Acute and Chronic Renal Failure Self Learning Module 2008

ACUTE AND CHRONIC RENAL FAILURE
SELF LEARNING MODULE
Abbotsford Regional Hospital Clinical Education
Rona Miller, 2008 Page 1 of 46

Table of Contents
INTRODUCTION 3
PURPOSE 3
OBJECTIVES 4
PRE TEST 5
PART A: ANATOMY & PHYSIOLOGY 7
PART B: ACUTE RENAL FAILURE 11
Causes of ARF 12
Stages of ARF 16
Assessment of ARF 18
Lab Tests 23
Diagnostic Tests 24
Nursing Care of Patients with ARF 25
ARF Treatment 27
PART C: CHRONIC RENAL FAILURE 29
Stages of Chronic Renal Failure 29
Causes of Chronic Renal Failure 30
Clinical Manifestations of Chronic Renal Failure 31
Nursing Care of Patients with Chronic Renal Failure 33
REFERENCES 36
POST TEST 37
ANSWER KEY 41
EVALUATION FORM 44
INTRODUCTION
The learning module includes a definition of renal failure, acute and chronic, a
review of the pathophysiology of renal failure, common patient symptoms, diagnostics
and medications generally prescribed to manage the symptoms of renal failure. It is the
hope that a review of this educational module will enhance your working knowledge of
renal failure and the current recommendations for the management of renal failure. The
module is divided into THREE MAIN SECTIONS; Part A—Anatomy and Physiology
Review, Part B—Acute Renal Failure, and Part C-Chronic Renal Failure.
Once you have completed the learning module, please
complete the evaluation form in order to better improve this
module to meet your leaning needs. Please return the
completed evaluation to your CNE by placing the evaluation in
an internal mail envelope and addressing it to your CNE.
PURPOSE
The purpose of this learning module is to provide you with:
a. A review of the pathophysiology of acute renal failure and chronic renal failure.
b. A review of risk factors for acute renal failure and chronic renal failure.
c. A review of signs and symptoms of acute renal failure and chronic renal failure.
d. Assessment parameters of patients with renal failure.
e. A review of the diagnostic tests used to diagnose and determine the severity of
acute renal failure and chronic renal failure.
f. An overview of the treatment of acute renal failure and chronic renal failure,
including pharmacotherapy and non-pharmacological interventions.
OBJECTIVES
At the completion of this learning package, you will be able to:
i. Explain the pathophysiology of acute renal failure and chronic renal failure.
ii. Differentiate between acute renal failure and chronic renal failure.
iii. Understand risk factors for acute renal failure and chronic renal failure.
iv. Discuss how acute renal failure and chronic renal failure is diagnosed and
classified.
v. Understand treatment goals and relevant laboratory and diagnostic tests.
vi. Describe common treatments for acute renal failure and chronic renal failure
including lifestyle modification and medication.
Now please take a few minutes to complete the Pretest.
PRETEST
1. A patient is admitted to the hospital with chronic renal disease. The nurse
understands that this condition is characterized by
a. Progressive irreversible destruction of the kidneys.

b. A rapid decrease in urinary output with an elevated BUN.
c. An increasing creatinine clearance with a decrease in urinary output.
d. Prostration, somnolence, and confusion with coma and imminent death.
2. Prerenal causes of acute renal failure include
a. Prostate cancer and calculi formation.

b. Hypovolemia and myocardial infarction.
c. Acute glomerulonephritis and neoplasms.
d. Septic shock and nephrotoxic injury from drugs.
3. During the oliguric phase of acute renal failure, the nurse monitors the patient for
a. Hypernatremia and CNS depression.

b. Pulmonary edema and ECG changes.
c. Kussmaul respirations and hypotension.
d. Urine with high specific gravity and low sodium concentration.
4. If a patient is in the diuretic phase of acute renal failure, the nurse must monitor for
which serum electrolyte imbalances?
a. Hyperkalemia and hyponatremia.

b. Hyperkalemia and hypernatremia.
c. Hypokalemia and hyponatremia.
d. Hypokalemia and hypernatremia.
5. A systemic effect of chronic renal disease that is usually reversed by the initiation of
dialysis is
a. Anemia.
b. Hyperlipidemia.
c. Psychological changes.
d. Nausea and vomiting.
6. Measures indicated in the conservative therapy of chronic renal disease are
a. Decreased fluid, carbohydrate, and protein intake.
b. Increased fluid intake and decreased carbohydrate and protein intake.
c. Decreased fluid and protein intake and increased carbohydrate intake.
d. Decreased fluid and carbohydrate intake and increased protein intake.
7. Two major causes of intrarenal acute renal failure are
a. Dehydration and increased cardiac output.

b. Calculi in the ureters and hypovolemic shock.
c. Aminoglycoside antibiotics and radiocontrast dye administration.
d. An obstructed foley catheter and benign prostatic hypertrophy.
8. During which phase of acute tubular necrosis are hyperkalemia, gastrointestinal

bleeding, infection, and vascular volume overload major potential problems?
a. Onset phase.
b. Oliguric phase.
c. Diuretic phase.
d. Recovery phase.
9. Which of the following statement is true about chronic renal disease?
a. Sometimes it is reversible.
b. Hypertension is the most common cause.
c. Ultimately, it leads to end-stage renal disease (ESRD).
d. It has a sudden onset.
10. The causes of metabolic acidosis in renal failure include
a. Increased renal secretion and excretion of hydrogen ions.

