Vol. 18 • Issue 7
• Page 30
In 2004, the Centers for Medicare and Medicaid Services enacted reimbursement changes that made it profitable for nephrology practices to employ NPs. NPs function in every aspect of nephrology care, including chronic kidney disease (CKD) clinics, dialysis centers and transplant practices.
Prevalence of Kidney Disease
CKD is more prevalent than heart failure or diabetes and affects 27 million U.S. residents.1 In addition, kidney disease is a major health expense. Patients on dialysis make up 1% of the Medicare population but account for 7% of Medicare costs.1High-risk groups include people with diabetes, hypertension, recurrent urinary tract infections or urinary obstruction, systemic illnesses that affect the kidney, or family history of kidney disease.2
Physiology of the Kidney
The kidneys are located between the twelfth thoracic and third lumbar vertebrae in front of and beside the vertebral column. An adult kidney is approximately 5 cm to 7 cm wide, 11 cm to 13 cm long and 2.5 cm thick. Each kidney weighs between 120 g and 160 g. Under normal circumstances, 20% to 25% of cardiac output or about 1,200 mL per minute flows through the kidneys. This means the body's total blood supply circulates through the kidneys approximately 12 times each hour.3 The kidneys are essential to maintaining homeostasis. They regulate the osmolarity of the body's fluid and maintain electrolyte balance and acidity. The kidneys do more than excrete wastes and foreign substances; they are also a major factor in the elimination of drugs. In addition, the kidneys are the major source for renin, erythropoietin and 1,25-dihydroxyvitamin D3(vitamin D3. Renin is involved in salt balance and blood pressure regulation. Erythropoietin stimulates the production of red blood cells. Vitamin D3is the active form of vitamin D and is essential to the balance of calcium and phosphorus.4
Stages of Kidney Disease
CKD is usually progressive. Kidney damage is defined as abnormalities in blood or urine tests, in imaging studies or pathologic exam. The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) defines CKD as kidney damage lasting more than 3 months with or without a decrease in estimated glomerular filtration rate (eGFR) or an eGFR less than 60 mL/min/1.73 m2with or without signs of kidney damage. The eGFR rate represents the total functioning of kidney nephrons and how much blood they filter. The rate, expressed as mL/min/m2of body surface area (BSA) is estimated by measuring the clearance of a substance, usually creatinine, from the blood. Generally, eGFR is expressed as mL/min/1.73m2 and is estimated according to published formulas.2
reatinine alone was once considered a determinant of kidney health. But it is a poor indicator of GFR. Certain populations, usually with increased muscle mass (e.g., young men on a high-protein diet) may have an elevated creatinine without kidney damage. Older adults, frail patients and those on low-protein diets may have normal or near normal creatinine and advanced kidney disease. The ingestion of cooked meats can affect serum creatinine levels.2 These often are normal until 50% of GFR is lost.5
CKD is classified in five stages, according to severity. Patients who are in Stage 5 and are on dialysis were formerly referred to as being in end-stage renal disease (ESRD).2
Diabetes and CKD
Approximately 21 million people in the United States, or 7% of the population, has diabetes; approximately 26 million have CKD.6 Diabetes is the leading cause of CKD, accounting for approximately 45% of cases.7 Diabetic nephropathy occurs in about 20% to 40% of people with diabetes and is defined as an elevated albumin excretion rate.8 Low albumin levels (an early manifestation of diabetic nephropathy) may be present on standard dipsticks for many years as eGFR declines. Guidelines suggest annual albumin screening in people with diabetes. Initial screening should begin 5 years after the diagnosis of type 1 diabetes or at the time of diagnosis in type 2 diabetes.2
Screening should include measurements of urinary albumin:creatinine ratio (ACR) in a spot urine sample, measurement of serum creatinine and estimation of GFR. An elevated ACR should be confirmed in the absence of urinary tract infection with two additional first-void specimens collected during the next 3 to 6 months. To confirm classification, two of the three samples should fall within the microalbuminuria or macroalbuminuria range. In most patients with diabetes, CKD is attributed to diabetes if macroalbuminuria is present or if microalbuminuria is present in addition to diabetic retinopathy and type 1 diabetes of at least 10 years.
Other causes of CKD should be considered in the presence of the following:6
• absence of diabetic retinopathy
• low or rapidly decreasing eGFR
• rapidly increasing proteinuria or nephrotic syndrome
• refractory hypertension
• presence of active urinary sediment
• signs of other systemic disease
• more than 30% reduction in eGFR within 2 to 3 months of angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB).
