Running head: CHRONIC KIDNEY DISEASE

Chronic Kidney Disease: An Overview

Sally Clas, Naomi Everett, Linda Nelson, Angel Nicholson
Frostburg State University
Nursing 401
Spring 2013

CHRONIC KIDNEY DISEASE

Chronic Kidney Disease: An Overview

Chronic Kidney Disease and its Pathophysiology
Lewis, Heitkemper, Dirksen, O'Brien, & Bucher (2007) summarize the kidneys primary
purpose as the regulation of homeostasis by filtering the blood (i.e., regulate extracellular fluid
volume and composition and maintain blood pressure and acid-base balance). Normal kidney
function consists of multiple processes: filtration, reabsorption, secretion, and excretion.
Filtration occurs at the glomerulus. Its semipermeable membrane does not allow for very large
components of blood (i.e., blood cells, platelets, and plasma proteins) to cross the membrane into
the filtrate, thus sequestering them within the blood vessel. Reabsorption of glucose, amino
acids, small proteins, electrolytes, and water takes place in the proximal tubule and Loop of
Henle. The distal tubule is responsible for the secretion of potassium (K+), hydrogen ions (H+),
and ammonia. Reabsorption of bicarbonate (HCO3-), calcium (Ca2+), phosphate ions (PO42-),
sodium (Na+), and K+ occur in the distal tubule as well. In addition to urine formation, the
kidneys secrete erythropoietin, renin and activate vitamin D. Erythropoietin is produced by the
kidneys in response to hypoxia and a decrease in renal blood flow, which in turn stimulates
production of red blood cells. The kidneys produce renin in response to decreases in renal
perfusion, arterial blood pressure, extracellular fluid, and serum Na+ or an increase in urine
Na+. The renin-angiotensin-aldosterone response manages blood pressure by regulating water
and Na+ retention. Vitamin D activation is a two-step process, the first occurring in the liver and
the second occurring in the kidneys.
The National Kidney Foundation (NKF) defines chronic kidney disease (CKD) as
kidney damage or a glomerular filtration rate of less than 60 mL/min per 1.73 m3 for 3 months
or longer. Kidney damage is defined as pathologic abnormalities of markers for damage,

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including abnormalities in blood or urine test or imaging studies (as cited in Broscious &
Castagnola, 2006, p. 18). Broscious and Castagnola (2006) explain the leading causes of CKD in
the United States are diabetes mellitus and hypertension. Both cause damage to the kidneys
ability to effectively filter, reabsorb, secrete, and excrete. Damage to the glomerulus increases its
permeability, allowing albumin (protein) and blood cells to escape the blood vessel resulting in
proteinuria and hematuria. Decrease in glomerular filtration rate (GFR) affects the ability of the
kidneys to excrete water. Both serum protein loss and increase in water retention contribute to
fluid volume overload. Retention of water and an increase in renin related to damage to the
renin-angiotensin-aldosterone system leads to hypertension (HTN). Metabolic acidosis results
from impaired ability to excrete H+. Electrolyte imbalances result from impaired excretion of
both K+ and PO42- and impaired Vitamin D activation that results in a decrease in the bodys
ability to absorb Ca2+ from the intestinal track. Impaired glomerular function results in an
increase in urea reabsorption; uremia contributes to anemia as it shortens the lifespan of the red
blood cell and impairs platelet aggregation. Decrease in the ability of the kidneys to secrete
erythropoietin contributes to anemia as well.
Broscious and Castagnolas (2006) review of laboratory tests in CKD reveal evidence of
impairment of the multiple metabolic processes of the kidneys. Blood urea nitrogen (BUN) and
creatinine, nitrogenous byproducts of protein metabolism, are elevated as a result of increased
retention of these byproducts and are indicative of uremia. Elevated K+ and PO42- result from
impaired excretion. Increase in water retention affects serum Na+ (dilutional
hyponatremia). Decrease in Ca+ is caused by its inverse relationship with PO42-, loss of serum
albumin as Ca+ binds to this protein, and decreased activation of Vitamin D. Anemia is
monitored through hemoglobin and hematocrit levels. These levels are expected to be low in the

