Chronic Kidney Disease For the PCM

1
Chronic Kidney DiseaseFor the PCM

• YOU Can Make a Difference!

CMYuan, 2007
2
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.

3
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 without kidney damage.

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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

5
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)

6
NKF-K/DOQI Stages of CKD
Primary Care Focus is here!
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Prevalence of GFR Categories in the USA(There is
a lot of CKD!)
Stage 3 CKD
8
Prevalence of CKD by GFR in the USA(There is a
lot of CKD!)
Coresh, et al, Am J Kidney Dis. 2003 41 1-12
9
Causes of ESRD in the USA Prevalent Counts and
Adjusted Rates by Primary Diagnosis
2006 ADR USRDS
10
Trends in the size of the Medicare CKD
population, by diabetic statusFigure 1.1
USRDS
700,000
600,000
Non-diabetic
500,000
en
f
400,000
b
Diabetic
300,000
num
And the numbers are increasing
200,000
ma
s
E
100,000
0
92-93
93-94
94-95
95-96
96-97
97-98
98-99
99-00
00-01
Cohort defining Period
Patients continuously enrolled in Medicare Part A
Part B in any two consecutive calendar years
from 1992 to 2001 (entry period), alive on the
last day of the entry period. Patients enrolled
in an HMO or diagnosed with ESRD any time during
the entry period are excluded. Estimates of the
general Medicare population are based on the 5
percent Medicare sample.
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CKD Patients Are More Likely to Die than to
Progress to ESRD
5 year follow-up
N27998
Keith, et al, Arch Int Med 2004 164659-663
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 16489-95.

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So what do we do about this?
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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/
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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

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Who should we screen?
17
How should we screen?
18
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.

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Factors Affecting Serum Creatinine Concentration
Increase Decrease

• Kidney Disease
• Ketoacidosis
• Ingestion of cooked meat
• Drugs
• Trimethoprim
• Cimetidine
• Flucytosine
• Some cephalosporins

• Reduced Muscle Mass
• Malnutrition

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Remember. GFR normally decreases with age!
21
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!

22
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/KDOQ
I/gfr.cfm
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TA-DA!(Your on-line link to the MDRD GFR
calculator)
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.

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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 SCr 1.2 mg/dl?

ClCr140-20144/72 x 1.2 200 cc/min
MDRD GFR Value99 mL/min/1.73 m2

• 93 year old Caucasian female nursing home
  resident, weighing
• 44 kg with a SCr 1.2 mg/dl.

ClCr 140-9344/72 x 1.2 x 0.85 20 cc/min
MDRD GFR Value45 mL/min/1.73 m2
26
Patient meets definition of Chronic Kidney
Disease?
YES NO
Risk Factor Reduction
Determine Stage of CKD Determine underlying
cause Identify risk factors for progression
Identify comorbidites
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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.

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A Simple Laboratory Evaluation!
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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

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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.

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So Now What Do You Do? (Theres a lot you can
do!)
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CKD Clinical Action Plan On-Line
http//www.kidney.org/professionals/kdoqi/cap/inde
x.html
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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

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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.

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Management of Patients with Chronic Kidney Disease
36
PROGRESSIVE RENAL DAMAGE The Final Common
Pathway
RENAL INJURY
Reduction in nephron mass
Glomerular capillary hypertension
Increased glomerular permeability to
macromolecules
Increased BP
Increased filtration of plasma proteins
Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
RENAL SCARRING
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Patient characteristics associated with increased
rate of GFR decline
Nonmodifiable Modifiable

• African American race
• Male gender
• Older age
• Lower baseline level of kidney function

• Higher level of proteinuria
• Higher BP
• Poor glycemic control
• Smoking

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• 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
• Strict glucose control in diabetes
• Strict blood pressure control
• ACEI and ARBs
• Interventions that may be effective, but studies
  are inconclusive, include
• Dietary protein restriction
• Lipid-lowering therapy
• 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.

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Slowing Progression The Earlier, the Better
40
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!
41
Measuring ProteinuriaGet into the right spot!
When you get to this point, Dont continue to get
microalbumin!
42
PROGRESSIVE RENAL DAMAGE The Final Common
Pathway
RENAL INJURY
ACEI ARB
Reduction in nephron mass
Glomerular capillary hypertension
Increased glomerular permeability to
macromolecules
ACEI ARB
Increased BP
Increased filtration of plasma proteins
Proteinuria
Excessive tubular protein reabsorption
Tubulointerstitial inflammation
ACEI ARB
RENAL SCARRING
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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
• 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/e
xpress.pdf
44
Controlling HypertensionGUIDELINE 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 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.

