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Nursing:
doi: 10.1097/01.NURSE.0000371121.30888.0e
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Understanding the stages of chronic kidney disease

Castner, Debra MSN, RN, APNC, CNN

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Author Information

Debra Castner is a nurse practitioner for Jersey Coast Nephrology and Hypertension Associates in Brick, N.J.

The author has disclosed that she has no financial relationships related to this article.

Adapted and updated from Castner D, Douglas C. Now onstage: chronic kidney disease. Nursing. 2005;35(12):1–63.

LUCIA RUIZ, 64, had an acute myocardial infarction (AMI) a year ago, so she's now seeing her primary care provider every 3 months. She's obese, with a body mass index of 35, and takes an oral antihyperglycemic agent to manage type 2 diabetes. Her BP was 140/80 at her last visit; today it's 146/88. Results of her most recent blood work and urinalysis also reveal chronic kidney disease (CKD).

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According to the National Kidney Foundation, either of the following conditions indicates CKD:1

* a glomerular filtration rate (GFR) less than 60 mL/min/1.73 m2 for 3 or more months, with or without kidney damage (normal GFR, 90 mL/min/1.73 m2 or greater). Ms. Ruiz has a GFR of 44.6 mL/min/1.73 m2

* structural or functional kidney abnormalities, with or without a decrease in GFR, lasting 3 or more months.

CKD is a slowly progressive disease that can occur over many years or decades. It leads to the need for renal replacement therapy (dialysis), renal transplant, or end-of-life care. Patients who don't progress to end-stage renal failure are likely to die from cardiovascular causes. In contrast to CKD, acute kidney injury happens suddenly and is reversible in many cases.2

This article will help you to recognize CKD and understand its stages so you can help your patient to modify risk factors, prevent further kidney damage, and manage complications. First, consider the scope of the problem.

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A growing problem

Over the past decade, the number of Americans with kidney failure has doubled. Those starting dialysis or having a first kidney transplant have increased by 50%. Currently, 26 million Americans have CKD, and millions more are at risk. Approximately 111,000 patients were newly diagnosed with end-stage renal disease (ESRD) in 1 year, with a 1-year increase in total ESRD patients of 4%. ESRD patients are those requiring dialysis or transplant.3-5

Protein—and particularly albumin—in the urine is a marker of damage to the renal glomeruli. (To understand why, see A closer look at the glomerulus.) Recent evidence also suggests that urinary protein may promote injury to the renal tubules, interstitial inflammation, and eventual kidney fibrosis.2

To help clinicians screen patients for kidney damage, collect data, and prevent or delay complications of CKD, the National Kidney Foundation has established five stages of CKD with management guidelines for each.1 (See Focus on the stages of CKD.) Using this framework, healthcare providers can slow the progression of CKD to stage 5 kidney failure, also known as ESRD.

Figure. A closer loo...
Figure. A closer loo...
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Recognizing risks

One of the most effective ways to help prevent ESRD is to recognize early CKD signs and risk factors for CKD and to make sure patients are referred to a nephrologist by stage 3 CKD or sooner.1,3 Many of the risk factors for CKD, including diabetes, untreated hypertension, smoking, obesity, poverty, and age over 65 years, are also risk factors for other diseases, such as cardiovascular disease.

For patients like Ms. Ruiz, heart disease can advance the progression of CKD. A cardiac event such as an AMI or a chronic disorder such as heart failure can decrease cardiac output, causing decreased renal perfusion and renal ischemia.

Other diseases that can lead to CKD include systemic lupus erythematosus, systemic sclerosis (scleroderma), primary amyloidosis, chronic pyelonephritis, hepatitis B or C, and multiple myeloma.

Exposure to nephrotoxic substances, especially in someone with one or more of these diseases, increases risk. These substances may be in environmental toxins, intravascular iodinated contrast media, and certain prescribed or over-the-counter medications, including antibiotics, such as aminoglycosides, and nonsteroidal anti-inflammatory drugs (NSAIDs).

Family history is important too. Some disorders such as polycystic kidney disease are hereditary, so relatives of patients with hereditary kidney disease should be screened.

Anyone with risk factors for CKD needs frequent screening and education about modifiable risk factors, such as hypertension, hyperglycemia, dyslipidemia, obesity, excessive protein and sodium intake, and exposure to nephrotoxins.

