Look at CKD Risk

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www.tnpj.com12 The Nurse Practitioner Vol. 30, No. 4

Contact Hours 3.0/0.5

he kidneys are one of the bodys most importantexcretory organs. The kidneys are also instru-

mental in reabsorption to maintain water bal-

ance, electrolyte balance, acid-base balance, and blood

pressure regulation via the renin-angiotensin-aldosterone

system.

The incidence of kidney disease is on the rise. In the

United States,kidney failure is becoming increasingly com-

mon and is associated with poor health outcomes and

high medical expenditures.The number of patients treated

with dialysis or transplantation is projected to increase

from 340,000 in 1999 to 651,000 in 2010.1

Because of the

increase in end-stage renal disease (ESRD),which requires

dialysis or transplantation, the National Kidney Founda-

tion (NKF) wrote an extensive guideline for the identifi-cation and treatment of renal disease. This approximately

200-page guideline, K/DOQI Clinical Practice Guide-

lines for Chronic Kidney Disease: Evaluation, Classifica-

tion, and Stratification, can be found in its entirety at

http://www.kidney.org/professionals/doqi/kdoqi.2

Pathophysiology/Etiology

Chronic kidney disease (CKD) is a pathophysiologic

process that results in the inexorable attrition of nephron

number and function, ultimately leading to ESRD.3 The

pathophysiology of CKD involves initiating mechanismsspecific to the underlying etiology, as well as a set of pro-

gressive mechanisms that are a common consequencefollowing long-term reduction of renal mass, irrespec-

tive of etiology.This reduction in renal mass causes struc-

tural and functional hypertrophy of surviving nephrons.

This compensatory hypertrophy is mediated by vasoac-

tive molecules, cytokines, and growth factors, and is ini-

tially due to adaptive hyperfiltration, in turn mediated

by increases in glomerular capillary pressure and flow.4

These short-term adaptations eventually prove maladap-

tive because they predispose to sclerosis of the remain-

ing viable nephron population. Increased intrarenal

activity of the renin-angiotensin axis appears to con-tribute to both the initial adaptive

hyperfiltration and to the subse-

quent maladaptive hypertrophy and

sclerosis.4

The most common causes of

CKD are diabetes and hypertension,

accounting for close to 70% of all

CKD cases.5 Because renal disease is

on the rise and affects so many Americans, primary care

providers should evaluate the risk of renal disease in each

patient at each visit (see Table: Evaluating Kidney Dis-ease Risk). Evaluation should be directed at determining

the type and severity of CKD. Complications of CKD,

especially irreversible kidney failure, involve the whole

body and include conditions such as high blood pres-

sure, anemia, protein energy malnutrition, bone disease

and disorders of calcium and phosphorous metabolism,

neuropathy, and a decrease in overall functioning and

well being.6

Chronic kidney disease should be established based

on the occurrence of kidney damage and the level of kid-

ney function (glomerular filtration rate [GFR]), regard-less of the diagnosis (see Table: Definition of Chronic

T

Evaluating ChronicKidney Disease RiskSusan Simmons Holcomb, PhD, ARNP, BC

The most common causes of chronic kidney

disease are diabetes and hypertension,

accounting for close to 70% of all CKD cases.


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Chronic Kidney Disease

Kidney Disease).1 The NKF classifications of CKD stages

encourage communication between clinicians and help

clear up vague terms such as chronic renal insufficiency

and chronic renal failure. The guidelines also allow clin-

icians to talk with patients so that they will understand

their disease. Using the word kidney instead of renal,for example, is easier for patients to understand. Also, pa-

tients are becoming used to dealing with numbers for cho-

lesterol, blood pressure measurements, and blood sugar

levels. Knowing their GFR and implementing lifestyle

modifications, patients can attempt to slow the disease

and take control of their health.1

The incidence of CKD is varied, however it is most

common in the elderly, indicating that CKD risk increases

with age. One reason for this may be unrecognized chronic

renal ischemia due to renovascular disease.4 Other risk

groups include non-caucasians (especially African Amer-icans, Hispanics, and Native Americans), men, diabetics,

and hypertensive individuals. Kidney failure from dia-

betes is the leading cause of CKD regardless of ethnicity

except in African Americans. In African Americans, hy-

pertension is the leading cause of kidney insufficiency

and failure.3

Sometimes, CKD can be a result of antibody-medi-ated or cell-mediated immunological problems. Chronic

kidney disease may also be a result of medications or other

illnesses. Generally, the etiology elicits information re-

garding the pathology of the kidney disease. Disease of

the kidneys can be classified as glomerular disease, vascu-

lar disease, tubulointerstitial disease, and cystic disease

(see Tables:Causes of Kidney Disease and Tests of Kid-

ney Structure and Function).