45
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

46
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
Controls
Controls
Controls
Controls
GFR vs. Time
BP vs. Time
AER vs. Time
47
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 m2).
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
48
JNC-7 recommends a goal blood pressure of mm Hg for individuals with high blood pressure
and CKD.
http//www.nhlbi.nih.gov/guidelines/hypertension/e
xpress.pdf
49
Recommendations for Controlling HTN in
Non-Diabetic CKD
Population BP Goal Nondrug Rx Drug RX CKD
200mg/g Ratio BMI25 kg/m2 Then diuretic Mod
EtOH Then BB or CCB Stop Smoking Exerci
se CKD no proteinuria Loop Then ACEI/ARB Then BB or CCB
KDOQI Table 118, Guideline 9
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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

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Interventions that delay progression of CKD
Strict Glycemic Control

• Recommended Therapy
• HgbA1c
• Additional information in 2001 ADA Clinical
  Practice Guidelines
• www.diabetes.org/clinicalrecommendations/Supplemen
  t101/S3.htm

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Management of Patients with Chronic Kidney Disease
53
When to Expect Complications
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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
  measurement should include Hb level.
• Anemia should be treated according to the
  K/DOQITM guidelines for anemia of CKD.

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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.

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Prevention of Uremic ComplicationsAnemia 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).

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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 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).

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Prevention of Uremic ComplicationsOsteodystrophy

• Osteitis fibrosis cystica, due to 2o HPT, is
  major form of bone disease.
• Check indices of bone and mineral metabolism at
  GFR
• iPTH the earliest marker
• Hypocalcemia, hyperphosphatemia
• Phosphorus control is cornerstone of treatment

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Prevention of Uremic ComplicationsOsteodystrophy
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

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Management of Renal Osteodystrophy is Very
Complex!
http//www.kidney.org/professionals/KDOQI/guidelin
es_bone/index.htm
62
GUIDELINE 9. ASSOCIATION OF LEVEL OF GFR WITH
NUTRITIONAL STATUS

• 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 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 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."

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Prevention of Uremic ComplicationsMalnutrition

• 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.

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Prevention of Uremic ComplicationsNutrition
Guidelines

• Protein intake
• 0.75g/kg/d (RDA)
• GFR
• Energy intake
• RDA depends on energy expenditure
• GFR
• Patients with less than recommended intake need
  frequent follow-up of nutritional status

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Prevention of Uremic ComplicationsJust 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!

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Management of Patients with Chronic Kidney Disease
67
GUIDELINE 15. ASSOCIATION OF CHRONIC KIDNEY
DISEASE WITH CARDIOVASCULAR DISEASE

• 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.

68
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.
69
Modification of ComorbidityCardiovascular
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

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GFR and relative risk for CVD-related death.
Wannamethee625 risk is for SCr ? 1.5 mg vs
SCr ? 1.3 mg. Culleton622 risk is for SCr ? 1.5
mg and ? 1.4 mg vs. women respectively. Upper limit for SCr was 3.0
mg. Mann637 risk is for SC ?  1.4 mg vs mg. Ruilope634 risk is for SCr 1.5 mg vs ?
1.5 mg. Upper limit for SCr was 3.0 mg.
Fried640 risk is for SCr ? 1.5 mg versus SCr ?
0.9 mg. Hemmelgarn642 risk is for SCr 2.3
mg/dL vs ? 2.3 mg/dL.
73
Proteinuria and relative risk for cardiovascular
disease. Where possible, results presented are
from multivariable analyses. Agewall650,
Ljungman647 Unadjusted results shown. Data not
available to calculate age or multivariable
adjusted risk.
74
Modification of ComorbidityCardiovascular
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.

75
Management of Dyslipidemia in CKD
http//www.kidney.org/professionals/KDOQI/guidelin
es_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,
2852486-2497.
76
Management of Patients with Chronic Kidney Disease
77
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 m2 (CKD Stages 4-5)!

Mandatory Referral to Nephrologist guideline,
Niagara Health Quality Coalition, NY
78
Fig 11. Level of GFR at initiation of replacement
therapy (USRDS). Data from Obrador et al.77
Diabetics
Medicare Eligible
Most should have started
79
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.

80
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.

81
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!