Factors that can't be modified include age, premature birth, heredity, and ethnicity. Hispanic Americans, African Americans, Pacific Islanders, and American Indians have a higher incidence of CKD leading to kidney failure than other ethnic groups, and aging increases the risk.1,6

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Triggers tip the balance

Various mechanisms can trigger CKD, but diabetes, hypertension, and glomerulonephritis top the list, in that order.1,3,4

Diabetic nephropathy begins when hyperglycemic osmotic polyuria causes increased tubular pressure and shear stress, especially in the collecting ducts, and compensatory cellular hypertrophy increases the GFR. People with type 1 diabetes commonly develop microalbuminuria (increased urinary albumin too subtle to detect with conventional tests) within 5 years of the onset of diabetes. Within 10 to 15 years, the problem can progress to overt nephropathy, with urine total-protein excretion exceeding the normal (less than 150 mg/24 h). After having diabetes for 15 years, one-third of people with type 1 diabetes develop kidney disease.7

The disease course varies more in patients with type 2 diabetes. Some patients have microalbuminuria at diagnosis because of delays in diagnosing diabetes and other factors affecting protein excretion, but progression to advanced renal disease is less likely. Without intervention, about 30% of patients with type 2 diabetes develop overt nephropathy, and about 20% of those with nephropathy develop ESRD after 20 years. Most patients with diabetes who require dialysis have type 2 diabetes but only because it's more prevalent than type 1 diabetes.2,8

Hypertensive nephrosclerosis occurs when small arteries and arterioles in the kidney are injured, probably from the effects of chronic hypertension. The damage may be due to two pathophysiologic processes acting in the kidney at the same time.

* Narrowed arteries and arterioles, caused by chronic hypertension, decrease glomerular blood flow, resulting in glomerular ischemia and nephrosclerosis.

* With loss of renal function due to decreasing renal mass, the remaining nephrons may try to compensate with arteriolar vasodilation to increase blood flow to the glomeruli. The results are increased glomerular pressure and filtration, and progressive thickening of the glomerular vessels. The high pressure within the vessels may weaken them and cause hemorrhaging. This bleeding can destroy large areas of the kidneys, leading to progressive deterioration of renal function. Hypertension can be both a cause of kidney disease and a complication of it.

Renal ischemia due to such conditions as renal artery stenosis or low cardiac output states activates the renin-angiotensin-aldosterone system (RAAS), which can further elevate BP and progressively damage the renal vessels. Spontaneous urinary sodium excretion early in the course of malignant hypertension leads to volume depletion with activation of the RAAS, which leads to catecholamine release to further elevate BP. Angiotensin II, an active element in the RAAS system and a potent vasoconstrictor, may have direct toxic effects on the vasculature. Activation of the clotting cascade within the lumen of damaged vessels may lead to fibrin deposition with localized intravascular coagulation.9

Glomerulonephritis, inflammation of the glomerulus, is the third leading cause of kidney failure.1–5 Many disorders that cause unregulated and uncontrolled inflammation can destroy the glomeruli. Regardless of how the process begins, locally activated cellular, immunologic, and biochemical mediators of inflammation do the damage.

Focus on the stages ...
Focus on the stages ...
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The location, type, and intensity of injury to the glomeruli vary from one person to another. At one extreme, the capillary wall or mesangium (the membrane supporting the capillary loops in the glomerulus) undergoes mild structural change with minimal cellular damage. The other extreme consists of intense mesangial cell proliferation, white blood cell (WBC) infiltration, capillary wall damage, and exudate.2

The rate at which glomerulonephritis progresses also varies among individuals, but abnormal changes at the tissue level generally follow this pattern:

* early phase, cellular infiltration, exudative reactions

* chronic phase, macrophage/monocyte infiltration, varying degrees of parenchymal cell proliferation

* late phase, structural sclerotic and fibrotic changes.10

Predictors for renal recovery are the degree of kidney function remaining and kidney size. If the kidneys are smaller than normal and are at a later CKD stage, recovery is less likely.2

Although glomerular antigen-antibody complex formation and deposition are responsible for most cases of glomerulonephritis, the role of substances called circulating permeability factors, which seem to be involved in development of abnormal glomerular permeability to plasma proteins (causing proteinuria), is being investigated in certain noninflammatory glomerulopathies.10

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Tune in to subtle clues

Considered a silent disease, CKD can progress quietly over months or several years. Many patients are diagnosed while being evaluated for another condition. Signs and symptoms depend on the cause of CKD, the stage of disease, and the patient's medical condition.