b. Decreased reabsorption of bicarbonate.
c. Increased exhalation of carbon dioxide.
d. A decrease in catabolism.
No peeking at the answers until you have completed the Pretest. The answers
can be found on page 42. If you correctly answered 9 or
more—you do not need to complete this module although
it is recommended that you do-there is interesting and
informative information in the module to enable you to
provide evidence based nursing care to your patients
with acute renal failure and chronic renal failure!
PART A: ANATOMY AND PHYSIOLOGY REVIEW
Prior to reviewing renal failure let’s first review normal kidney function.
Urinary System
The urinary system consists of two kidneys, two ureters, a urinary bladder, and a
urethra. The system maintains homeostasis by removing waste products and by either
conserving or excreting fluid and electrolytes.
Kidney
The kidneys are two bean-shaped

organs positioned retroperitoneally
in the posterior abdominal wall at the
level of the 12th thoracic vertebra to
the third lumbar vertebra. Each
kidney weighs about 4-6 ounces
(115-175g) and is about 12 cm (5
inches) long. The right kidney, with
the liver above it, is lower than the
left. An adrenal gland lies on top of
each kidney.
The kidney consists of the cortex, medulla and pelvis. The cortex and medulla
are called the renal parenchyma. The medulla contains the renal pyramids or collecting
ducts. The cortex and medulla contain the nephrons, which are primarily composed of
tubular structures and blood vessels surrounding the nephrons. The nephrons produce
urine. The renal artery supplies the blood supply to the kidneys.
Nephron
The nephron is the functional unit of the kidney. Each nephron is composed of
three major structures: a glomerulus, tubular apparatus, and collecting duct. There are
approximately 1.25 million nephrons in each kidney composed of vascular (blood flow)
and tubular (urine flow) systems that promote the formation of urine. The vascular
system of a nephron includes the glomerulus and vasa recta. The glomerulus is
composed of a tight cluster of capillaries and the afferent and efferent loops.
Surrounding each glomerulus is a Bowman’s capsule, the initial structure of the

tubular system. Connected to the Bowman’s capsule is the proximal convoluted tubule
which becomes the Loop of Henle. At the distal end of the Loop of Henle is the distal
convoluted tubule.
The primary function of the nephron is to filter waste products from the blood as it
flows through the kidneys.
Glomerular Filtration
Glomerulur filtration is the process by which fluid and solutes are moved from the
vascular system into the tubular system of the nephron, from an area of high pressure
to an area of low pressure. The glomerulus is a high pressure, semipermeable capillary
bed. Glomerular filtrate consists of:
• Water (H2O), hydrogen ions(H+)

• Electrolytes: sodium (Na+), potassium (K+), calcium (Ca++), magnesium (Mg++),
chloride (Cl - ), bicarbonate (HCO3- ), phosphate (PO4- )
• Waste products: urea, creatinine, uric acid
• Metabolic substances: glucose and amino acids
Functions of the Kidneys

Excretion
Removal of the waste products of metabolism: urea and creatinine.
Removal of excess fluid: concentration and dilution of urine.
Regulation of acid‐base balance: excretion of hydrogen ions and
conservation of bicarbonate ions.
Regulation of electrolyte levels, for example, potassium.
Secretion
Regulation of blood pressure: renin‐angiotensin mechanism.
Regulation of red blood cell production: erythropoietin.
Regulation of calcium metabolism: activated vitamin D.
Time Out 1
Fluid and electrolytes are moved from the vascular system
into the tubular system of the nephron by:
a. Tubular reabsorption
b. Glomerular filtration
c. Vascular resistance
d. Tubular secretion

PART B: ACUTE RENAL FAILURE
If toxins build up I could stop

working!!
Renal disease is a condition arising from many
causes, and often progresses to kidney failure
that requires dialysis or transplantation to
sustain life. Renal disease impacts all body
systems and, combined with the treatment,
affects the person's diet, energy level, self
image, ability to work, and overall lifestyle. It
also affects family members, as their diet, income and roles may also change. When
you understand the various causes and life-threatening effects, you can provide nursing
care that supports recovery.
ACUTE RENAL FAILURE (ARF) is a sudden loss of kidney function with a

buildup of toxic waste products, such as urea and creatinine, in the blood. Unlike
chronic renal failure, in which 90% to 95% of nephrons cease to function permanently
over time, ARF occurs when the kidneys are strained suddenly, causing 50% or more of
the nephrons to lose function so fast that the body can't compensate. It is often
reversible if diagnosed and treated early. However, in some cases damage is
permanent and renal failure becomes chronic.
Although ARF most often affects elderly people, the clinical course and survival
rate are similar in patients of all ages. Occurring in 5% of hospitalized patients, ARF can
lead to complications and death, typically from overwhelming infection or
cardiopulmonary problems. Management of ARF is largely limited to symptom control in
the hope that renal tissues will regenerate and normal function will be restored. Thus,
ARF represents a situation where prevention is undoubtedly better than

cure. An understanding of the likely mechanisms and locations of renal injury can help
in planning preventative strategies and may indicate an opportunity for early intervention
to prevent onset of ARF.
READ ON to learn more about how ARF