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presence of uremia and decreased erythropoietin production. Arterial blood gas (ABG) analysis
may indicate metabolic acidosis. Normal functioning kidneys will excrete H+ and retain
HCO3-. Glomerular damage causes impaired excretion of H+ (which results in low pH). In CKD,
acid-base balance is maintained by the retention of HCO3-, which can result in metabolic
acidosis. Urinalysis results for both proteinuria and hematuria is expected related to increased
permeability of the glomerulus.
Chronic Kidney Disease and the Cardiovascular System
CKD that is untreated or uncontrolled can have drastic effects on the organ systems of the
body. One such system is the cardiovascular system. In the early stages of kidney disease,
coronary artery disease (CAD), left ventricular hypertrophy (LVH), atherosclerosis,
cerebrovascular accident (CVA), and HTN can occur. LVH, atherosclerosis, and HTN are also
considered risk factors for the development of kidney disease. LVH is due to an increase in
myocardial workload over prolonged periods of time. Left ventricular hypertension results from
systemic hypertension and can develop into cardiomyopathy. LVH can occur in the early stages
of the disease, or at later stages when dialysis therapy is warranted.
HTN is the leading cause of CKD. The National Kidney Foundation (2013) notes that
CKD may also be a causative factor in the development of HTN. The kidneys aid the
cardiovascular system in its regulation of blood pressure. A diagnosis of HTN is made when
there are persistent elevations of systolic and diastolic blood pressure. According to McCarley
and Salai (2005), hypertension is a blood pressure greater than 130/80 mm Hg. A persistent,
increased workload on the heart due to vasoconstriction causes HTN. Micro albuminuria, a
presence of albumin in the urine, is known to increase the prevalence of hypertension (McCarley
and Salai, 2005). HTN can lead to a CVA or stroke in some people.

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In addition to the above-mentioned pathologies, persons with CKD may be predisposed

to the development of atherosclerosis and CAD. According to the National Institutes of Health
(2011), atherosclerosis affects the arteries, which carry oxygenated blood to all body systems.
Atherosclerosis is a build up of plaque inside the walls of arteries. This build up results in a
narrowing of the lumen that causes a smaller diameter for blood to travel thus reducing the
oxygen rich supply of blood to important body systems (National Institutes of Health, 2011).
CAD is a result of atherosclerosis and plaque in the coronary arteries. This plaque buildup may
lead to clot formation and myocardial infarction (National Institutes of Health, 2011). A
symptom of CKD, uremia can cause atherosclerosis. McCarley and Salai (2005) noted that
studies of patients with CKD and uremia have shown this population to be four times more likely
to have the presence of heavily calcified plaques.
Chronic Kidney Disease and the Endocrine System
CDK also affects the endocrine system, preventing the kidneys from releasing important
endocrine hormones. The kidneys maintain fluid balance in the body by regulating and
continuously exchanging water and solutes inside and around cellular membranes. The endocrine
system and its hormones assist in the kidneys role in maintaining this delicate fluid balance. A
malfunction within these hormones may cause a variation in the Na+ and K+ levels that can lead
to HTN. This control depends on the responses of the osmoreceptors and changes they detect in
osmolality.
According to Lippincott Williams & Wilkins (2009), one of the hormones involved with
fluid balance is the antidiuretic hormone (ADH) that is formed by the hypothalamus and stored
by the pituitary gland. ADH increases water permeability of the distal and collecting tubules of
the kidneys, which causes water reabsorption in the body. When the ADH concentration in

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plasma is increased, the tubules are more permeable to water. This leads to an increased water
absorption that results in a small volume of highly concentrated urine, which exhibits a high
specific gravity. According to Lippincott Williams & Wilkins (2009), if the ADH concentration
is decreased, the tubules will be less permeable to water and thus more water will be excreted;
which will cause less concentrated urine with a low specific gravity. Diabetes insipidus is caused
by a deficiency of ADH. When ADH is absent, fluid is excreted in large quantities (4-16 L/day)
of diluted urine instead of being reabsorbed. This is known as polyuria. In an attempt to replace
the extreme fluid loss associated with polyuria, polydipsia develops. Polydipsia is characterized
by excessive thirst or the consumption of large amounts of fluid. Nephrogenic diabetes insipidus,
a common result of renal disease, occurs when the kidneys are unable to respond to ADH.
Aldosterone is another hormone important to kidney function. Aldosterone is produced
and released by the adrenal cortex. It regulates water reabsorption in the distal tubules and
changes the concentration of urine by increasing or decreasing Na+ reabsorption. High plasma
concentrations of aldosterone increase Na+ reabsorption, while low plasma levels promote the
excretion of water and Na+ in urine. Aldosterone also assists in the regulation of K+ by the distal
tubules. High aldosterone concentrations can increase the excretion of K+. K+ can also be altered
by foods high in K+, the number of hydrogen ions secreted, the amount of Na+ in the distal
tubules, the GFR, and the amount of K+ within the cells.
The kidneys are responsible for generating renin, thrombopoietin, erythropoietin, and
calcitriol. The kidneys assist in regulating blood pressure by producing and secreting renin in
response to sympathetic or parasympathetic reactions. According to Rubin and Strayer (2005),
renin forms angiotensin I, which is then converted into angiotensin II; a more potent vasopressor.
Angiotensin II raises low arterial blood pressure by increasing peripheral vasoconstriction and

