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Chronic Kidney Disease

RIZKI ALIANA AGUSTINA


Goals and Objectives
Review the K/DOQI definition and
classification of chronic kidney disease
(CKD)
Review the prevalence and causes of
CKD in the US.
Understand the primary evaluation and
management of patients with CKD.
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
GFR < 60 mL/min/1.73 m
2
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 for proteinuria
Urine dipstick for protein

Negative
Positive
(Urine protein >300mg/l)
On 2 separate occasions
(exclude other causes)
Overt Nephropathy
Quantify excretion rate
24HUP
3-6 monthly follow-up of
microalbuminuria
Optimise glycaemic control
Strict Bp control
ACE/ARB
Stop smoking
Lifestyle modification
Treat hyperlipidaemia
Avoid excessive protein intake
Monitor renal function
Monitor other endorgan
damage
Screen for
Microalbuminuria
(on early morning spot urine)
Negative
Yearly test
Positive
Retest twice in 3-6/12
Exclude other cause
If 2 of test are positive
Diagnosis of microalbuminuria
Is established
Significance of proteinuria
A dominant risk factor for deterioration of
renal failure (besides HT)

Marker of Increased Risk for CV mortality
and morbidity (DM & non-DM)
e.g. Microalbuminuria is associated with a 100-
150% increase in death rate
(Mogensen CE, New Eng. J. Med 1984;310:310-60)
Evaluation of Symptomatic Haematuria
Detection of Microscopic hematuria
>5RBC/hpf or +ve dipstik test
Primary care investigation
History
Examination
Renal function
Urine microscopy and culture
Consider Urological referral
Exclude benign causes :
Menstruating women
Women with UTI
False +ve result
Recent strenous exercise
Sexual activity, viral illness,trauma etc
Proteinuria
Red cell cast/dysmorphic red blood cells
Renal Impairment
Nephrological referral

Isolated microscopis,
hematuria and age > 40
yricroscopic
haematuria and age
>40 years
Pathophysiology
Repeated injury to kidney

Symptoms
Hematuria
Flank pain
Edema
Hypertension
Signs of uremia
Lethargy and fatigue
Loss of appetite
If asymptomatic may have elevated serum
creatinine concentration or an abnormal
urinalysis

Risk Factors
Age of more than 60 years
Hypertension and Diabetes
Responsible for 2/3 of cases
Cardiovascular disease
Family history of the disease.
Race and ethnicity
Highest incidence is for African Americans
Hispanics have higher incidence rates of ESRD
than non-Hispanics.


NKF-K/DOQI Stages of CKD
Stage Description GFR
(mL/min/1.73m2
)
1 Kidney damage with
normal or GFR
> 90
2 Mild GFR 60-89
3 Moderate GFR 30-59
4 Severe GFR 15-29
5 Kidney Failure < 15 or dialysis
Primary Care
Focus is here!
Prevalence of CKD by GFR in the USA
(There is a lot of CKD!)
Stage Description GFR
(mL/min/1.73m2)
Prevalence Prevalence
(%)
1 Kidney damage
with normal or
GFR
> 90 5.9 million 3.3%
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
Causes of ESRD in the USA:
Prevalent Counts and Adjusted
Rates by Primary Diagnosis
2006 ADR: USRDS
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.

So what do we do about this?
Chronic Kidney Disease
In 1999, the NKF approved a proposal for K/DOQI,
Kidney Disease Outcomes Quality Initiative (an
evolution of the DOQI (Dialysis Outcomes Quality
Initiative).
The purpose was to develop clinical practice
guidelines for the spectrum of kidney diseases.
In February 2002, Clinical Practice Guidelines for
Chronic Kidney Disease (CKD): Evaluation,
Classification, and Stratification were published.
Find the KDOQI guidelines at
http://www.kidney.org/professionals/KDOQI/
Guideline 1. Definition and Stages of
Chronic Kidney Disease
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 (glomerular filtration rate [GFR]),
irrespective of diagnosis.
Among patients with CKD, the stage of disease
should be assigned based on the level of kidney
function, irrespective of diagnosis, according to the
K/DOQI CKD classification
Who should we screen?
How should we screen?
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.
I ncrease Decrease
Factors Affecting Serum Creatinine
Concentration
Kidney Disease
Ketoacidosis
Ingestion of cooked meat
Drugs:
Trimethoprim
Cimetidine
Flucytosine
Some cephalosporins
Reduced Muscle Mass
Malnutrition
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
Cl
Cr
(cc/min) = [140-age] x IBW/72 x S
Cr
x [0.85 if
female]

Used almost universally as the basis for drug
dosing!