develops and what you can do to support
recovery.
CAUSES OF ACUTE RENAL FAILURE

Acute renal failure has many causes and many effects. Although ARF has many
causes, ischemia and toxicity are the most common. Depending on where the problem
originates, ARF can be classified as prerenal, intrarenal, or postrenal.
Prerenal ARF, also known as prerenal azotemia, is the most common type. It
occurs when decreased blood flow to the kidneys causes ischemia of the nephrons.
Blood loss, severe dehydration, septicemia, and cardiogenic shock are common
underlying causes. Fortunately, restoring renal blood flow and glomerular ultrafiltration
can rapidly reverse prerenal ARF. Another important cause of prerenal ARF involves
the use of nonsteroidal anti-inflammatory drugs, cyclooxygenase inhibitors, or
angiotensin-converting enzyme inhibitors. These drugs can impair renal autoregulatory
responses by blocking the production of prostaglandins, which are necessary to
maintain renal perfusion. The risk of problems related to therapy with these drugs is
high in the elderly and those with renal insufficiency, heart failure, and advanced liver
disease.
Intrarenal ARF is caused by problems involving the renal parenchyma. Although
prerenal ARF can trigger this condition, the major cause of intrarenal ARF and ARF in
general is acute tubular necrosis (ATN)---damage to the renal tubules caused by
ischemia or toxins. Although the terms ARF and ATN are often used interchangeably,
they don't mean the same thing. As many as 20% to 30% of patients with ARF caused
by ischemia or nephrotoxicity do not have evidence of tubular necrosis.
Diseases involving the large renal vessels (such as renal artery stenosis) and the
small vessels and glomeruli (as in glomerulonephritis) are among the ischemic causes
of intrarenal ARF. Nephrotoxic substances that can trigger intrarenal ARF include
radiocontrast media, cyclosporine, antibiotics (especially aminoglycosides), and
chemotherapy. Other nephrotoxic substances include heavy metals, such as mercury
and arsenic.
Postrenal ARF refers to renal dysfunction caused by conditions that block urine
flow, causing it to back up into the kidneys. To initiate renal failure, the obstruction must
block urine outflow bilaterally or unilaterally when there is only one functioning kidney.
Prostatic hypertrophy, ureteral obstruction (usually bilateral), and bladder outlet
obstruction are common causes.
CAUSES OF ACUTE RENAL FAILURE
PRERENAL FAILURE INTRARENAL POSTRENAL

FAILURE FAILURE
Cardiovascular Acute tubular Ureteral obstruction

disorders necrosis • Blood clots
• Arrhythmias • Ischemic damage to renal • Calculi
• Cardiac tamponade tissue from unrecognized • Edema or inflammation
• Cardiogenic shock or poorly treated prerenal • Necrotic renal papillae
• Heart failure failure • Retroperitoneal fibrosis or
• Myocardial infarction • Nephrotoxins, including hemorrhage
analgesics; antibiotics, such • Surgery (accidental
Hypovolemia as gentamicin; heavy ligation)
• Burns metals, such as lead; • Tumor
• Dehydration radiographic contrast media • Uric acid crystals
• Diuretic overuse • Obstetric complications,
• Hemorrhage i.e. eclampsia, postpartum Bladder obstruction
• Hypovolemic shock renal failure • Anticholinergic drugs
• Trauma • Myoglobin release, as in • Autonomic nerve
crush injury, sepsis, and dysfunction
Peripheral transfusion reaction • Infection
• Tumor
vasodilation
• Antihypertensive drugs Other parenchymal
• Sepsis disorders Urethral obstruction
• Acute glomerulonephritis • Prostatic hyperplasia or
• Acute interstitial nephritis tumor
Renovascular
• Acute pyelonephritis • Strictures
obstruction
• Bilateral renal vein
• Arterial embolism
thrombosis
• Arterial or venous
• Malignant nephrosclerosis
thrombosis
• Papillary necrosis
• Tumor
• Periarteritis nodosa
(inflammatory disease of
Severe the arteries)
vasoconstriction • Renal myeloma
• Disseminated • Sickle-cell disease
intravascular • Systemic lupus
coagulation erythematosus
• Eclampsia • Vasculitis
• Malignant hypertension
• Vasculitis
Medications that can cause Acute Renal Failure
Acute tubular necrosis
• Aminoglycosides (such as amikacin, gentamicin, tobramycin)

• Radiographic contrast media
• Antineoplastics (such as cisplatin)
• Amphotericin
Hemodynamically mediated renal failure
• Angiotensin-converting enzyme inhibitors