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stimulating the secretion of aldosterone. This increased uptake of aldosterone promotes the
reabsorption of water and sodium to correct the fluid deficit and renal ischemia from the
decreased blood flow of a MAP <60. High blood pressure damages the blood vessels and causes
nephrosclerosis, which is a leading cause of renal failure. HTN can be caused by fluid and
electrolyte imbalances as well as renin angiotensin hyperactivity. Thrombopoietin is a hormone
that increases the production and secretion of platelets, which in turn speeds up the healing
capabilities within the body. Erythropoietin is a hormone that prompts the bone marrow to
increase red blood cell production and nutrients when the oxygen supply in the blood is in
demand. Loss of renal function results in chronic anemia and hypocalcemia; this is a direct result
of decreased erythropoietin. Calcitriol increases the bodys absorption of calcium. The kidneys
assist in the conversion of vitamin D to its active form. Activated vitamin D helps to regulate
calcium and phosphorus balance and bone metabolism. When the kidneys fail hypophosphatemia
and hypocalcemia occur.
Patient Education Material: Chronic Kidney Disease
According to Estes (2010), In 2004, an estimated 69.7% of the U.S. population was
Euro-American (predicted to be only 52.8% by the year 2050) and 30.3% were members of
ethnic and cultural minority groups: 12.3% African Americans, 13% Hispanic (the fastest
growing minority group in the U.S.), 4.2% Asian and Pacific Islander, and 0.8% American
Indian (p. 122). As the racial, ethnic, and cultural diversification of American society
accelerates at an unprecedented rate, the health care delivery system must adapt and parallel
these changes to effectively communicate and educate these expanding groups.
McCray (2005) defines health literacy as the degree to which an individual has the
capacity to obtain, communicate, process, and understand basic health information and services

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to make appropriate health decisions (p. 152). Every day people are challenged with lifechanging health decisions. These decisions often are made in the typical places of doctors
offices, clinics, and hospitals. They are also made in atypical places such as at shopping malls,
around water coolers at work, during social events, and family gatherings. Many decisions are
based upon materials found on the Internet. The essential steps in making proper health decisions
consist of obtaining, communicating, processing, and understanding health information.
The National Kidney Foundation, a major voluntary nonprofit health organization, is
dedicated to preventing kidney and urinary tract diseases, improving the health and well-being of
individuals and families affected by kidney disease and increasing the availability of all organs
for transplantation (http://www.kidney.org/about/mission.cfm). The Appendix of this paper
contains a selection of patient education retrieved from the NKF webpage labeled, About
Chronic Kidney Disease. This information, along with many other articles on the website, is
available in English and Spanish languages. It also includes a listing of persons who are most
vulnerable to the development of CKD; African Americans, Hispanics, Pacific Islanders, Native
Americans, and seniors.
About Chronic Kidney Disease was evaluated according to the Simple Measure of
Gobbledegook (SMOG) readability formula to determine the readability of its text. The
readability formula carries out calculations on text, which are based primarily on sentence and
word length. The results are given as a numerical score. Other factors which play a role in the
understanding of what is being read, such as reader motivation, size and type of print, layout of
the written material, previous knowledge of the subject, and writer style are not measured in
this formula (NIACE, 2009). There are two versions of the SMOG readability test, an original
and newer version. The original SMOG formula gives a score based on the years of education