Hypertension and CKD
Hypertension is the second leading cause of CKD, and uncontrolled hypertension contributes to the progression.6,8 More than 50% to 75% of people with CKD have a systolic blood pressure higher than 140 mm Hg.2 Among patients with diabetes or CKD, systolic blood pressure of 130 mm Hg or higher or diastolic readings of 80 mm Hg or higher constitute hypertension. In patients without kidney disease, systolic blood pressure of 140 mm Hg or higher or diastolic readings of 90 mm Hg or higher constitute hypertension.9,10
Evaluation of people with CKD or hypertension should include measurement of blood pressure, GFR and proteinuria at each encounter.2 The goals of therapy are to reduce blood pressure, reduce CVD risk and slow the progression of CKD. The reduction of albuminuria appears to be the most important goal that can be achieved through blood pressure control.11
Advancing Age and CKD
In the fourth decade, function decreases by approximately 8 mL/minute/1.73m2 This loss is often accelerated by such risk factors as hypertension, smoking, atherosclerotic vascular disease and lead exposure. Likewise, renal mass declines after the fourth decade.12Kidney function declines by about 10 mL/min/1.73 m2 per decade despite the absence of markers of kidney damage, such as findings of abnormal structure (imaging) or abnormal function (blood tests, urinalysis).13
As stated, serum creatinine is not a good measure of kidney function in older adults. Using an eGFR is a better measurement of kidney function.14 However, providers should be cautious when using estimating calculations to estimate GFR because they may lead to overdiagnosis. A rapid decline in GFR in older adults may be associated with high mortality independent of eGFR and other demographic variables. Evidence suggests that modest declines in eGFR or albuminuria are associated with cardiovascular disease (CVD).15 Therefore, it is important to address CKD and CVD risk in older adults by treating modifiable risk factors and implementing strategies to reduce CVD.
Cardiovascular Disease and CKD
People with CKD face a more significant risk for CVD than those without kidney disease.8 Patients with CKD have a greater likelihood of dying from comorbidities related to kidney disease than progressing to ESRD.16 Several traditional and nontraditional risk factors for cardiovascular disease exist in people with CKD. Modifiable risk factors associated with decline in kidney function include proteinuria, uncontrolled hypertension, poor glycemic control, obesity and smoking.8 Diabetes is an important risk factor for CVD; people with CKD and diabetes should be considered at highest risk for CVD events.6
Other Complications
As kidney function declines, other complications develop, such as edema, sodium retention, hyperkalemia, metabolic acidosis, bone disorders and anemia, as well as gastrointestinal, immunologic, neurologic, endocrine, skin and hormonal effects.17
Treatment and Referral
Referral is warranted when the eGFR is less than 30 mL/min/1.73m2 (some sources recommend 60 mL/min/1.73m2. Other indications for referral include proteinuria, uncontrolled hypertension or a loss of 15% or more in renal function in 3 months. Diabetes patients with an eGFR less than 60 mL/min/1.73m2 and anemia often benefit from referral.5 Because many labs provide the eGFR as part of the metabolic panel report, identifying the at-risk population is easier than in the past, when the NP had to check the eGFR separately on each patient. Essential laboratory values include a metabolic profile, phosphorus and urine protein. Traditionally, the 24-hour urine has been used to determine the presence of proteinuria. Because these are somewhat problematic to obtain, a random albumin:creatinine sample is usually adequate. The 24-hour urine collection is a good indicator of sodium ingestion, which is valuable in treating the patient with hypertension. Order a complete blood count as well. In the presence of anemia, iron studies are necessary. If the anemic patient's iron studies are normal, further laboratory testing should include B12levels and folate. In the case of anemia, stools should be checked.
The physical exam should include vital signs, a lung exam and assessment for edema. Assess for jugular vein distension. The cardiac portion of the exam should look for a new murmur or signs of heart failure. Patients with CKD sometimes present with fatigue, malaise, nocturia, gastrointestinal upset, itching, shortness of breath, edema and restless legs.
Although most patients with CKD do not require renal replacement, early intervention can slow the progression of CKD and decrease CVD risk.5 Many of the recommended interventions apply to all patients regardless of renal status. They include smoking cessation, weight control, blood pressure control, increased physical activity, nutrition (emphasis on sodium restriction), moderate alcohol use, and blood glucose and cholesterol control.5 Patients with CKD may present with a sudden worsening of renal function from many reasons. Hypertension, proteinuria and hematuria raise suspicion for glomerular disease. These patients often require further testing and in most instances should be referred.18
Dehydration is common in patients with heart failure and often results from overdiuresis. ACE inhibitors can cause decline in renal function. This often is transient, but it is essential for patients to return for blood work 2 to 4 weeks after introducing or increasing this type of medication.
Nutrition
CKD patients, especially those in stages 3 through 5, often have compromised nutritional status. As the disease progresses, dietary restrictions arise, particularly sodium, phosphorus and potassium. A renal dietitian is an invaluable asset. Sodium restrictions are essential regardless of renal status, and phosphorus restrictions are appropriate. Follow potassium levels, especially when adjusting hypertension medications.
Medications in CKD
A number of medications should be avoided or used with extreme caution in patients with CKD, due to the risk for worsening renal function. In addition, several medications require dose adjustments due to the predominance of renal elimination.