• Angiotensin 11 receptor blockers
• Nonsteroidal anti-inflammatory medications (NSAIDs)
Glomerular disease
• NSAIDs
• Gold
• Hydralazine
Tubulorinterstitial disease
• Methicillin
• NSAIDs
• Cyclosporine
• Lithium
While different causes of acute renal failure are easily

defined, it should be recognized that ARF is frequently the
result of a combination of events, rather than a single
cause. Hence, it may be valuable to identify patient
groups that are at risk of developing ARF so that
preventative measures can be instituted for them. The elderly are considered
particularly at risk of developing ARF due to an age-related reduction in water content
related to loss of muscle mass. Also, there is commonly a reduction in thirst sensation
removing a stimulus for the elderly to maintain adequate hydration. Age-related
changes in the kidney also result in a reduction in the ability to concentrate urine.
Furthermore, the elderly often present to hospital with multiple system disorders, such
as atherosclerosis and cardiac failure, which may reduce renal blood flow.
In summary, there are 3 main causes of acute renal failure: prerenal, which
stems from decreased renal perfusion; intrarenal (usually ATN), caused by problems
involving the renal tissue; and postrenal, which results from obstruction of the urine flow.
Should acute renal failure be left unrecognized or untreated, increased kidney damage
will result with the consequence of permanent damage regardless of the cause.
Time Out 2
Congestive heart failure, hemorrhage, and shock are
examples of possible etiologic factors for development
of which type(s) of renal failure?
Stages of Acute Renal Failure

Changes in renal function can be considered on a continuum that ranges from
mild renal impairment to complete renal failure. Renal failure begins when the kidneys
are not able to meet the demands of dietary or metabolic stress. The progressive
course of acute renal failure can be divided into four stages: onset, oliguric/anuric;
diuretic (early and late), and convalescent.
Onset Stage
The onset stage begins at the time of injury. During this stage, the patient is
acutely ill due to the underlying disorder, as well as the rapid onset of acute renal
failure. There is a decrease in urine output to approximately 20% of normal. This stage
lasts approximately 2 days and ends when the oliguric/anuric stages begins or when
azotemia (accumulation of uremic toxins—urea, uric acid and creatinine-in the blood)
develops in the absence of oliguric/anuric stage.
Oliguric/Anuric Stage
This stage begins when the patient’s urine output falls to less than 400 mLs/24
hrs, which usually occurs by about 48 hours postinjury. This stage can last one to two
weeks, until the early diuresis stage begins. Anuria refers to when the urine output falls
to less than 50 mLs/24 hrs. The longer the patient stays in the oliguric/anuric stage, the
higher the risk of irreversible renal damage and chronic renal failure.
During this stage, the GFR significantly decreases and metabolites, such as
creatinine, urea and potassium, rapidly accumulate since they are normally excreted
through the kidneys. Fluid excess develops in the extracellular and intracellular
compartments, which can result in edema, congestive heart failure, and water
intoxication. Due to significant improvements in the treatment regimen for improving
heart performance and circulatory failure, not all patients with acute renal failure go
through the oliguric/anuric stage.
Diuretic Stage
This stage is divided into two phases based on time: the early diuretic stage and
the late (recovery) stage.
Early Diuretic Stage

The onset of the early diuretic stage begins when the patient’s urine output
increases to over 400mLs/24hrs. It continues until the BUN and creatinine stabilize and
lasts approximately 1 to 2 weeks. During the early diuretic stage, the renal tubules are
beginning to heal and regain their integrity. As this stage progresses, urine output
maybe 1 to 2 Litres/24hrs due to the inability of the kidneys to concentrate urine and the
diuretic effect of the elevated BUN. Fluid and electrolyte levels become difficult to
manage.
Late (Recovery) Diuretic Stage

This stage begins when the patient’s BUN and creatinine begin to decrease. It
continues until the BUN and creatinine levels return to normal, which takes
approximately 10 days. During this stage, renal function continues to improve as the
nephrons heal. A high urine output continues, which requires ongoing monitoring of fluid
and electrolyte balance.
Convalescent Stage
The convalescent stage begins when the patient’s laboratory values have
returned to normal. It ends with the return of normal renal function, lasting 6 months to a
year. During this stage, the patient’s urine output returns to normal with the return of the
patient’s ability to concentrate urine. However, the kidneys are extremely vulnerable
during this stage, and therefore, it is important to avoid the use of nephrotoxic agents.
The patient requires close monitoring and management of fluid and electrolytes and
evaluation of the degree of permanent renal damage.
ASSESSMENT of ACUTE RENAL FAILURE
In the acutely ill patient, renal dysfunction often has an

insidious onset. It may be first suspected when urine
output stays below normal despite attempts to
increase it. It also may be detected when
electrolyte or BUN values develop abnormal
trends.
Nursing History
Important recent history data to be aware of include:
• Recent use of nephrotoxic substances (nephrotoxic antibiotics, particularly