Diagnosis

Diagnosis of CKD is traditionally based on pathology andetiology. A simplified classification emphasizes diseases in

www.tnpj.com The Nurse Practitioner April 2005 13


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ney failure is identified when the GFR falls to 15 to 30

mL/min/1.73 m2. End-stage renal failure is characterized

by a GFR of less than 15 mL/min/1.73 m2

(see Table:GFR and Chronic Kidney Disease).2 Equations for mea-

suring GFR in adults are the Cockcroft-Gault or the Mod-

ification of Diet in Renal Disease (MDRD) equations

(see Table: Equations for Estimation of GFR).2,4 Mea-

surement of GFR based on serum creatinine concentra-

tion using these equations is comparable, if not more

reliable, than 24-hour creatinine clearance.2

The GFR is not without drawbacks.In some patients,

substantial kidney damage can occur without a change

in the GFR. Normal GFR also varies with age, sex, race,

and body size. Children reach adult values for GFR byapproximately 2 years of age. Women generally have GFR

values 8% lower than males. In young adulthood, be-

tween 20 to 30 years of age, GFR begins to decline by ap-

proximately 1 mL/min/1.73 m2

per year, so that anexpected GFR by age 70 in males is 70 mL/min/1.73 m2.

Chronic kidney disease is identified when the GFR has

been < 60 mL/min/1.73 m2 for at least 3 months.1,4

Proteinuria

Proteinuria is not only a marker of kidney damage, it also

seems to be a marker for cardiovascular disease, as noted in

the Hoorn Study, and may be toxic to the kidney itself.6-8

Early on, the presence of protein is reversible, so follow-

ing urine protein at least annually is recommended in all

patients at risk for CKD.1

At the beginning of CKD, macro-protein, most commonly found on a urine dipstick, will

Tests of Kidney Structure and Function

Test

Urinalysis (UA)

Complete blood count (CBC)

Chemistry panel

Glomerular filtration rate (GFR)

Kidney-ureters-bladder x-ray (KUB)

Renal ultrasonography

Intravenous pyelogram (IVP)

Computed tomography (CT scan)

Magnetic resonance imaging (MRI)

Arteriogram

Kidney biopsy

Importance

Red cells and casts may indicate glomerular disease. Casts only originate in the

kidneys and form as a result of gelation within the tubules. Casts can trap other

materials when they are formed. The type of cast gives a clue to where in the kid-

ney the cast was made: glomerular, tubulointerstitial, or vascular.

White blood cells can be seen in interstitial nephropathies

Pyuria

Protein should not be noted

Anemia is noted in CKD

Change in electrolytes

Change in blood sugar

Measures serum creatinine and creatinine clearance. Note that creatinine is de-

pendent upon age, muscle mass, and starvation

May help to discover kidney calculi (stones), kidney size, or masses (solid or fluid-

filled)

Measures kidney size

Detects hydronephrosis

Detects tumors

Shows cystic disease

To discover gross anatomical abnormalities such as in polycystic kidneys,

nephrolithiasis, etc.

Not utilized for initial screening related to problems with dye toxicity in the form

of allergic reactions, salt overload, and fluid overload

Shows obstructions

Shows tumors, cysts, and stones

With contrast, may show kidney artery stenosis

Shows tumors and cysts

Useful if CKD thought to be due to kidney vascular disease

May help if diagnosis and treatment is uncertain. Considered the gold standard to

diagnose the specific type of kidney disease.


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not be noted; the guidelines instead recommend follow-

ing microalbumin. A spot, untimed, or random urine

collection to measure albumin-to-creatinine ratio should

be done, preferably on the first morning urine.2,7 Urinary

protein excretion varies throughout the day, leading to

variations in albumin-to-creatinine.A first-morning spec-

imen most closely correlates with a 24-hour protein ex-

cretion, making it the preference over randomly timed

specimens. An albumin-to-creatinine ratio of > 30 mg/g

is considered a strong indicator of kidney disease with a

need for intervention to halt and reverse imminent kid-

ney disease, as well as cardiovascular assessment and in-tervention.7 Interventions to reduce microalbumin include

maintaining blood pressure at less than 130/80 mmHg

(125/70 mmHg if macroproteinuria present), use of kid-

ney-protective medications, reducing salt intake, and re-

ducing protein intake.

