g T im e ly D ia ly s is I n it ia t io n
GUIDELINE 13. LOSS OF KIDNEY FUNCTION IN CKD
Interventions to slow the progression should be considered in all patients with CKD
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. Lipid-lowering therapy;
3. Partial correction of anemia.
Attempts should be made to prevent acute renal failure:
•Volume depletion;
•IV contrast;
•Some antibiotics (for example, aminoglycosides and amphotericin B);
•NSAIDs, including COX 2 inhibitors;
•Other drugs: ACEI, ARBs, calcineurin inhibitors
•Obstruction.
eGFR should be obtained at least yearly in CKD, and more often in patients with:
•GFR <60 mL/min/1.73 m2;
•Fast GFR decline in the past
•Risk factors for faster progression;
•Ongoing treatment to slow progression;
•Exposure to risk factors for acute GFR decline.
Slowing Progression
The Earlier, the Better…
Interventions that delay progression of
CKD: ACEI 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 diseases!
PROGRESSIVE RENAL DAMAGE:
The Final Common Pathway
RENAL INJURY
ACEI Reduction in nephron mass

ARB
Glomerular capillary hypertension
Increased glomerular permeability

Increased BP ACEI
to macromolecules ARB
Increased filtration of plasma proteins
Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
ACEI
RENAL SCARRING
ARB
Interventions that delay progression
of CKD: ACEI and ARBs
 Diabetic Kidney Disease
 ACEI or ARB in all diabetic patients with microalbuminuria
 ACEI (alt ARB) for 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 Guideline 8, Table 110
-JNC 7, 2003
http://www.nhlbi.nih.gov/guidelines/hypertension/express.pdf
Controlling Hypertension
GUIDELINE 7. ASSOCIATION OF LEVEL OF GFR WITH
HYPERTENSION
-HTN is both a cause and a complication of CKD.

-HTN may develop early during the course of CKD and is
associated with adverse outcomes—in particular, faster loss of
kidney function and development of CVD.
-Blood pressure should be closely monitored in all patients with
chronic kidney disease.
-Treatment of high blood pressure in CKD should include
specification of target BP levels, nonpharmacologic therapy,
and specific antihypertensive agents for the prevention of
progression of kidney disease and development of
cardiovascular disease.
Recommendations for Controlling HTN in
Non-Diabetic CKD
Population BP Goal Nondrug Rx Drug RX
CKD + >200mg/g <130/80 Reduce salt ACEI/ARB

Prot/Cr Ratio BMI≤25 kg/m2 Then diuretic
Mod EtOH Then BB or CCB
Stop Smoking
Exercise
CKD + no proteinuria <130/80 Same Thiazide/Loop
Then ACEI/ARB
Then BB or CCB
KDOQI Table 118, Guideline 9

Kidney Disease
Anemia and CKD
• Anemia usually develops during the course of chronic
kidney disease and may be associated with adverse
outcomes.
• Anemia is one of the modifiable complications of CKD .
• All individuals with hemoglobin (Hb) levels lower than
physiologic norms are considered anemic.
 Erythropoietin deficiency is the primary cause of anemia of CKD.
 The NKF recommends that evaluation for anemia should occur
when GFR <60 mL/min/1.73 m2; measurement should include
Hb level.
 Anemia should be treated according to the K/DOQI TM guidelines
for anemia of CKD.
K/DOQI: Evaluation and Management of
Anemia
 For Adults with ≥ Stage 3 CKD:
 Assess Hemoglobin level
 If anemia (HgB ≤ 12)
 RBC indices/CBC
 Reticulocyte count
 Iron studies
 Test for occult GI bleeding as indicated
 Medical evaluation of comorbid conditions
 Erythropoetin levels are usually NOT indicated.
Prevention of Uremic Complications:
Anemia Therapy
 Subcutaneous administration of erythropoietin
once to thrice weekly (sometimes less).
 Supplemental oral or IV iron to keep ferritin >
100 and iron saturation >20%.
 Monthly monitoring of Hgb, iron stores.
 Monthly adjustments in EPO dose and
frequency to meet target Hgb 11-12 g/dl
(HCT 33-36%).
GUIDELINE 10. ASSOCIATION OF LEVEL OF GFR WITH
BONE DISEASE AND DISORDERS OF CALCIUM AND
PHOSPHORUS METABOLISM
•Bone disease and disorders of calcium and phosphorus