A thorough health history and head-to-toe physical assessment may reveal altered cognitive ability and concentration, fatigue, headache, cold intolerance, a metallic or "off" taste, halitosis, dyspnea, palpitations, angina, hypertension, irregular pulse, nausea, vomiting, hiccups, weight loss, anorexia, increased or decreased urine output, nocturia, generalized pruritus, abnormally pale or darkened skin, nail changes, thinning hair, dry skin, bruising, increased bleeding, muscle twitching or cramping, and edema.2,11 Emotional signs and symptoms include depression, denial, anxiety, and agitation.

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Interpreting test results

Diagnostic studies can help establish the cause of chronic or acute kidney disease and are used to stage CKD when it's identified.

Urine dipstick for protein. A patient with persistent urine protein should have a workup for CKD. Persistent proteinuria is defined as 1+ protein on standard dipstick two or more times over a 3-month period.

A patient with diabetes should have a 24-hour microalbuminuria test to screen for early stages of kidney disease. Ms. Ruiz's test result is 35 mg/L (normal, less than 30 mg/L).

Routine urinalysis can reveal low specific gravity in advanced kidney disease and abnormal amounts of WBCs or the presence of red blood cells (RBCs), bacteria, casts, or protein. Specific gravity is an important gauge of the kidneys' ability to concentrate urine, a process that decreases with declining renal tubular function. An abnormal number of WBCs may be due to chronic pyelonephritis; RBCs may signal glomerulonephritis. Casts are present in some types of acute renal failure but not typically in CKD.2

Albumin-to-creatinine ratio. Regardless of the patient's hydration status, a urine test for albumin-to-creatinine ratio provides an accurate estimate of the albumin excretion rate. A ratio greater than 300 mg albumin/1 g creatinine in someone who doesn't have diabetes signals CKD. Because people with diabetes have a high incidence of renal failure, a patient with diabetes whose ratio is greater than 30 mg albumin/1 g creatinine should receive evaluation and treatment by a nephrologist.3,5

Serum creatinine, blood urea nitrogen (BUN), and albumin levels. Increased serum creatinine and BUN levels signal decreased kidney function. The serum albumin level decreases as albumin excretion in the kidneys increases.

Estimated GFR, a relatively accurate reflection of kidney function, gauges the rate at which the kidneys filter blood. Using the MDRD (Modification of Diet in Renal Disease) equation or the Cockcroft-Gault formula, the healthcare provider uses the patient's serum creatinine level and factors such as age, weight, sex, and race to calculate GFR. (These formulas are available at http://www.nephron.com and http://www.kidney.org/professionals/kdoqi/gfr_calculator.cfm.)

Blood chemistries. A liver profile, thyroid function tests, and electrolyte, calcium, phosphorus, magnesium, glucose, and parathyroid hormone (PTH) levels are checked to rule out other abnormalities. An elevated PTH level signals secondary hyperparathyroidism. This occurs in later stages of CKD because decreased serum calcium levels due to impaired calcium absorption and vitamin D synthesis trigger increased PTH secretion, which can cause a form of bone disease known as renal osteodystrophy. Untreated renal osteodystrophy accelerates hypertension and calcification of the arterial walls, leads to bone changes, and can cause joint and bone pain. A patient with this condition is treated with vitamin D analogue, a pharmaceutically developed form of vitamin D cleaved from vitamin D-25 in the healthy kidney.

A complete blood cell count and iron indices can determine if the patient has anemia, one of the most common complications of CKD. Anemia occurs when the diseased kidneys produce less of the hormone erythropoietin needed to stimulate adequate RBC production by the bone marrow. Treatment with erythropoietin injections and iron replacement therapy is crucial to reduce the risk of cardiovascular disease, the most common cause of death in patients with CKD or any type of kidney failure, and to help reduce fatigue, dyspnea, and cognitive delay. Overcorrecting patients with CKD or ESRD to a hemoglobin greater than 12 has been associated with higher death rates from AMI and stroke, which reinforces the need for lab monitoring and careful patient assessment.12,13

Additional blood tests to help identify underlying disease as a cause of CKD include complement studies, antinuclear antibody titers, and protein electrophoresis.

Imaging studies to evaluate the anatomy and function of the kidneys and to help determine the cause of CKD include X-rays of the kidneys, ureters, and bladder; a renal ultrasound, scan, or angiography; and an abdominal computed tomography scan or magnetic resonance imaging. Although small, atrophied kidneys indicate a progressive disease process, the kidneys can also be normal size or enlarged in diabetic kidney disease. Abnormally shaped kidneys or a missing kidney may indicate a familial disorder or birth defect.

A chest X-ray and 12-lead ECG can detect an enlarged heart or left ventricular hypertrophy, or dysrhythmia, conditions that can limit blood flow to the kidneys, causing renal ischemia.

