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Evaluating Chronic Kidney Disease Risk


Susan Simmons Holcomb, PhD, ARNP, BC

he kidneys are one of the bodys most important excretory organs. The kidneys are also instrumental in reabsorption to maintain water balance, 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 common 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

gressive mechanisms that are a common consequence following long-term reduction of renal mass, irrespective of etiology. This reduction in renal mass causes structural and functional hypertrophy of surviving nephrons. This compensatory hypertrophy is mediated by vasoactive molecules, cytokines, and growth factors, and is initially due to adaptive hyperfiltration, in turn mediated by increases in glomerular capillary pressure and flow.4 These short-term adaptations eventually prove maladaptive because they predispose to sclerosis of the remaining viable nephron population. Increased intrarenal activity of the renin-angiotensin axis appears to contribute to both the initial adaptive hyperfiltration and to the subseThe most common causes of chronic kidney quent maladaptive hypertrophy and sclerosis.4 disease are diabetes and hypertension, The most common causes of accounting for close to 70% of all CKD cases. CKD are diabetes and hypertension, accounting for close to 70% of all CKD cases.5 Because renal disease is increase in end-stage renal disease (ESRD), which requires on the rise and affects so many Americans, primary care dialysis or transplantation, the National Kidney Founda- providers should evaluate the risk of renal disease in each tion (NKF) wrote an extensive guideline for the identifi- patient at each visit (see Table: Evaluating Kidney Discation and treatment of renal disease. This approximately ease Risk). Evaluation should be directed at determining 200-page guideline, K/DOQI Clinical Practice Guide- the type and severity of CKD. Complications of CKD, lines for Chronic Kidney Disease: Evaluation, Classificaespecially irreversible kidney failure, involve the whole tion, and Stratification, can be found in its entirety at body and include conditions such as high blood preshttp://www.kidney.org/professionals/doqi/kdoqi.2 sure, anemia, protein energy malnutrition, bone disease and disorders of calcium and phosphorous metabolism, neuropathy, and a decrease in overall functioning and Pathophysiology/Etiology Chronic kidney disease (CKD) is a pathophysiologic well being.6 process that results in the inexorable attrition of nephron Chronic kidney disease should be established based number and function, ultimately leading to ESRD.3 The on the occurrence of kidney damage and the level of kidpathophysiology of CKD involves initiating mechanisms ney function (glomerular filtration rate [GFR]), regardspecific to the underlying etiology, as well as a set of proless of the diagnosis (see Table: Definition of Chronic

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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 clinicians 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, patients are becoming used to dealing with numbers for cholesterol, 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 Americans, Hispanics, and Native Americans), men, diabetics,
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and hypertensive individuals. Kidney failure from diabetes is the leading cause of CKD regardless of ethnicity except in African Americans. In African Americans, hypertension is the leading cause of kidney insufficiency and failure.3 Sometimes, CKD can be a result of antibody-mediated or cell-mediated immunological problems. Chronic kidney disease may also be a result of medications or other illnesses. Generally, the etiology elicits information regarding the pathology of the kidney disease. Disease of the kidneys can be classified as glomerular disease, vascular disease, tubulointerstitial disease, and cystic disease (see Tables: Causes of Kidney Disease and Tests of Kidney Structure and Function).
Diagnosis Diagnosis of CKD is traditionally based on pathology and etiology. A simplified classification emphasizes diseases in
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Chronic Kidney Disease

Evaluating Kidney Disease Risk2,7


Questions to Ask Risk factors for kidney disease present (i.e. diabetes, hypertension, kidney diseases, cancer, kidney calculi, infections, glomerulonephritis)? If risk factors are present, what is the glomerular filtration rate (GFR)? Is proteinuria present? If risk factors are present, is the blood pressure < 130/80 mmHg? Is an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin-receptor blocker (ARB) indicated? Potential Initiation Risk Factors for CKD Advanced age Non-Caucasian (African American, American Indian, Hispanic, Asian, or Pacific Islander) Certain chemical and environmental exposures, and/or nephrotoxic or illicit drugs Low socioeconomic and educational level Diabetes Hypertension Autoimmune diseases Systemic infections Frequent urinary tract infections Kidney calculi Lower urinary tract obstruction Kidney neoplasia Reduction in kidney mass Family medical history of CKD Recovery from acute kidney failure Progression Risk Factors Higher level of proteinuria Higher blood pressure levels Poor glycemic control in diabetes Tobacco abuse