Kidney protective medications that can also reduce

hypertension include angiotensin-converting enzyme in-

hibitors (ACEIs), angiotensin receptor blockers (ARBs),

and nondihydroypyridine calcium channel blockers. If

the use of ACEIs is associated with hyperkalemia, potas-

sium levels may be effectively reduced by avoiding potas-sium and NSAIDs, as well as giving diuretics such as

loop diuretics twice a day.7 In the first few weeks of be-

ginning an ACEI, the serum creatinine may rise by as

much as 30%. This rise may be more beneficial than

detrimental and may be considered kidney-protective.7

If however, a potassium and/or creatinine rise cannot

be contained or lowered, consider changing to another

kidney-protective medication.7 An ARB may be an ap-

propriate alternative for patients who demonstrate in-

tolerance to an ACEI. Angiotensin receptor blockers canalso be considered first-line thera-

pies. Combining an ACEI and ARB

can be synergistic, although the

long-term effects of such a combi-

nation are unknown.7 In general,

nondihydropyridine calcium chan-

nel blockers can be used in patients

who do not tolerate ACEIs or ARBs,

or in whom treatment with these medications has not

shown significant reduction in proteinuria or blood

pressure.9

Clinical Manifestations

Initially, the patient with CKD may be asymptomatic. As

the disease progresses, symptoms of CKD may include

fatigue, nausea, anorexia, nocturia, pruritus, insomnia,

confusion, and changes in taste, especially having a metal-

lic taste in the mouth. Symptoms can be related to ane-

mia,changes in the neuromuscular system,and electrolyte

and hormonal (especially parathyroid) imbalances. Salt

and water imbalances can manifest as edema, increased

blood pressure, ascites, heart failure, and/or pericardialeffusion. Neurologically, the changes in electrolytes, fluid

GFR and Chronic Kidney Disease2

Stage

1

2

3

4

5

*Includes actions from preceeding stages

Abbreviations: GFR: glomerular filtration rate; CKD: chronic kidney disease; CVD: cardiovascular disease

Description

At increased risk

Kidney damage with

normal or GFR

Kidney damage with

mild GFR

Moderate GFR

Severe GFR

Kidney failure

GFR (mL/min/1.73m2)

> 90

(with CKD risk factors)

> 90

60-89

30-59

15-29

< 15 (or dialysis)

Action*

Screening

CKD risk reduction

Diagnosis and treatment

Treatment of comorbid conditions, slowing

progression, CVD risk reduction

Estimating progression

Evaluating and treating complications

Preparation for kidney replacement therapy

Replacement (if uremia present)

Early on, the presence of protein is reversible,

so following urine protein at least annually is

recommended in all patients at risk for CKD.

continued on p. 23


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balance, and acid-base balance can be noted as asterixis,confusion, lethargy, orthostatic hypotension, gastropare-

sis, diminished deep tendon reflexes, hypothesia, and/or

paresthesias. Anemia may cause pallor, shortness-of-

breath, and/or chest pain.

Complications of CKD seem to progress and stem

from a declining GFR. Complications include cardiovas-

cular disease, anemia, malnutrition, osteoporosis, and

neuropathy. In kidney failure, these complications are

manifested and referred to as uremia or uremic syn-

drome. Prior to overt failure, these complications may

or may not be present and if present, may show them-selves in varying degrees.

For reasons unknown, any de-

gree of CKD, even mild disease, is as-

sociated with a marked increase in

cardiovascular mortality.2,7 This in-

crease in risk is independent of other

comorbid factors such as diabetes,

hypertension, and hyperhomocys-

teinemia. However, the risk of cardiovascular disease rises

even more in the presence of these comorbid conditions

and also rises as the GFR declines, proteinuria increases,and anemia develops. Cardiovascular disease (CVD) is the

leading cause of death in patients with kidney failure and

is higher in these patients than in the general population.