Get it at
http://www.kidney.org/professionals/KDOQI/gfr.cfm
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/1.73m
2
= 186 x [P
cr
]
-1.154
x [age]
-0.203
x
[0.742 if female] x [1.212 if AfAm]
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 1.73m
2
BSA
The Cockcroft-Gault equation estimates
CrCl.
CrCl is best used for drug dosing decisions--
drug dosing is usually indexed to CrCl.
Comparing the Cockcroft-Gault and MDRD:
Do these patients have the same level of renal
function?
20 year old AfAm Washington Redskins tackle, weighing 144 kg
with a S
Cr
1.2 mg/dl?
Cl
Cr
=[140-20][144]/72 x [1.2] =200 cc/min
93 year old Caucasian female nursing home resident, weighing
44 kg with a S
Cr
1.2 mg/dl.
Cl
Cr
= [140-93][44]/72 x [1.2] x 0.85 = 20 cc/min
MDRD GFR Value:99 mL/min/1.73 m2
MDRD GFR Value:45 mL/min/1.73 m2
YES NO
Risk Factor Reduction
Determine Stage of CKD
Determine underlying cause
Identify risk factors for
progression
Identify comorbidites
Patient meets definition of Chronic
Kidney Disease?
Tools for Determining the Cause of
Chronic Kidney Disease
CKD is often silent. Assessment relies on
laboratory testing and imaging.
A Good History! ROS, existence of chronic
diseases (DM, HTN, CHF, cirrhosis),
medication review, accurate PMH and FH of
kidney disease.
Helpful Physical Examination! BP, evidence of
co-morbid conditions and complications of
CKD.
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.

So Now What Do You Do?
(Theres a lot you can do!)
CKD Clinical Action Plan On-Line
http://www.kidney.org/professionals/kdoqi/cap/index.html
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
Clinical Action Plan
A Clinical Action Plan should be developed for each patient,
based on the stage of CKD (see Table 33).
Patients with CKD should be evaluated to determine:
Diagnosis
Comorbid Conditions
Severity, assessed by level of kidney function
Complications, related to level of kidney function
Risk for loss of kidney function
Risk for cardiovascular disease
Review of medications should be performed at all visits.
Self-management behaviors should be incorporated into the
treatment plan at all stages of chronic kidney disease.
Management of Patients with Chronic
Kidney Disease
Blood glucose control
BP Control
ARBs
ACE Inhibitors
Interventions that delay progression
Reduced Functioning and Well-being
Malnutrition
Osteodystrophy
Anemia
Prevention of Uremic Complications
(GFR < 60 cc/min/1.73 m2)
Cardiovascular Disease
Modifcation of Comorbidity
Pre-emptive Transplantation
Kidney Transplant Evaluation
Timely Dialysis Initiation
Timely Dialysis Access Placement
Choice of Dialysis Modality
Education
An "ESRD Clinic"
Preparation for Renal Replacement Therapy
(GRF < 30 cc/min/1.73m2)
Early Detection of CKD
RENAL INJURY
Reduction in nephron mass
Glomerular capillary hypertension
Increased glomerular permeability
to macromolecules
Increased filtration of plasma proteins
Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
RENAL SCARRING
PROGRESSIVE RENAL DAMAGE:
The Final Common Pathway
Increased BP
Nonmodifiable Modifiable
Patient characteristics associated
with increased rate of GFR decline
African American
race
Male gender
Older age
Lower baseline level
of kidney function



Higher level of
proteinuria
Higher BP
Poor glycemic
control
Smoking


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!
Measuring ProteinuriaGet into the right spot!
When you get to this point,
Dont continue to get microalbumin!
RENAL INJURY
Reduction in nephron mass
Glomerular capillary hypertension
Increased glomerular permeability
to macromolecules
Increased filtration of plasma proteins
Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
RENAL SCARRING
PROGRESSIVE RENAL DAMAGE:
The Final Common Pathway
Increased BP
ACEI
ARB
ACEI
ARB
ACEI
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

-HTN is both a cause and a complication of CKD.
-HTN may develop early during the course of CKD and is
associated with adverse outcomesin 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.

Controlling Hypertension
GUIDELINE 7. ASSOCIATION OF LEVEL OF GFR WITH
HYPERTENSION

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
Relationship between BP and progression of diabetic nephropathy.
BP, albumin excretion rate, and GFR in patients with type 1 DMs randomly assigned to a
reduction in MAP of 10 mm Hg using metoprolol at 100 to 400 mg/d, hydralazine at 50 to
200 mg/d, and furosemide at 80 to 500 mg/d versus no antihypertensive therapy. Solid
circles represent the treated group. Open circles represent the control group. Vertical lines
represent standard error. Study was stopped earlier in the control group because of faster
decline in GFR. Reprinted with permission.
253