Definition of Chronic Kidney Disease2


Criteria 1. Kidney damage for > 3 months, as defined by structural or functional abnormalities of the kidney, with or without decreased glomerular filtration rate (GFR), manifested by either: Pathological abnormalities; or Markers of kidney damage, including abnormalities in the composition of the blood or urine, or abnormalities in imaging tests 2. GFR < 60 mL/min/1.73 m2 for > 3 months, with or without kidney damage

Causes of Kidney Disease


Medical Conditions Diabetes Hypertension HIV Immunological Conditions Lupus Collagen vascular disease Infectious Beta-hemolytic streptococci Urinary tract infections (UTIs) Systemic infections Inherited Polycystic disease Alports syndrome (nephritis and hearing loss) Ethnicity African American, Native American, Hispanic Medications Antibiotics aminoglycosides, penicillins, tetracyclines Analgesics aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) Diuretics Contrast dyes Medication toxicity Miscellaneous Chronic kidney calculi Other kidney system obstruction Smoking Older age (> 60 years old) Cancer Low birth weight Low income and/or education

the native kidneys (broadly divided into those that are diabetic or nondiabetic in origin) and kidney disease in the transplant patient.1 Creatinine measurements can indicate kidney disease. Mean, normal serum creatinine levels are 0.96 mg/dL for women and 1.17 mg/dL for men. The definition of kidney disease is a creatinine level above 1.5 mg/dL, however this definition does not take into account gender differences. Kidney damage can occur even before the serum creatinine reaches 1.5 mg/dL,especially in the elderly.Since serum creatinine is affected by the GFR, which is in turn affected by age, gender, race, body size, diet, certain drugs, and laboratory procedures, it is not a great predictor of kidney function by itself.2
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Currently, a better measurement of kidney disease is to use the GFR. Kidney disease can also be defined as a GFR of 30 to 60 mL/min/1.73 m2, with a normal GFR in the range of 100 to 140 mL/min/1.73 m2. Chronic kidwww.tnpj.com

Chronic Kidney Disease

Tests of Kidney Structure and Function


Test Urinalysis (UA) 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 kidney 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 dependent upon age, muscle mass, and starvation May help to discover kidney calculi (stones), kidney size, or masses (solid or fluidfilled) Measures kidney size Detects hydronephrosis Detects tumors Shows cystic disease

Complete blood count (CBC) Chemistry panel

Glomerular filtration rate (GFR)

Kidney-ureters-bladder x-ray (KUB)

Renal ultrasonography

Intravenous pyelogram (IVP)

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

Computed tomography (CT scan)

Magnetic resonance imaging (MRI) Shows tumors and cysts Arteriogram Kidney biopsy 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.

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 measuring GFR in adults are the Cockcroft-Gault or the Modification of Diet in Renal Disease (MDRD) equations (see Table: Equations for Estimation of GFR).2,4 Measurement of GFR based on serum creatinine concentration 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 by approximately 2 years of age. Women generally have GFR
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values 8% lower than males. In young adulthood, between 20 to 30 years of age, GFR begins to decline by approximately 1 mL/min/1.73 m2 per year, so that an expected 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 following urine protein at least annually is recommended in all patients at risk for CKD.1 At the beginning of CKD, macroprotein, most commonly found on a urine dipstick, will
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Chronic Kidney Disease

GFR and Chronic Kidney Disease2


Stage Description At increased risk GFR (mL/min/1.73m2) > 90 (with CKD risk factors) > 90 Action* Screening CKD risk reduction Diagnosis and treatment Treatment of comorbid conditions, slowing progression, CVD risk reduction Estimating progression

Kidney damage with normal or GFR

Kidney damage with mild GFR Moderate GFR Severe GFR Kidney failure

60-89

3 4 5

30-59 15-29 < 15 (or dialysis)

Evaluating and treating complications Preparation for kidney replacement therapy Replacement (if uremia present)