Intervening to prevent CKD or to slow its progression is

obviously extremely important since CVD is the number

one killer of Americans.2

Strict blood sugar control can also halt progression

of CKD. In diabetics whose urine microalbumin excre-

tion has progressed to >30 mg/day, it is known that pro-

teinuria will ensue within 5 to 10 years.10 There also seems

to be a correlation between hyperlipidemia and progres-sive CKD.11

Anemia Management

Anemia in CKD is related primarily to erythropoietin de-

ficiency. However, other causes of anemia can include iron

deficiency, blood loss, and deficiencies of folate and/or vi-

tamin B12

. Patients with anemia may also have thalassemia,

G6PD deficiency, or sickle cell disease.Anemia commonlyoccurs with CKD and may develop at any time during the

course of the disease. It is also known to progress as the

kidney disease progresses if interventions aimed at its re-

versal are not carried out. Anemia of chronic disease, such

as CKD,is the second most common type of anemia world-

wide, after iron deficiency anemia. Management of ane-

mia is based on the cause.

Erythropoietin deficiency is reversed by injecting ery-

thropoietin-stimulating proteins such somatropin (Nu-

tropin) or darbepoetin alpha (Aranesp).2,4 When initiating

either erythropoietin or darbepoetin, hemoglobin mea-surements should be done every 1 to 2 weeks following

initiation or change in dose.2 Once therapeutic levels of

11 to 12 g/dL have been reached, measurements of hemo-

globin can be monitored as deemed sufficient by the

provider and patient. Hypertension can occur with ad-

ministration of either erythropoietin or darbepoetin. If

hypertension occurs, reduce blood pressure using antihy-

pertensives. If blood pressure cannot be adequately re-

duced, then treatment with erythropoietin or darbepoetin

must be stopped.2,7,8

Anemia is an independent predictor of CVD in pa-

tients with kidney insufficiency, leading to left ventricu-

lar hypertrophy (LVH). In one study, almost 40% of

patients with kidney insufficiency already had LVH at thetime of diagnosis.The reason for the development of LVH

is probably the bodys trial to compensate for decreasing

oxygenation via anemia.8

Malnourished patients or patients with high dietary

intake of sodium and/or protein should receive nutri-

tional counseling. Malnutrition is a common finding in

patients with kidney disease. It is hypothesized that both

metabolic and hormonal changes in CKD patients de-

crease appetite, which leads to decreased nutrient intake

and malnutrition. Many patients have nausea from gas-

trointestinal changes or changes with taste, and thereforedo not want to eat. Metabolic acidosis combined with a

Equations for Estimation of GFR4

1. Equation from the Modification of Diet in Renal

Disease (MDRD) study*

Estimated GFR

(mL/min/1.73m2) = 1.86 X (PCr)-1.154 X (age)-0.203Multiply by 0.742 for women

Multiply by 1.21 for African Americans

2. Cockcroft-Gault equation

Estimated creatinine clearance (mL/min)=

(140 age) X body weight (kg)

72 X PCr

(mg/dL)

Multiply by 0.85 for women

* Equation is available in handheld calculators and in tabular form

Anemia commonly occurs with chronic kidney

disease and may develop at any time during

the course of the disease.

continued from p. 18


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decreased protein intake can increase protein breakdown

in CKD patients. Metabolic acidosis also squelches albu-

min synthesis, which is needed as a building block formuscle mass. In addition, declining kidney function is

known to adversely affect insulin and growth hormone,

two factors also needed for growth and repair. As the GFR

decreases, levels of C-reactive protein increase, making

adequate nutrition for repair even more imporant.2,8

In nondialyzed patients with GFRs < 25 mL/min/

1.73m2, protein intake should be 0.60 g protein/kg/d, not

to exceed 0.75 g protein/kg/d. In these same individuals,

daily caloric intake should be 35 kcal/kg/d if less than 60

years of age, and 30 to 35 kcal/kg/d in patients 60 years

of age or older. It has been suggested that lowering uri-nary protein to less than 2,500 mg per day may help de-

lay progression of CKD.8 In patients with higher GFRs,

protein intake should be 0.75 g/kg/d. Patients with higher

GFRs should adjust daily caloric intake to maintain or

lose weight, if needed. Sodium should be reduced in all

kidney patients.2

Another potential complication of chronic kidney in-sufficiency is changes in bone development, including os-

teoporosis,due to a decrease in synthesis of vitamin D and

resultant increase in secretion of parathyroid hormone

(PTH). Changes in calcium-phosphorus ratios and hy-

perparathyroidism can also cause calcification ofthe blood

vessels, which will worsen CVD. In CKD, phosphorus is

not excreted properly, and the increase in serum phos-

phorus level directly affects vitamin D synthesis.Also,cal-

cium is not as readily absorbed from the gastrointestinal

tract. The combined low calcium, high phosphorus, and

low vitamin D result in secondary hyperparathyroidismfrom stimulation of PTH and proliferation of parathy-