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needed to understand a piece of writing. The newer version gives a readability index that can be
correlated to the National Adult Literacy Standards (NALS). The educational article About
Chronic Kidney Disease scored equivalent to an eighth grade level according to the older SMOG
version. Via the newer version, it scored a readability index of approximately 16. This is slightly
greater than a level 2 on the NALS. At a level 2, adults can read straightforward texts of variable
lengths on diverse topics reliably and autonomously. They are also able to read and obtain
information from different sources. As noted by Stossel, Segar, Gliatto, Fallar, & Karani (2012),
countless patient educational materials (PEMs) found on the internet are written at high school or
college reading levels, rendering them inaccessible to the average US resident, who reads at or
below an 8th grade level (p. 1165). To meet the needs of average consumers, an adaptation to a
fifth grade reading level would be beneficial. This could be achieved by the use of simple and
two syllable words. One example of doing so in About Chronic Kidney Disease would be using
the words high blood pressure in place of hypertension. Bullet formatting in the listing of the
symptoms of CKD was an effective strategy when supplying information. Shorter sentences in
the text also make it easier to understand.
McCray (2005) noted, some studies have shown that low-literacy individuals have less
knowledge of their health conditions and treatment regimens, have lower self-management skills,
have higher rates of chronic illness, and do not effectively participate in preventative care (p.
155). For the majority of health care professionals, reading and comprehending information is a
predictable part of the usual routine that assumptions are made regarding patients adequacies in
reading and understanding information. It is important that all health care professionals are
educated to the prevalence and consequences of inadequate health literacy. Persons who struggle

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with health literacy need to be compassionately identified so that barriers can be broken and their
literacy needs are met.

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References

Broscious, S. K., & Castagnola, J. (2006). Chronic kidney disease: Acute manifestations and role
of critical care nurses. Critical Care Nurse, 26(4), 17-27. Retrieved February 11, 2013,
from http://ccn.aacnjournals.org/content/26/4/17.full.pdf+html
Estes, M. E. (2010). Health Assessment & Physical Examination (4th ed.). Clifton Park, NY:
Delmar.
Lewis, S., Heitkemper, M., Dirksen, S., O'Brien, P., & Bucher, L. (2007). Medical-surgical
nursing: Assessment and management of clinical problems (7th ed.). St. Louis, Mo:
Mosby Elsevier.
Lippincott Williams & Wilkins. (2009). Pathophysiology made incredibly easy (4th ed.).
Philadelphia, PA: Wolters Kluwer.
McCarley, P., & Salai, P. (2005, April). Cardiovascular disease in chronic kidney disease:
Recognizing and reducing the risk of a common CKD comorbidity. American Journal of
Nursing, 105(4), 40-52.
McCray, A. T. (2005). Promoting health literacy. Journal of the American Medical Informatics
Association, 12(2), 152-163. Retrieved from http://dx.doi.org/10.1197/jamia.M1687
National Institute of Adult Continuing Education (NIACE) (2009). Readability: How to produce
clear written materials for a range of readers. Retrieved from
http://www.niace.org.uk/misc/SMOG-calculator/smogcalc.php
What is atherosclerosis? (2011). National Institutes of Health. Retrieved February 7, 2013, from
http://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis

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High blood pressure and chronic kidney disease in children: A guide for parents. (2013).
National Kidney Foundation. Retrieved February 11, 2013, from
http://www.kidney.org/atoz/content/hbpchildren.cfm
Rubin, R. & Strayer, D. (2005). Rubins Pathology: Clinicopathologic Foundations of Medicine,
(4th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
Stossel, L., Segar, N., Gliatto, P., Fallar, R., & Karani, R. (2012, September 27). Readability of
patient education materials available at point of care. JGIM: Journal of Internal General
Medicine, 27, 1165-70.