BP vs. Time
Controls
AER vs. Time
GFR vs. Time
Controls
Controls
Controls
Relationship between MAP and GFR decline (Non-diabetic Pts).
Mean GFR decline and achieved follow-up BP in MDRD Study A (patients with
baseline GFR 25 to 55 mL/min/1.73 m
2
). Regression lines relating the estimated
mean GFR decline over 3 years to mean follow-up MAP for groups of patients
defined according to baseline proteinuria. Within each group, a 3-slope model
was used with break points at 92 and 98 mm Hg. Reprinted with permission.
255

Nephrotic
JNC-7 recommends a goal blood pressure of
<130/80 mm Hg for individuals with high blood
pressure and CKD.

http://www.nhlbi.nih.gov/guidelines/hypertension/express.pdf
Population BP Goal Nondrug Rx Drug RX

CKD + >200mg/g <130/80 Reduce salt ACEI/ARB
Prot/Cr Ratio BMI25 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
Recommendations for Controlling HTN in
Non-Diabetic CKD
KDOQI Table 118, Guideline 9
Interventions that delay progression
of CKD: 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
Interventions that delay progression
of CKD: Strict Glycemic Control
Recommended Therapy:
HgbA
1c
< 7%
Additional information in 2001 ADA Clinical
Practice Guidelines
www.diabetes.org/clinicalrecommendations/Supplem
ent101/S3.htm


Management of Patients with Chronic
Kidney Disease
Blood glucose control
BP Control
ARBs
ACE Inhibitors
Interventions that delay progression
Reduced Functioning and Well-being
Malnutrition
Osteodystrophy
Anemia
Prevention of Uremic Complications
(GFR < 60 cc/min/1.73 m2)
Cardiovascular Disease
Modifcation of Comorbidity
Pre-emptive Transplantation
Kidney Transplant Evaluation
Timely Dialysis Initiation
Timely Dialysis Access Placement
Choice of Dialysis Modality
Education
An "ESRD Clinic"
Preparation for Renal Replacement Therapy
(GRF < 30 cc/min/1.73m2)
Early Detection of CKD
When to Expect Complications
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 m
2
; 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%).

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 m
2
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 treatedsee K/DOQI Clinical Practice
Guidelines on Bone Metabolism and Disease in Chronic Kidney
Disease (October, 2004).

GUIDELINE 10. ASSOCIATION OF LEVEL OF GFR WITH
BONE DISEASE AND DISORDERS OF CALCIUM AND
PHOSPHORUS METABOLISM
Prevention of Uremic Complications:
Osteodystrophy
Osteitis fibrosis cystica, due to 2
o
HPT, is
major form of bone disease.
Check indices of bone and mineral
metabolism at GFR < 60 cc/min/1.73m
2:
iPTH the earliest marker
Hypocalcemia, hyperphosphatemia
Phosphorus control is cornerstone of treatment

Prevention of Uremic Complications:
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, HCO
3
> 23 mEq/l



Management of
Renal
Osteodystrophy
is Very
Complex!
http://www.kidney.org/profess
ionals/KDOQI/guidelines_bo
ne/index.htm
Protein energy malnutrition develops during the course of chronic kidney
disease and is associated with adverse outcomes. Low protein and calorie
intake is an important cause of malnutrition in chronic kidney disease.
Patients with GFR <60 mL/min/1.73 m
2
should undergo assessment of
dietary protein and energy intake and nutritional status:
Guideline 23. Panels of Nutritional Measures for Nondialyzed Patients:
"For individuals with CRF (GFR <20 mL/min) protein-energy
nutritional status should be evaluated by serial measurements of a panel of
markers including at least one value from each of the following clusters:
(1) Serum albumin;
(2) Edema-free actual body weight, percent standard (NHANES II)
body weight, or subjective global assessment (SGA); and
(3) Normalized protein nitrogen appearance (nPNA) or dietary
interviews and diaries. (Evidence and Opinion)"
Guideline 26. Intensive Nutritional Counseling for Chronic Renal
Failure: "The nutritional status of individuals with CRF should be
monitored at regular intervals."
GUIDELINE 9. ASSOCIATION OF LEVEL OF GFR WITH
NUTRITIONAL STATUS
Prevention of Uremic Complications:
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.
Prevention of Uremic Complications:
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
Prevention of Uremic Complications:
Just a Word About Immunizations
Dont forget to continue routine immunizations, e.g.
Tetanus
Pneumococcus
Influenza
Hepatitis B
Check for immunity first--ie, hepatitis B sAb, sAg, cAb
Those who are immune or have chronic infection do not
need the vaccine.
All others should receive the vaccine. Dont wait for dialysis!
Patients with advanced chronic kidney disease are less likely
to gain immunity from the vaccine. Consider for all Stage 3
or greater CKD patients!
Management of Patients with Chronic
Kidney Disease
Blood glucose control
BP Control
ARBs
ACE Inhibitors
Interventions that delay progression
Reduced Functioning and Well-being
Malnutrition
Osteodystrophy
Anemia
Prevention of Uremic Complications
(GFR < 60 cc/min/1.73 m2)
Cardiovascular Disease
Modifcation of Comorbidity
Pre-emptive Transplantation
Kidney Transplant Evaluation
Timely Dialysis Initiation
Timely Dialysis Access Placement
Choice of Dialysis Modality
Education
An "ESRD Clinic"
Preparation for Renal Replacement Therapy
(GRF < 30 cc/min/1.73m2)
Early Detection of CKD
Patients with CKD, irrespective of diagnosis, are at increased risk of
cardiovascular disease (CVD), including coronary heart disease,
cerebrovascular disease, peripheral vascular disease, and heart failure.
Both traditional and chronic kidney disease related (nontraditional) CVD
risk factors may contribute to this increased risk.
-All patients with CKD should be considered in the highest risk group
for CVD, irrespective of levels of traditional CVD risk factors.
-All patients with CKD should undergo assessment of CVD risk factors,
including:
Measurement of traditional CVD risk factors in all patients;
Individual decision-making regarding measurement of selected
CKD-related CVD risk factors in some patients.
-Recommendations for CVD risk factor reduction should take into
account the highest-risk status of patients with chronic kidney disease.