*Includes actions from preceeding stages Abbreviations: GFR: glomerular filtration rate; CKD: chronic kidney disease; CVD: cardiovascular disease

loop diuretics twice a day.7 In the first few weeks of beginning 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 appropriate alternative for patients who demonstrate intolerance to an ACEI. Angiotensin receptor blockers can also be considered first-line therapies. Combining an ACEI and ARB Early on, the presence of protein is reversible, can be synergistic, although the long-term effects of such a combiso following urine protein at least annually is nation are unknown.7 In general, recommended in all patients at risk for CKD. nondihydropyridine calcium channel blockers can be used in patients who do not tolerate ACEIs or ARBs, is considered a strong indicator of kidney disease with a or in whom treatment with these medications has not need for intervention to halt and reverse imminent kidshown significant reduction in proteinuria or blood ney disease, as well as cardiovascular assessment and inpressure.9 7 tervention. Interventions to reduce microalbumin include maintaining blood pressure at less than 130/80 mmHg Clinical Manifestations (125/70 mmHg if macroproteinuria present), use of kidInitially, the patient with CKD may be asymptomatic. As ney-protective medications, reducing salt intake, and re- the disease progresses, symptoms of CKD may include ducing protein intake. fatigue, nausea, anorexia, nocturia, pruritus, insomnia, Kidney protective medications that can also reduce confusion, and changes in taste, especially having a metalhypertension include angiotensin-converting enzyme in- lic taste in the mouth. Symptoms can be related to anehibitors (ACEIs), angiotensin receptor blockers (ARBs), mia, changes in the neuromuscular system, and electrolyte and nondihydroypyridine calcium channel blockers. If and hormonal (especially parathyroid) imbalances. Salt the use of ACEIs is associated with hyperkalemia, potasand water imbalances can manifest as edema, increased sium levels may be effectively reduced by avoiding potas- blood pressure, ascites, heart failure, and/or pericardial sium and NSAIDs, as well as giving diuretics such as effusion. Neurologically, the changes in electrolytes, fluid not be noted; the guidelines instead recommend following 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 specimen most closely correlates with a 24-hour protein excretion, making it the preference over randomly timed specimens. An albumin-to-creatinine ratio of > 30 mg/g
continued on p. 23

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continued from p. 18

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)-0.203 Multiply 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

balance, and acid-base balance can be noted as asterixis, confusion, lethargy, orthostatic hypotension, gastroparesis, diminished deep tendon reflexes, hypothesia, and/or paresthesias. Anemia may cause pallor, shortness-ofbreath, and/or chest pain. Complications of CKD seem to progress and stem from a declining GFR. Complications include cardiovascular disease, anemia, malnutrition, osteoporosis, and neuropathy. In kidney failure, these complications are manifested and referred to as uremia or uremic syndrome. Prior to overt failure, these complications may or may not be present and if present, may show themselves in varying degrees. For reasons unknown, any deAnemia commonly occurs with chronic kidney gree of CKD, even mild disease, is associated with a marked increase in disease and may develop at any time during cardiovascular mortality.2,7 This inthe course of the disease. crease in risk is independent of other comorbid factors such as diabetes, hypertension, and hyperhomocysteinemia. However, the risk of cardiovascular disease rises tients with kidney insufficiency, leading to left ventricueven more in the presence of these comorbid conditions lar hypertrophy (LVH). In one study, almost 40% of and also rises as the GFR declines, proteinuria increases, patients with kidney insufficiency already had LVH at the and anemia develops. Cardiovascular disease (CVD) is the time of diagnosis. The reason for the development of LVH leading cause of death in patients with kidney failure and is probably the bodys trial to compensate for decreasing is higher in these patients than in the general population. oxygenation via anemia.8 Intervening to prevent CKD or to slow its progression is Malnourished patients or patients with high dietary obviously extremely important since CVD is the number intake of sodium and/or protein should receive nutrione killer of Americans.2 tional counseling. Malnutrition is a common finding in Strict blood sugar control can also halt progression patients with kidney disease. It is hypothesized that both of CKD. In diabetics whose urine microalbumin excremetabolic and hormonal changes in CKD patients detion has progressed to >30 mg/day, it is known that pro- crease appetite, which leads to decreased nutrient intake teinuria will ensue within 5 to 10 years.10 There also seems and malnutrition. Many patients have nausea from gasto be a correlation between hyperlipidemia and progres- trointestinal changes or changes with taste, and therefore sive CKD.11 do not want to eat. Metabolic acidosis combined with a
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Anemia Management Anemia in CKD is related primarily to erythropoietin deficiency. However, other causes of anemia can include iron deficiency, blood loss, and deficiencies of folate and/or vitamin B12. Patients with anemia may also have thalassemia, G6PD deficiency, or sickle cell disease. Anemia commonly occurs 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 reversal are not carried out. Anemia of chronic disease, such as CKD,is the second most common type of anemia worldwide, after iron deficiency anemia. Management of anemia is based on the cause. Erythropoietin deficiency is reversed by injecting erythropoietin-stimulating proteins such somatropin (Nutropin) or darbepoetin alpha (Aranesp).2,4 When initiating either erythropoietin or darbepoetin, hemoglobin measurements 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 hemoglobin can be monitored as deemed sufficient by the provider and patient. Hypertension can occur with administration of either erythropoietin or darbepoetin. If hypertension occurs, reduce blood pressure using antihypertensives. If blood pressure cannot be adequately reduced, then treatment with erythropoietin or darbepoetin must be stopped.2,7,8 Anemia is an independent predictor of CVD in pa-