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Appendix

ABOUT CHRONIC KIDNEY DISEASE

Chronic kidney disease (CKD) is a condition characterized by a gradual loss of kidney
function over time.
What is chronic kidney disease (CKD)?
Chronic kidney disease includes conditions that damage your kidneys and decrease their ability
to keep you healthy by doing the jobs listed. If kidney disease gets worse, wastes can build to
high levels in your blood and make you feel sick. You may develop complications like high
blood pressure, anemia (low blood count), weak bones, poor nutritional health and nerve
damage. Also, kidney disease increases your risk of having heart and blood vessel disease. These
problems may happen slowly over a long period of time. Chronic kidney disease may be caused
by diabetes, high blood pressure and other disorders. Early detection and treatment can often
keep chronic kidney disease from getting worse. When kidney disease progresses, it may
eventually lead to kidney failure, which requires dialysis or a kidney transplant to maintain life.
The Facts About Chronic Kidney Disease (CKD)
26 million American adults have CKD and millions of others are at increased risk.
Early detection can help prevent the progression of kidney disease to kidney failure.
Heart disease is the major cause of death for all people with CKD.
Glomerular filtration rate (GFR) is the best estimate of kidney function.
Hypertension causes CKD and CKD causes hypertension.
Persistent proteinuria (protein in the urine) means CKD is present.
High risk groups include those with diabetes, hypertension and family history of kidney
disease.
African Americans, Hispanics, Pacific Islanders, Native Americans and seniors are at
increased risk.
Three simple tests can detect CKD: blood pressure, urine albumin and serum creatinine.
What causes CKD?
The two main causes of chronic kidney disease are diabetes and high blood pressure, which are
responsible for up to two-thirds of the cases. Diabetes happens when your blood sugar is too
high, causing damage to many organs in your body, including the kidneys and heart, as well as
blood vessels, nerves and eyes. High blood pressure, or hypertension, occurs when the pressure
of your blood against the walls of your blood vessels increases. If uncontrolled, or poorly
controlled, high blood pressure can be a leading cause of heart attacks, strokes and chronic
kidney disease. Also, chronic kidney disease can cause high blood pressure.
Other conditions that affect the kidneys are:
Glomerulonephritis, a group of diseases that cause inflammation and damage to the kidney's
filtering units. These disorders are the third most common type of kidney disease.
Inherited diseases, such as polycystic kidney disease, which causes large cysts to form in the

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kidneys and damage the surrounding tissue.

Malformations that occur as a baby develops in its mother's womb. For example, a narrowing
may occur that prevents normal outflow of urine and causes urine to flow back up to the
kidney. This causes infections and may damage the kidneys.
Lupus and other diseases that affect the body's immune system.
Obstructions caused by problems like kidney stones, tumors or an enlarged prostate gland in
men.
Repeated urinary infections.
What are the symptoms of CKD?
Most people may not have any severe symptoms until their kidney disease is advanced.
However, you may notice that you:
feel more tired and have less energy
have trouble concentrating
have a poor appetite
have trouble sleeping
have muscle cramping at night
have swollen feet and ankles
have puffiness around your eyes, especially in the morning
have dry, itchy skin
need to urinate more often, especially at night.
Anyone can get chronic kidney disease at any age. However, some people are more likely than
others to develop kidney disease. You may have an increased risk for kidney disease if you:
have diabetes
have high blood pressure
have a family history of chronic kidney disease
are older
belong to a population group that has a high rate of diabetes or high blood pressure, such as
African Americans, Hispanic Americans, Asian, Pacific Islanders, and American Indians.
Learn more About Glomerular Filtration Rate (GFR)
GFRglomerular filtration rate is the best test to measure your level of kidney function and
determine your stage of kidney disease. Your doctor can calculate it from the results of your
blood creatinine test, your age, race, gender and other factors.
The earlier kidney disease is detected, the better the chance of slowing or stopping its
progression.
What happens if my test results show I may have chronic kidney disease?
Your doctor will want to pinpoint your diagnosis and check your kidney function to help plan

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your treatment. The doctor may do the following:

Calculate your Glomerular Filtration Rate (GFR), which is the best way to tell how much
kidney function you have. You do not need to have another test to know your GFR. Your
doctor can calculate it from your blood creatinine, your age, race, gender and other
factors. Your GFR tells your doctor your stage of kidney disease and helps the doctor
plan your treatment.
Perform an ultrasound or CT scan to get a picture of your kidneys and urinary tract. This tells
your doctor whether your kidneys are too large or too small, whether you have a problem
like a kidney stone or tumor and whether there are any problems in the structure of your
kidneys and urinary tract.
Perform a kidney biopsy, which is done in some cases to check for a specific type of kidney
disease, see how much kidney damage has occurred and help plan treatment. To do a
biopsy, the doctor removes small pieces of kidney tissue and looks at them under a
microscope.
Your doctor may also ask you to see a kidney specialist who will consult on your case and help
manage your care.
http://www.kidney.org/kidneydisease/aboutckd.cfm