Medications that may worsen renal function include, but are not limited to, NSAIDs, intravenous contrast dyes and aminogylcosides.19 Because the kidneys are already compromised, patients with CKD are at high risk for further decline in kidney function.20 Iodinated contrast media used in imaging services can cause worsening renal function in patients with CKD. When use of a contrast media cannot be avoided, employ methods to reduce the risk (e.g., adequate hydration, pretreatment with acetylcysteine).19,21 Aminoglycoside antibiotics may cause nephrotoxicity in 10% to 20% of patients. Avoid this by using appropriate kinetic dosing calculations that adjust for renal function and monitoring drug levels closely.19 Dose adjustments are also recommended for many medications because the kidney, along with the liver, is a primary route of drug elimination. Drugs that are commonly used in this population and require dose adjustments include select diabetes medications, ACE inhibitors, some beta blockers, spironolactone (Aldactone), statins, fibric acids, gout medications, meperidine (Demerol), morphine, several antibiotics, enoxaparin (Lovenox), gabapentin (Neurontin), metoclopramide (Reglan), and ranitidine (Zantac).22,23 Due to the large number of drugs requiring dose adjustments, consult published references when dosing medications for a patient with CKD.
Putting It Into Practice
Early recognition and treatment of CKD may delay or prevent progression to ESRD. It is essential that detection and appropriate referrals begin in primary care.
References
1. United States Renal Data System. Annual Report Atlas of Chronic Kidney Disease 2009. Bethesda, Md.: National Institutes of Health; 2009.
2. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification and stratification. Am J Kidney Dis. 2002;39(2 Suppl 1):S1-266.
3. Schira M. The Kidney. In: Counts CS, ed. Core Curriculum for Nephrology Nurses. Pitman, N.J.: American Nephrology Nurses Association; 2008: 5-7.
4. Briggs JP, et al. Overview of kidney function and structure. In: Greenberg A, ed. Primer on Kidney Diseases. Philadelphia, Pa.: Elsevier Sanders; 2005: 2-19.
5. Kidney Health of Australia. Chronic kidney management in general practice. Available at: http://www.kidney.org.au/HealthProfessionals/PublicationsforHealthProfessionals/tabid/635/Default.aspx. Accessed March 23, 2010.
6. National Kidney Foundation. K/DOQI clinical practice guidelines and clinical practice recommendations for diabetes and chronic kidney disease. Am J Kidney Dis. 2007;49(2 Suppl 2):S12-154.
7. United States Renal Data System. Annual Report Atlas of Chronic Kidney Disease 2006. Bethesda, Md.: National Institutes of Health; 2006.
8. Sarnak MJ, et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure, Clinical Cardiology and Epidemiology and Prevention. Hypertension. 2003;42(5):1050-1065.
9. Chobanian AV, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-1252.
10. National Kidney Foundation. Kidney Early Evaluation Program Annual Data Report 2006. New York, NY: National Kidney Foundation; 2006.
11. National Kidney Foundation. K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 Suppl 1):S1-S290.
12. Yuan FE, Anderson S. The kidney in aging. In: Greenberg A, ed. Primer on Kidney Diseases. Philadelphia, Pa.: Elsevier Saunders; 2005: 436-442.
13. Manjunath G, et al. Level of kidney function as a risk factor for atherosclerotic cardiovascular outcomes in the community. J Am Coll Cardiol. 2003;41(1):47-55.
14. Fox CH, et al. Improving chronic kidney disease care in primary care practices: an upstate New York practice based research network (UNYNET) study. J Am Board Fam Med. 2008;21(6):522-530.
15. Rifkin DE, et al. Rapid kidney function decline and mortality risk in older adults. Arch Intern Med. 2008;168(20):2212-2218.
16. Keith DS, et al. Longitudinal follow-up and outcomes among a population with chronic kidney disease in a large managed care organization. Arch Intern Med. 2004;164(6):659-663.
17. Schieppati A, et al. Pathophysiology and management of chronic kidney disease. In: Greenberg A, ed. Primer on Kidney Diseases. Philadelphia, Pa.: Elsevier Sanders; 2005: 444-454.
18. Agrawal M, Swartz R. Acute renal failure. Am Fam Physician. 2000;61(7):2077-2088.
19. Guo X, Nzerue C. How to prevent, recognize, and treat drug-induced nephrotoxicity. Cleve Clin J Med. 2002;69(4):289-297.
20. Ejaz P, et al. NSAIDs and kidney. J Assoc Physicians India. 2004;52:632-640.
21. Reddan D, et al. Contrast-induced nephropathy and its prevention: what do we really know from evidence-based findings? J Nephrol. 2009;22(3):333-351.
22. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.
23. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.
Jane Davis is an adult nurse practitioner who specializes in nephrology. She practices in the division of nephrology at the University of Alabama in Birmingham. Anne Marie Liles is a pharmacist in the department of pharmacy practice at Auburn University in Auburn, Ala. Debra Hain is a gerontologic nurse practitioner who specializes in nephrology. She is an assistant professor of nursing at Florida Atlantic University in Boca Raton and practices in the department of nephrology at Cleveland Clinic in Weston, Fla.
|