aminoglycosides)
• Recent exposure to heavy metals or organic solvents
• Recent hypotensive episode of greater than 30 minutes
• Presence of tumor or multiple clots that might cause renovascular or urine
outflow obstruction bilaterally.
Acute renal failure affects multiple body functions and systems. The collective
term used to describe the clinical manifestation of renal failure is uremia. Caring for a
patient with ARF is challenging. Renal impairment often affects various body systems,
therefore the patient will have signs and symptoms of renal disease and problems with
other organs and systems. The following is a brief description of the effects of renal
failure on body systems and related clinical manifestations.
RenalThe
Effects
key renal effect of ARF is decreased urine output that leads to fluid retention
and edema. The classic sign, oliguria (less than 400 ml of urine output in 24 hours)
means the kidneys aren't producing enough urine to excrete waste products. However,
some patients experience nonoliguric ARF (usually seen in prerenal azotemia and
rarely in intrarenal ARF). In this condition, blood urea nitrogen (BUN) and creatinine
build up in the blood and the volume of urine output varies. Restoring intravascular
volume and maintaining adequate cardiac output and blood pressure generally stop
progression of nonoliguric ARF, so renal replacement therapy-hemodialysis or
continuous arteriovenous hemofiltration-is not necessary.
The kidneys impaired ability to remove waste products from the blood causes
levels of toxins such as BUN and creatinine to rise. Because many processes, such as
protein metabolism, internal bleeding, and infection, increase BUN levels, this is a less
accurate indicator of renal function than creatinine, which is a by-product of muscle
metabolism alone. Keep in mind, however, that if muscle mass is decreased, as in a
thin or debilitated patients, so is creatinine production, and creatinine levels may stay in
the normal range even though their kidneys are impaired. Trends in creatinine levels are
a better gauge of renal function. Other abnormal lab results suggesting ARF include
metabolic acidosis and electrolyte imbalances, such as hyponatremia, hyperkalemia,
hyperphosphatemia, hypocalcemia, and hypermagnesemia.
Neurologic Effects
Metabolic wastes building up in the blood can affect your patient’s mental status.
Look for changes in the level of consciousness, which could progress to coma. Sensory
changes and weakness in the extremities signal uremic neuropathy.
Neurologic Clinical Manifestations

• Decreased alertness, energy and thought processing
• Decreased level of consciousness that progresses from drowsiness to coma
• Seizures
• Itching, tingling, numbness, twitching of extremities.
Cardiovascular and Pulmonary Effects
Hypertension, pulmonary edema, peripheral edema, and arrhythmias are among

the cardiovascular effects of ARF. As decreased urine output causes fluid retention, the
patient develops hypertension. If the heart cannot pump the additional volume, heart
failure ensues. Renin overproduction also causes hypertension. When renal ischemia is
present, the rennin-angiotensin system is triggered, which results in increased blood
pressure and increased renal blood flow.
Fluid volume excess and electrolyte imbalances are the basis of most
cardiovascular symptoms. The presence of fluid excess may cause congestive heart
failure accompanied by peripheral and pulmonary edema. Electrolyte imbalances can
precipitate cardiac arrhythmias.
Hyperkalemia occurs when the kidneys fail to excrete excess potassium. Be on
the alert for signs and symptoms such as muscle weakness, loss of muscle tone, and
neuromuscular irritability, including tingling in the lips or fingertips. Changes in the
electrocardiogram, such as a flattened p wave, prolonged QRS complex, and tall, tented
T waves, also signal hyperkalemia. Often, though, hyperkalemia does not cause
symptoms, so monitoring the patient’s serum potassium level is critical. A level greater
than 6 mEq/liter could trigger bradycardia and/or heart block arrhythmia.
Cardiovascular and Pulmonary Clinical Manifestations
• Cardiovascular
Hypertension
Cardiac arrhythmias
Peripheral edema
Signs and symptoms of congestive heart failure
• Pulmonary
Adventitious breath sounds
Decreased cough reflex
Thick secretions
Kussmaul -type breathing pattern
Infiltrates on x-ray
Signs and symptoms of pneumonia
Pharmacotherapy to Treat Hyperkalemia
1. Regular Insulin Administration IV
Potassium moves into the cells when insulin is given. Glucose is given
concurrently to prevent hypoglycemia. When effects of insulin decrease, potassium
shifts back out of the cells.
2. Sodium Bicarbonate
Therapy can correct acidosis and causes shift of potassium into cells.
3. Calcium Gluconate IV
Therapy is given IV and generally used in advanced cardiac toxicity. Calcium
raises the threshold for excitation.
4. Sodium Polystyrene Sulfonate (Kayexalate)

Cation- exchange resin is administered po or retention enema. When resin is in
the bowel, potassium is exchanged for sodium.
Hematopoietic Effects
Anemia is the main hematologic effect of ARF. Contributing factors include
impaired red blood cell (RBC) production, hemolysis, bleeding, hemodilution, and
reduced RBC survival. The normal life span of RBCs, about 120 days, is shortened to
about 60 days in ARF. Because the damaged kidneys produce less and less
erythropoietin to stimulate RBC production, the lost RBCs are not replaced. Monitor the
patient for decreased hemoglobin and hematocrit levels and dyspnea due to insufficient
oxygenation.
Hematopoietic Clinical Manifestations
• Anemia
• Pale mucous membranes
• Fatigue, weakness
Gastrointestinal
Electrolyte imbalances and increasing levels of uremic toxins are the primary
causes of GI manifestations. As urea decomposes in the GI tract, it releases ammonia.
Ammonia in the GI tract is associated with capillary fragility and GI mucosal irritation. As
the ammonia level increases, small mucosal ulcerations may develop, causing GI
bleeding. Uremia also causes anorexia, nausea, and vomiting, which lead to poor
nutrition and loss of body mass and muscle.
Gastrointestinal Clinical Manifestations
• Weight loss
• Positive guaiac stools
• Anorexia
• Nausea and vomiting
• Constipation or diarrhea
Metabolic Acidosis
In renal failure the kidneys cannot synthesize ammonia, which is needed for
hydrogen ion excretion, or excrete acid products of metabolism. The serum bicarbonate
levels decrease as the bicarbonate is used up in buffering hydrogen ions. The patient
may develop Kussmaul respirations (rapid, deep respirations) to increase the excretion
of carbon dioxide.
Signs and Symptoms of ARF
Decreased urine output • Anuria or oliguria <400ml/day