A renal biopsy may be done so a pathologist can examine the patient's renal tissue under a microscope. If cellular changes indicate a reversible disease such as vasculitis, drug therapy may be recommended.

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Controlling CKD

Modifying risk factors, avoiding nephrotoxic substances, and protecting existing kidney function can help prevent or slow the progression of CKD. The following measures can help:

* Maintain BP at less than 130/80 mm Hg, the level the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends for someone with diabetes or CKD.14

* Regulate blood glucose levels if the patient has diabetes. The American Diabetes Association recommends aiming for a hemoglobin A1C level of 7% for nonpregnant adults in general.15

* Manage dyslipidemia.

* Encourage weight loss if the patient is overweight or obese.

* Develop a smoking cessation plan if the patient smokes.

* Adapt medication therapy as necessary and as ordered by decreasing doses or increasing the time between doses according to the patient's GFR. Educate the patient to avoid using NSAIDs or other medications that can impair renal function.

* Administer an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker to protect kidney function or as a first-line medication to treat hypertension or heart failure.

* Avoid intravascular iodinated contrast media whenever possible. If it must be used, the patient should receive treatment to protect the kidneys, such as using N-acetylcysteine prophylactically (off-label use) and adequately hydrating the patient before and after the study.

* Teach the patient to restrict dietary protein if ordered. A renal dietitian can help the patient develop a food plan, which typically limits sodium, potassium, and phosphorus, and restricts fluid intake.

* Administer treatment as ordered to correct anemia and abnormal calcium, phosphorus, and PTH levels.

* Encourage patients with diabetes to schedule follow-up visits with their primary care provider or endocrinologist.

* Suggest the patient be referred to a nephrologist if the GFR is 60 mL/min/1.73 m2 or less for development of a plan to slow progression of CKD.

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Nursing guidelines

When you care for a patient with known CKD, use the following approaches to prevent further kidney damage and manage complications:

* Review medications and dosages to make sure they're appropriate for the patient's stage of kidney impairment. (Some hospital computer and pharmacy systems signal an alert when dosages need to be decreased for a patient with kidney dysfunction.) Certain medications, such as metformin, bisphosphonates, and NSAIDs, aren't appropriate at all for patients in later stages of CKD. Good drug references include cautions and adjustments for patients with kidney disease.

* Assess your patient's exposure to intravascular iodinated contrast media, including testing in other facilities, because repeated exposures can hasten renal damage. If the patient has recently undergone intravascular contrast studies, ask the primary care provider to determine whether the benefit of further exposure is worth the risk. Protective measures can be ordered if additional studies are warranted.

* Monitor your patient's intake and output and adherence to any dietary restrictions. Weigh the patient daily before breakfast, as ordered, and report gains or losses of 3 pounds (1.4 kg) or more in 24 hours.

* Monitor BP to identify problems and gauge the patient's response to medication.

* Auscultate the lungs and heart. Inspiratory crackles and an S3 can indicate fluid overload. A cardiac dysrhythmia may indicate electrolyte imbalance.

* Educate your patient and family about CKD. Patients are more likely to succeed in limiting or slowing complications when they understand the disease and rationales for treatments. (See Teaching points.)

* Encourage the patient to learn about dialysis, even if it's not needed now. Many dialysis facilities offer classes on this important topic. Educate the patient about treatment options for renal failure, including home dialysis therapies such as peritoneal dialysis and home hemodialysis, and renal transplantation.

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Preparing for dialysis

Patients who are prepared with education and placement of an arteriovenous (AV) fistula before they need hemodialysis have lower mortality than patients who start emergency dialysis through a central venous access. In addition, patients who have the opportunity and time to decide which treatment best fits their lifestyle are more likely to select home therapies. See http://www.homedialysis.org for more information about home dialysis modalities.

When your patient has an AV fistula, follow facility policy and procedure to alert others not to use the extremity for procedures such as I.V. access, phlebotomy, injections, or BP readings. Explain to the patient how to protect the access arm as well.

If patients reach ESRD and believe that dialysis or renal transplant would adversely affect their quality of life, support their decision by referring them to a counselor, healthcare provider, and hospice program. Be sure to ask patients whom they want to include in conversations and planning about this decision. As with any chronic illness, encourage patients to consider advanced care planning.

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Prevention takes center stage

Ms. Ruiz has lost 10 pounds, she's controlling her blood glucose and BP at the recommended levels, and her primary care provider has added an ACE inhibitor to help manage heart disease. Scheduled for a cardiac stress test and her first appointment with a nephrologist, she's taking all the necessary steps to prevent the progression of CKD.