roid cells. Bone changes usually begin when the GFR

reaches 60 ml/min/1.73 m2 or less. Bone changes should

be suspected if PTH levels are elevated. Parathyroid hor-

mone, ionized calcium, magnesium, phosphorus, and al-

kaline phosphatase should therefore be closely monitored

and supplements or medications to protect the

bone initiated when indicated.2

Many forms of neuropathy are associated

with CKD. Among the most common neu-

ropathies are sleep disorders. Other neu-ropathies include encephalopathy, peripheral

polyneuropathy, and autonomic dysfunction.

The reasons for the development of neu-

ropathies in CKD patients are not well understood. In-

creased levels of urea, creatinine, and PTH, as well as

changes in electrolytes, fluid balance, and acid-base bal-

ance may interfere with nerve conduction. Symptoms

associated with encephalopathy can range from fatigue,

insomnia, and impaired memory and concentration to

convulsions and coma. Peripheral neuropathy symp-

toms include itching, burning, muscle cramps, and/ormuscle weakness. Autonomic changes include impaired

heart rate, orthostatic hypotension, and depressed gas-

trointestinal motility. Exam findings may include loss

of deep tendon reflexes, muscle wasting, changes in cog-

nition, and impaired sensation.2

Management

Treatment goals for CKD include treating the underlying

disease when able, slowing progression, preventing and

treating complications, and referral to a nephrologist and

kidney team early in the disease.A kidney evaluation and follow-up with a kidney team

Goals to Prevent Progression of Kidney Disease

Attain blood pressure of 125/75 mmHg

Achieve urine protein excretion rate of < 2,500 mg/24

hours

Keep LDL cholesterol to < 100 mg/dL

Maintain Hgb A1c < 6.5%

Keep Hct 36%

Maintain serum albumin > 4.0

Keep serum bicarbonate level 22-24 meq/L

Maintain normal serum calcium, magnesium, sodium,

potassium, and phosphorous levels

No smoking

Addition of ACEI to preserve kidney function

Minimize effects of medication on kidney function

- No or judicious use of NSAIDs

- Avoid antacids containing magnesium and aluminum

- Use the same pharmacy to fill medications so kidney

interactions can be followed

- No use of over-the-counter medications without prior

approval of the primary care provider or pharmacist

Maintain adequate nutrition

- Salt limit to 2-3 gm/d

- Fluid limit to 1-3 L/d

- Potassium limit to 2-2.4 gm/d

- Calcium 1-1.5 g/day- Vitamin D 800 international units/day

- Protein limit to 0.6-0.8 gm/kg/d (for most

0.75 gm/kg/d)

- Calories minimum of 35-45 kcal/kg/d

- Folic acid 1 mg

- Vitamin B12

250-500 mcg/d

- Phosphorous < 800 mg/d


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CE Test

Evaluating Chronic Kidney Disease Risk

Instructions:

Read the article beginning on page 12.

Take the test, recording your answers in the test answers

section (Section B) of the CE enrollment form. Each question

has only one correct answer.

Complete registration information (Section A) and course

evaluation (Section C).

Mail completed test with registration fee to: Lippincott

Williams & Wilkins, CE Group, 333 7th Avenue, 19th Floor,

New York, NY 10001. Within 3 to 4 weeks after your CE enrollment form is

received, you will be notified of your test results.

If you pass, you will receive a certificate of earned contact

hours and an answer key. If you fail, you have the option of

taking the test again at no additional cost.

A passing score for this test is 11 correct answers.

Need CE STAT? Visit http://www.nursingcenter.com for

immediate results, other CE activities, and your personal-

ized CE planner tool.

No Internet access? Call 1-800-933-6525, ext. 6617 or ext.

6621, for other rush service options.

Questions? Contact Lippincott Williams & Wilkins: 646-674-

6617 or 646-674-6621.