Weight gain • Increased urea and creatinine
• Peripheral edema or systemic
edema
Uremic symptoms of : • Weight loss
Anorexia • Poor diet intake
Nausea and vomiting • Dry, flaky skin
Fatigue • Pale yellow skin colour
Itchy skin • purpura
Metallic taste in mouth
Halitosis (bad breath)
Thirst/dry mouth • Raised blood pressure may
Breathlessness indicate fluid overload leading to
Fever pulmonary and peripheral edema
Ankle swelling • Lowered blood pressure may
Congestive heart failure indicate dehydration or sepsis
• Abnormal, irregular pulse may
indicate cardiac arrhythmias
• Increased respirations may
indicate metabolic acidosis
• Raised temperature is a sign of
infection
Confusion • Depressed level of consciousness
Twitching or seizures
Irritability, convulsions • Electrolyte imbalance
Laboratory Tests
The diagnosis and management of renal failure are mainly dependent on
laboratory tests, measuring uremic toxins, and renal excretion
Laboratory Tests Abnormal Trends

Serum
Blood urea nitrogen Increased
Creatinine Increased
Uric Acid Increased
Sodium Decreased
Potassium Increased
Calcium Decreased
Chloride Increased
Phosphorus Increased
Albumin Decreased
pH Decreased
Bicarbonate Decreased
Urine
Protein Increased
Creatinine Clearance Decreased
Urea Clearance Decreased
GFR Decreased
Diagnostic Tests
The patient with acute renal failure may require radiographic or invasive
procedures to help verify the exact cause of acute renal failure. The following are some
of the more common tests performed to help make a differential diagnosis:
Tests of Renal Function
TEST IMPORTANCE

Urinalysis • Red cells and casts may indicate
glomerular disease.
• White blood cells can be seen in
interstitial nephropathies
• Pyuria
• Protein, if present, is an important
marker of renal disease

Complete Blood Count • Low Hgb and hematocrit levels are
noted in CRF

Chemistry Panel • Changes in electrolytes
• Changes in blood glucose

• Measures the byproducts of
Glomerular Filtration Rate (GFR) metabolism: creatinine and blood urea
nitrogen

Kidney‐Ureter‐Bladder X‐ray (KUB) • May help to discover renal calculi,
kidney size, or masses

Renal Ultrasonography
• Measures kidney size

• Detects hydronephrosis

• Detects lesions

• Shows cystic disease

Intravenous Pyelogram (IVP)
• Reveals gross anatomic abnormalities,
such as those found with polycystic
kidneys
• Not utilized for initial screening related
to problems with dye toxicity in the
form of allergic reactions, salt overload,
and fluid overload
• Obstruction

Computed Tomography (CT) • Tumors, cysts and stones
• With contrast may show renal artery
stenosis

TEST IMPORTANCE

Arteriogram • Useful if renal insufficiency is thought
to be caused by renal vascular disease

Renal Biopsy • May help if diagnosis and treatment are
uncertain; considered gold standard to
diagnosis the specific type of renal
disease

Nursing Care of Patients with ARF
In most cases of ARF, normal kidney function returns

naturally within weeks. The treatment goals are to
eliminate the cause of ARF and support the patient’s
kidney function and other affected body systems.
Regardless of the type of ARF affecting the patient, provide the following supportive
measures:
Maintain fluid and electrolyte balance. Accurately assessing fluid balance is critical,
so strictly monitor the patient’s weight along with fluid intake and output.
Assess for edema, which is often dependent (in the legs and feet if the patient is sitting or in
the sacral region if supine) but also may appear around the eyes. Document the color and
clarity of the urine.
Monitor fluid and electrolytes. A patient with ARF has an increased risk of hyperkalemia,
hyponatremia, and volume overload, so closely monitor fluid and electrolyte levels. A trial of
diuretic therapy may remove excess fluid and electrolytes. Monitor the BUN and creatinine
levels. If ARF progresses to the point where waste products are building up in the body, the
patient may need renal replacement therapy such as hemodialysis or continuous arteriovenous
hemofiltration to remove them.
Maintain nutrition. Nutritional support is critical to combat malnutrition and water and
electrolyte imbalances. Protein‐calorie malnutrition is highly prevalent in patients with ARF.
When a patient is in a hypercatabolic state, the body breaks down muscle for protein, causing
the BUN and creatinine levels to increase even further. The recommended diet is low in protein
and sodium, higher in fats and carbohydrates.