GUIDELINE 15. ASSOCIATION OF CHRONIC KIDNEY DISEASE WITH
CARDIOVASCULAR DISEASE
The most common cause of death among
ESRD patients is CVD
Fig 5. Causes of death among period prevalent patients 19971999, 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.
Modification of Comorbidity:
Cardiovascular Disease
CVD is the cause of death in 40-50% ESRD
patients
ESRD CVD mortality rates 15x higher than
general population.
CVD is leading cause of death in patients with
CKD, regardless of stage.
HDFP, pts with Cr> 1.7mg/dl, 58% deaths CV
British Regional Heart Study, 50% deaths CV in
patients in upper decile of baseline Cr

GFR and relative risk for CVD-related death.
Wannamethee
625
: risk is for S
Cr
1.5 mg% vs S
Cr
1.3 mg%. Culleton
622
: risk is for S
Cr

1.5 mg% and 1.4 mg% vs. <1.5 and <1.4 in men and women respectively. Upper
limit for S
Cr
was 3.0 mg%. Mann
637
: risk is for S
C


1.4 mg% vs <1.4 mg%. Ruilope
634
:
risk is for S
Cr
>1.5 mg% vs 1.5 mg%. Upper limit for SCr was 3.0 mg%. Fried
640
: risk is
for S
Cr


1.5 mg% versus S
Cr
0.9 mg%. Hemmelgarn
642
: risk is for S
Cr
>2.3 mg/dL vs

2.3 mg/dL.
Proteinuria and relative risk for cardiovascular
disease.
Where possible, results presented are from multivariable
analyses. Agewall
650
, Ljungman
647
: Unadjusted results shown.
Data not available to calculate age or multivariable adjusted
risk.
Modification of Comorbidity:
Cardiovascular Disease
Patients with CKD should be considered
highest risk for CVD.
Aggressive intervention and management of
traditional CV risk factors is indicated.
This particularly includes dyslipidemias.
All adults with Stage1-5 CKD should be evaluated
for dyslipidemia.
Fasting lipid profile with total cholesterol, LDL,
HDL and triglycerides, at baseline, and at least
annually.

Management of Dyslipidemia in CKD
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.
http://www.kidney.org/professionals/KDOQI/guidelines_lipids/index.htm
Management of Patients with Chronic
Kidney Disease
Blood glucose control
BP Control
ARBs
ACE Inhibitors
Interventions that delay progression
Reduced Functioning and Well-being
Malnutrition
Osteodystrophy
Anemia
Prevention of Uremic Complications
(GFR < 60 cc/min/1.73 m2)
Cardiovascular Disease
Modifcation of Comorbidity
Pre-emptive Transplantation
Kidney Transplant Evaluation
Timely Dialysis Initiation
Timely Dialysis Access Placement
Choice of Dialysis Modality
Education
An "ESRD Clinic"
Preparation for Renal Replacement Therapy
(GRF < 30 cc/min/1.73m2)
Early Detection of CKD
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
m
2
(CKD Stages 4-5)!
Mandatory Referral to Nephrologist guideline, Niagara Health Quality Coalition, NY
Fig 11. Level of GFR at initiation of replacement therapy (USRDS). Data from Obrador et al.
77
Diabetics Medicare Eligible Most should
have started
Preparation for Renal Replacement
Therapy
(GFR < 30cc/min/1.73m
2
)
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/1.73m
2
)
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.

YOU, the PCM, CAN MAKE A Difference!