Registration Deadline:April 30, 2007

Provider Accreditation:

This Continuing Nursing Education (CNE) activity for 3.0 contact hours

is provided by Lippincott Williams & Wilkins, which is accredited as a

provider of continuing education in nursing by the American Nurses

Credentialing Centers Commission on Accreditation and by the

American Association of Critical-Care Nurses (AACN 00012278, CERP

Category A). This activity is also provider approved by the California

Board of Registered Nursing, Provider Number CEP 11749 for 3.0 con-

tact hours. LWW is also an approved provider of CNE in Alabama,

Florida, and Iowa and holds the following provider numbers: AL#ABNP0114, FL #FBN2454, IA #75. All of its home study activities are

classified for Texas nursing continuing education requirements as Type

I. This activity has been assigned 0.5 pharmacology credit.

Your certificate is valid in all states. This means that your certificate of

earned contact hours is valid no matter where you live.

Payment and Discounts:

The registration fee for this test is $19.95.

If you take two or more tests in any nursing journal published by

LWW and send in your CE enrollment forms together, you may deduct

$0.75 from the price of each test.

We offer special discounts for as few as six tests and institutional

bulk discounts for multiple tests. Call 1-800-933-6525, ext. 6617 or ext.

6621, for more information.

is important. In a landmark study, the National Institutes

of Health found that mortality and morbidity were re-

duced in patients with CKD when aggressively treated

and followed by a kidney team. Factors that affected mor-

tality and morbidity included many that are reversible or

controllable such as anemia, acidosis, hypertension, mal-nutrition (hypoalbuminemia), renal osteodystrophy (de-

fective bone development), hyperlipidemia, smoking, and

hyperglycemia (see Table: Goals to Prevent Progression

of Kidney Disease).

Chronic kidney disease is an extremely prevalent dis-

order and represents a significant challenge to healthcare.

The treatment approach for a patient with CKD should

include identification and treatment of the reversible

causes of further kidney function decline, slow the pro-

gression of disease, and treat the manifestations of CKD.

The plan of care should not only incorporate pharma-cotherapy, but also multiple therapeutic modalities with

continuous patient education and monitoring.

REFERENCES

1. Johnson CAJ,Levey AS,Coresh J,et al: Clinical practice guidelines for chronickidney disease in adults: Part 1. Definition, disease stages, evaluation, treat-ment, and risk factors. Am Fam Phys 2004; 70(5):869-76.

2. National Kidney Foundation K/DOQI.KDOQI CKD clinical practice guide-lines for chronic kidney disease: evaluation, classification and stratification.National Kidney Foundation 2002. Found at: http://www.kidney.org. Ac-cessed January 26, 2005.

3. Ferrone M: Pharmaceutical interventions in chronic kidney disease. USPharm 2004;11:HS34-45.

4. Kasper DL, Braunwald E, Fauci AS, et al: Harrisons internal medicine. NewYork, N.Y. McGraw-Hill, 2005: 1653-63.

5. Kidney-Failure-Symptoms. Causes of acute renal failure and chronic renalinsufficiency. Found at: http://www.kidney-failure-symptoms.com.AccessedJanuary 26, 2005.

6. Henry R, Kostense P, Bos G, et al: Mild renal insufficiency is associated withincreased cardiovascular mortality. The Hoorn Study. Kidney Int 2002; 62:14021407.

7. Hebert CJ.: Preventing kidney failure: Primary care physicians must inter-vene earlier. Cleveland Clinic Journal of Medicine April 2003; 70(4):33744.Erratum in: Cleveland Clinic Journal of Medicine June 2003; 70(6):501.

8. Schmitz P: Progressive renal insufficiency. Postgraduate medicine online.July 2000. Found at: http://www.postgradmed.com. Accessed January 26,2005.

9. Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint Na-tional Committee on Prevention, Detection, Evaluation, and Treatment ofHigh Blood Pressure. Hypertension 2003;42:1206-52.

10. Ueda H,Ishimura E,Shoji T, et al: Factors affecting progression of renal fail-ure in patients with type 2 diabetes. Diabetes Care 2003; 26:1530-1534.

11. Appel GB, Appel AS: Dyslipidemia in chronic kidney disease and end-stagerenal disease: A review.Dialysis & Transplantation 2004; 33(11):714-19.

AUTHOR DISCLOSURE

The author has disclosed that she has no significant relationship or financial in-terest in any commercial companies that pertain to this education activity.

ABOUT THE AUTHOR

Dr.Holcomb is a Nurse Practitioner at the Walk-In Health Care Clinic of Olathe,Olathe, Kan.,and a Consultant for Continuing Nursing Education at Kansas CityKansas Community College.

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