Dietary restrictions typically include 2 to 4 grams/day of sodium to prevent further water
retention, reduced potassium intake to decrease the risk of cardiac arrhythmias, and limited
phosphorus intake and possibly use of phosphate binders with meals to prevent further
reductions in blood calcium levels.
Provide emotional support and teaching. For both the patient and family, ARF is sudden,
unexpected, and traumatic. Provide emotional support and teach them about the medications,
nutritional needs, fluid restriction, and other treatments.
Recovery If all goes well, recovery from ARF may take 3 to 12 months. But if the underlying
cause of ARF can't be corrected and nephron damage continues, the patient will develop
chronic renal failure, which calls for maintenance dialysis or a kidney transplant.
Strategies for Prevention of ARF

Maintain renal blood flow by ensuring adequate hydration and blood
volume in all patients.
Maintain an awareness of potential mechanisms of injury leading to ARF
& identify patients at risk of ARF.
Maintain close monitoring of fluid balance and serum biochemistry for
those at risk.
Monitor diuretic use, particularly in the elderly, to ensure adequate
hydration and blood volume is maintained. Closely monitor hydration and
blood volume before, during and after surgery.
Monitor serum levels or potentially nephrotoxic drugs. Ensure adequate
hydration for all patients receiving radiographic contrast dyes.
Time Out 3

List at least 4 nursing diagnoses that apply to the
patient with acute renal failure.
Acute Renal Failure Treatment

A major portion of the management of acute renal failure focuses on maintaining
fluid and electrolytes within acceptable levels. During the oliguric/anuric stage, severe
kidney dysfunction can cause life threatening abnormalities in fluid, electrolyte and
uremic toxin levels. Medical management of acute renal failure varies with the type of
failure ( prerenal, intrarenal, or postrenal).
Diagnostic tests are performed to determine the type of renal failure (i.e.
decreased renal function secondary to postshock state [prerenal], versus parenchymal
tubular damage [intrarenal]). To differentiate between these two causes of renal failure,
a diuretic challenge may be given, using either mannitol (an osmotic diuretic) or
furosemide ( a loop diuretic). If the kidneys are able to respond to this diuretic challenge
by increasing urine output, fluid replacement and additional diuretics are given to treat a
prerenal type of problem. However, if the kidneys do not respond to the diuretic
challenge, acute tubular necrosis (ATN) is seriously considered as the cause of the
acute renal failure and dialysis may be a viable treatment option. Patients who
experience the oliguric/anuric stage for 4 -5 days generally require dialysis.
There are 3 main types of dialysis: hemodialysis, continuous renal replacement
therapy, and peritoneal dialysis. It is beyond the scope of this module to
comprehensively discuss these types of dialysis and instead a brief description of them
is provided.
Hemodialysis
Hemodialysis involves circulating the patient's blood outside of the body through
an extracorporeal circuit (ECC), or dialysis circuit. The ECC is made up of plastic blood
tubing, a filter known as a dialyzer (or artificial kidney), and a dialysis machine that
monitors and maintains blood flow and administers dialysate. Dialysate is a sterile
chemical solution that is used to draw waste products out of the blood. The patient's
blood leaves the body through the vein and travels through the ECC and the dialyzer,
where fluid removal takes place.
During dialysis, waste products in the bloodstream are carried out of the body. At
the same time, electrolytes and other chemicals are added to the blood. The purified,
chemically-balanced blood is then returned to the body.
A dialysis treatment usually lasts three to four hours, depending on the type of
dialyzer used and the physical condition of the patient. Dialysis is used several times a
week until acute kidney failure is reversed. Blood pressure changes associated with
hemodialysis may pose a risk for patients with heart problems.
Continuous Renal Replacement Therapy (Hemofiltration)
Continuous renal replacement therapy (CRRT), is a slow, continuous blood

filtration therapy used to control acute kidney failure in critically ill patients. Driven by the
patient’s own BP, it rarely causes hypotension. These patients are typically very sick
and may have heart problems or circulatory problems. They cannot handle the rapid
filtration rates of hemodialysis. They also frequently need antibiotics, nutrition,
vasopressors, and other fluids given through a vein to treat their primary condition.
Because hemofiltration is continuous, prescription fluids can be given to patients in
kidney failure without the risk of fluid overload.
Like hemodialysis, CRRT uses an ECC. A hollow fiber hemofilter is used instead
of a dialyzer to remove fluids and toxins. Instead of a dialysis machine, a blood pump
makes the blood flow through the ECC. The volume of blood circulating through the
ECC in hemofiltration is less than that in hemodialysis. Filtration rates are slower and
gentler on the circulatory system. CRRT treatment will generally be used until kidney
failure is reversed.
Peritoneal Dialysis
Peritoneal dialysis may be used if an acute kidney failure patient is stable and not
in immediate crisis. In peritoneal dialysis (PD), the lining of the patient's abdomen, the
peritoneum, acts as a blood filter. A flexible tube-like instrument (catheter) is surgically
inserted into the patient's abdomen. During treatment, the catheter is used to fill the
abdominal cavity with dialysate. Waste products and excess fluids move from the
patient's bloodstream into the dialysate solution. After a certain time period, the waste-
filled dialysate is drained from the abdomen, and replaced with clean dialysate. There
are three type of peritoneal dialysis, which vary according to treatment time and
administration method.
In summary, a general overview of the acute renal patient has been provided.
Active collaboration between physicians and nurses is required to prevent further
complications to the patient in acute renal failure. The nurse needs to perform frequent,
ongoing patient assessments to evaluate the function of multiple body systems,
implement and evaluate interventions based on physician orders, as well as
independent nursing actions based on patient needs. Four major complications need to
be consistently addressed: fluid overload, catabolic processes, electrolyte/acid-base
imbalance, and infection.
Continue to open the door to renal failure knowledge—

now we will move on to information on chronic renal
failure.
PART C: Chronic Renal Failure