The CKD staging system provides a solid basis for helping a patient with CKD manage the condition. Your recognition of the risk factors, patient education, and protective measures can help your patient prevent progression of CKD to a more critical stage.

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Teaching points

Use these techniques to help patients cope with CKD:

* Teach them about medications and lab results.

* Encourage them to get involved in their care and to ask questions. Teach patients to call the nephrologist or primary care provider when new medications are ordered to make sure the drug and dosing are appropriate. Understanding the significance of lab results and self-monitoring BP and blood glucose levels empowers patients.

* Encourage patients to work with members of the interdisciplinary team, such as the dietitian for meal planning and the social worker for financial information and support.

* Teach patients with an AV fistula to keep the site clean, recognize the signs of infection, and check the fistula for blood flow. Make sure they know when to call the healthcare provider or dialysis center if a problem arises. Tell them to avoid activities that could injure the site, including carrying heavy objects, wearing tight sleeves, and sleeping on the access arm. Warn them not to let healthcare providers use that arm to take BP, draw blood, or give an injection.

* Patients who have a peritoneal catheter also need to keep the exit site clean and avoid heavy lifting or constipation to avoid increasing intra-abdominal pressure, which can lead to hernias or leakage of peritoneal fluid into tissue of the abdomen and pelvis. Warn them to stay out of lakes, hot tubs, or other water that's not chlorinated because of the risk of infection in the peritoneum.

* Discuss quality-of-life concerns, including hospice if appropriate and advance medical directives. Encourage patients to share end-of-life preferences with their family and healthcare providers.

* Tell patients how to find information from reliable sources such as the National Kidney Foundation, local resources, and support groups. Many health insurance providers have education programs for people with chronic diseases such as kidney disease and diabetes. Patients can call the insurer's member services or toll-free number to find out if their company offers such a program.

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REFERENCES

1. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Kidney Disease Outcomes Quality Initiative. Am J Kidney Dis. 2002;39(suppl 1):S1–S266

2. Molzahn AE, Butera E. Contemporary Nephrology Nursing: Principles and Practice. 2nd ed. Pitman, NJ: American Nephrology Nurses' Association; 2007.

3. National Kidney Disease and Urologic Diseases Information Clearinghouse (NKUDIC). NIH, 2006. http://www.kidney.niddk.nih.gov.

4. United States Renal Data System. Annual Data Report, 2009. http://www.usrds.org/adr.htm.

5. National Kidney Foundation. Chronic kidney disease (CKD). http://www.kidney.org/kidneydisease/ckd/index.cfm.

6. Healthy People 2010 Objectives: Chronic kidney disease. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). http://www.healthypeople.gov/Document/HTML/Volume1/04CKD.htm.

7. National Institute of Diabetes and Digestive and Kidney Diseases. Epidemiology of Diabetes Interventions and Complications Study (EDIC). http://www.niddk.nih.gov/patient/edic/edic-public.htm.

8. Molitch ME, DeFronzo RA, Franz MJ, et al.; American Diabetes Association. Neuropathy in diabetes. Diabetes Care. 2004;27(suppl 1):S79–S83.

9. Ferenza FC. Textor SC, Rosenthal D. Nephrosclerosis. http://emedicine.medscape.com/article/244342-overview.

10. Vielhauer V, Schlondorff D, Anders H-J. Disease mechanisms of glomerulonephritis: chemokines and chemokine receptors. Drug Discov Today Dis Mech. 2004;1(1):1–90.

11. Burrows-Hudson S, Prowant BF. Nephrology Nursing Standards of Practice and Guidelines for Care: A Comprehensive Document. Pitman, NJ: American Nephrology Nurses' Association; 2005.

12. Singh AK, Szczech L, Tang KL, et al; CHOIR investigators. Correction of anemia with epoetin alfa in chronic kidney disease. N Engl J Med. 2006;355(20):1–2098.

13. Drueke TB, Locatelli F, Clyne N, et al; CREATE investigators. N Engl J Med. 2006;355(20):1–2084.

14. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). http://www.nhlbi.nih.gov/guidelines/hypertension/index.htm.

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RESOURCES
American Association of Kidney Patients (AAKP) http://www.aakp.org

American Nephrology Nurses' Association (ANNA) http://www.annanurse.org



National Kidney and Urologic Diseases Information Clearinghouse http://www.kidney.niddk.nih.gov

National Kidney Foundation: Kidney Early Evaluation Program (KEEP) http://www.kidney.org/news/keep/index.cfm

© 2010 Lippincott Williams & Wilkins, Inc.

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