metabolism develop during the course of chronic kidney
disease and are associated with adverse outcomes.
-Patients with GFR <60 mL/min/1.73 m2 should be evaluated for
bone disease and disorders of calcium and phosphorus
metabolism.
-Patients with bone disease and disorders of bone metabolism
should be evaluated and treated—see K/DOQI Clinical Practice
Guidelines on Bone Metabolism and Disease in Chronic Kidney
Disease (October, 2004).
Osteodystrophy Therapy
 Restrict dietary phosphorus to 800-
1,000 mg/d
 Calcium-based phosphate binders (but
not with Vit D!) to combat hypocalcemia
and bind phosphorus
 Assure repletion of Vitamin D 25
 Avoid acidosis, HCO3> 23 mEq/l
Malnutrition
 Contributors to protein-energy
malnutrition(PEM) in CKD:
 low protein and calorie intake
 metabolic acidosis
 resistance to insulin, GH, IGF-1
 proinflammatory cytokines
 Assessment of nutritional status requires
multiple markers to assess protein status, fat
stores, body composition and dietary protein
and energy intake.
Nutrition Guidelines
 Protein intake
 0.75g/kg/d (RDA)
 GFR < 25 cc/min(Stages 4-5) consider 0.6g/kg/d
 Energy intake
 RDA depends on energy expenditure
 GFR < 25 cc/min(Stages 4-5) 30-35kcal/kg/d
 Patients with less than recommended intake
need frequent follow-up of nutritional status
Kidney Disease
The most common cause of death among
ESRD patients is CVD
Fig 5. Causes of death among period prevalent patients 1997–1999, treated

with hemodialysis, peritoneal dialysis, or kidney transplantation. Data are from
the USRDS 2001 Annual Data Report (www.usrds.org). Abbreviations: MI,
myocardial infarction; HD, heart disease.
Management of Dyslipidemia in CKD
http://www.kidney.org/professionals/KDOQI/guidelines_lipids/index.htm
Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Executive
Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel
on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel
III). JAMA, 2001, 285;2486-2497.
Kidney Disease
When to Refer!
 Consider co-management with a nephrologist if the
clinical action plan cannot be carried out.
 Consider subspecialty referral when*:
 Unexplained proteinuria (>1gm/day) or microalbumin/Cr ratio
>250mg albumin/gCr
 Unexplained macroscopic or microscopic hematuria
 Diabetes and macroalbuminuria
 Multiple and recurring kidney stones
 Rapidly deteriorating kidney function
 Difficult to control hypertension
 Refer to a nephrologist when GFR <30 mL/min/1.73
m2 (CKD Stages 4-5)!
Mandatory Referral to Nephrologist guideline, Niagara Health Quality Coalition, NY

Preparation for Renal Replacement
Therapy
(GFR < 30cc/min/1.73m2)
 Referral to a Nephrologist allows:
 Early identification of RRT modality.
 Evaluation for kidney transplantation with goal of
pre-emptive transplantation.
 REMEMBER, in eligible patients transplantation
confers a survival advantage over dialysis!
 Identification of social, functional or nutritional
needs.
Preparation for Renal Replacement
Therapy
(GFR < 30cc/min/1.73m2)
 Close coordination between PCM and
nephrologist allows:
 Timely placement of dialysis access
 Timely initiation of dialysis
 Timely referral for transplant evaluation
with preemptive transplant if possible.
Conclusions
 CKD is a public health problem with poor
outcomes and high cost. CKD is
underdiagnosed and undertreated in the U.S.
 Early CKD detection and intervention may
increase opportunities for the prevention of
ESRD and of complications of CKD, including
death.
Thank You

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Chronic Kidney Disease

Dr H Adhi Permana, SpPD

 Kidney damage for ≥ 3 months, defined by

 Markers of Kidney Damage?

Reduction in nephron mass

Glomerular capillary hypertension

Increased glomerular permeability

Increased filtration of plasma proteins

Excessive tubular protein reabsorption

 Used almost universally as the basis for drug

Determine Stage of CKD Risk Factor Reduction

ARBs O s te o d y s tro p h y K id n e y T r a n s p la n t E v a lu a t io n C h o ic e o f D ia ly s is M o d a lit y

Interventions proven to be effective include:

Should be employed in all proteinuric

ACEI Reduction in nephron mass

Increased glomerular permeability

Excessive tubular protein reabsorption

-HTN is both a cause and a complication of CKD.

Population BP Goal Nondrug Rx Drug RX

CKD + >200mg/g <130/80 Reduce salt ACEI/ARB

KDOQI Table 118, Guideline 9

ARBs O s te o d y s tro p h y K id n e y T r a n s p la n t E v a lu a t io n C h o ic e o f D ia ly s is M o d a lit y

•Bone disease and disorders of calcium and phosphorus

ARBs O s te o d y s tro p h y K id n e y T r a n s p la n t E v a lu a t io n C h o ic e o f D ia ly s is M o d a lit y

Fig 5. Causes of death among period prevalent patients 1997–1999, treated

ARBs O s te o d y s tro p h y K id n e y T r a n s p la n t E v a lu a t io n C h o ic e o f D ia ly s is M o d a lit y

Mandatory Referral to Nephrologist guideline, Niagara Health Quality Coalition, NY

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