Chronic Kidney Disease

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

decreased protein intake can increase protein breakdown in CKD patients. Metabolic acidosis also squelches albumin synthesis, which is needed as a building block for muscle 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 urinary protein to less than 2,500 mg per day may help de24 The Nurse Practitioner Vol. 30, No. 4

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 insufficiency is changes in bone development, including osteoporosis, due to a decrease in synthesis of vitamin D and resultant increase in secretion of parathyroid hormone (PTH). Changes in calcium-phosphorus ratios and hyperparathyroidism can also cause calcification of the blood vessels, which will worsen CVD. In CKD, phosphorus is not excreted properly, and the increase in serum phosphorus level directly affects vitamin D synthesis. Also, calcium is not as readily absorbed from the gastrointestinal tract. The combined low calcium, high phosphorus, and low vitamin D result in secondary hyperparathyroidism from stimulation of PTH and proliferation of parathyroid 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 hormone, ionized calcium, magnesium, phosphorus, and alkaline 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 neuropathies are sleep disorders. Other neuropathies include encephalopathy, peripheral polyneuropathy, and autonomic dysfunction. The reasons for the development of neuropathies in CKD patients are not well understood. Increased levels of urea, creatinine, and PTH, as well as changes in electrolytes, fluid balance, and acid-base balance 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 symptoms include itching, burning, muscle cramps, and/or muscle weakness. Autonomic changes include impaired heart rate, orthostatic hypotension, and depressed gastrointestinal motility. Exam findings may include loss of deep tendon reflexes, muscle wasting, changes in cognition, 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 www.tnpj.com

Chronic Kidney Disease

is important. In a landmark study, the National Institutes of Health found that mortality and morbidity were reduced in patients with CKD when aggressively treated and followed by a kidney team. Factors that affected mortality and morbidity included many that are reversible or controllable such as anemia, acidosis, hypertension, malnutrition (hypoalbuminemia), renal osteodystrophy (defective bone development), hyperlipidemia, smoking, and hyperglycemia (see Table: Goals to Prevent Progression of Kidney Disease). Chronic kidney disease is an extremely prevalent disorder 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 progression of disease, and treat the manifestations of CKD. The plan of care should not only incorporate pharmacotherapy, 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 chronic kidney disease in adults: Part 1. Definition, disease stages, evaluation, treatment, and risk factors. Am Fam Phys 2004; 70(5):869-76. 2. National Kidney Foundation K/DOQI. KDOQI CKD clinical practice guidelines for chronic kidney disease: evaluation, classification and stratification. National Kidney Foundation 2002. Found at: http://www.kidney.org. Accessed January 26, 2005.

3. Ferrone M: Pharmaceutical interventions in chronic kidney disease. US Pharm 2004;11:HS34-45. 4. Kasper DL, Braunwald E, Fauci AS, et al: Harrisons internal medicine. New York, N.Y. McGraw-Hill, 2005: 1653-63. 5. Kidney-Failure-Symptoms. Causes of acute renal failure and chronic renal insufficiency. Found at: http://www.kidney-failure-symptoms.com. Accessed January 26, 2005. 6. Henry R, Kostense P, Bos G, et al: Mild renal insufficiency is associated with increased cardiovascular mortality. The Hoorn Study. Kidney Int 2002; 62: 14021407. 7. Hebert CJ.: Preventing kidney failure: Primary care physicians must intervene 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 National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-52. 10. Ueda H, Ishimura E, Shoji T, et al: Factors affecting progression of renal failure in patients with type 2 diabetes. Diabetes Care 2003; 26:1530-1534. 11. Appel GB, Appel AS: Dyslipidemia in chronic kidney disease and end-stage renal disease: A review. Dialysis & Transplantation 2004; 33(11):714-19.

AUTHOR DISCLOSURE
The author has disclosed that she has no significant relationship or financial interest 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 City Kansas Community College.

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 personalized 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: 646-6746617 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 contact 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.

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