This section of the self learning module provides an overview of chronic kidney
disease in adults and outlines nursing management of patients with chronic renal
failure. Patient assessment, including the stages of chronic kidney disease, common
causes and risk factors, will also be discussed. The clinical manifestations and
treatment are similar to those used to treat acute renal failure and therefore will
only be briefly reviewed in this section of the module.
Chronic kidney disease, also called chronic renal failure (CRF), leads to
permanent loss of kidney function and can result from damage to the kidney tissue.
Chronic kidney disease can progress to established renal failure either rapidly, over a
period of months, or slowly over many years. It cannot be cured, but there are
interventions that can slow its progress and improve symptoms.
Stages of Chronic Renal Failure

Among individuals with chronic renal failure, the stages are defined based on the
level of kidney function.
Stages and Description of Chronic Renal Failure
DESCRIPTION GFR ACTION

(ml/min/1.73m2
At increased risk for Screening
CRF ≥ 90 (with CRF risk CRF risk reduction
factors)
Stage 1 Diagnosis &

Kidney damage with ≥90 treatment
normal or ↑ GFR Treatment of co
morbid conditions
CRF risk reduction
Stage 2 Kidney damage with Estimation of

mild ↓GFR 60-89 progression
Stage 3 Evaluation and

Moderate ↓GFR 30-59 treatment of
complications
Stage 4 Preparation for renal

Severe ↓GFR 15-29 replacement therapy
Stage 5 Renal replacement

Kidney failure <15 (or dialysis) (If uremia present)
The last stage of kidney failure (end stage renal disease [ESRD]) occurs when
the GFR is less than 15 mL/per minute. At this point renal replacement therapy (dialysis
or transplantation) is required. Although there are many different causes of chronic renal
failure, the end result is a systemic disease involving every body organ.
Causes of Chronic Renal Failure

An individual is born with approximately 2 million nephrons and can survive
without dialysis until almost 90% of the nephrons are destroyed. In most situations, the
individual passes through the early stages of CRF without recognizing the disease state
because the remaining nephrons hypertrophy to compensate. The prognosis of CRF is
highly variable given the cause(s), patient’s condition and age, and adequacy of medical
intervention and follow-up. The causes of chronic renal disease fall into the following
categories:
Systemic disease – this may include generalized diseases such as systemic lupus
erythematosus and vasculitis. Diabetes mellitus is the most common cause of about 20
per cent of renal disease in most countries. Progressive kidney damage may begin after
many years of poorly controlled high blood pressure and blood glucose.
High blood pressure – hypertension damages the kidneys, but this damage can be
halted or reversed in some cases by early detection and appropriate treatment
regimens.
Autoimmune disease – glomerulonephritis describes a group of diseases in which the

glomeruli (capillaries within the nephron) are damaged by the body’s immunological
response to tissue changes or infections.
Obstruction – anything that causes an obstruction to the free flow of urine within the
kidneys and renal tract can cause back pressure in the kidneys. Enlarged prostate is the
most common cause of obstruction in older men.
Urine infections – infections of urine caused by renal calculi, obstruction or

abnormalities of the urinary tract can result in scarring of the kidney and eventual kidney
failure
Genetic disease – polycystic kidney disease and other rare genetic diseases. Although
present from birth, polycystic kidney disease often does not cause symptoms until
middle age or later.
Cardiovascular disease--- is the most common cause of death in patients with chronic
kidney disease and established renal failure. Prompt recognition and treatment are
essential because cardiovascular disease – including coronary artery disease,
atherosclerosis, stroke and left ventricular hypertrophy – generally begins in the early
stages of chronic kidney disease. Risk reduction measures to prevent cardiovascular
disease may also delay the onset and progression of kidney disease. Lifestyle
modifications as well as appropriate medical interventions are important for the
management of patients with chronic kidney disease and cardiovascular disease.
Clinical Manifestations
As renal function deteriorates, every body system becomes affected. The clinical
manifestations are a result of retained substances, including urea, creatinine, phenols,
hormones, electrolytes, water, and many other substances. UREMIA is a syndrome that
incorporates all the signs and symptoms seen in various systems throughout the body
in chronic renal failure. It is important to recognize that the manifestations of uremia
vary among patients, according to the cause of the kidney damage, co-morbid
conditions, age, and degree of compliance with the medical treatment regimen. The
symptoms of chronic renal failure vary according to the disease stage. The signs and
symptoms are usually “silent” in the early stages and are evident only when the GFR
decreases below 60mL/min/1.73m2 (Stage 3). Therefore, early and ongoing
assessment of those individuals with risk factors is essential. The clinical manifestations
of chronic renal failure are similar to those of acute renal failure and for a more in-depth
presentation of them please refer back to the acute renal failure section of the module.
The following is a schematic overview of the clinical manifestations of chronic renal
failure:
Time Out 4 True or False
1. The number one cause of ESRD is hypertension.
2. Hemoglobin and hematocrit levels are typically
high in patients with ESRD.

Treatment Goals
Chronic renal failure is irreversible, and eventually patients will require renal
replacement therapy. However, even successful dialysis and transplant does not
eliminate possible death from complications of renal failure or its treatment. After the
correction of contributing factors to chronic renal failure, control of blood pressure and
fluid and dietary adjustments are the mainstays of conservative medical management of
the patient in chronic renal failure.The 5 main goals of treatment are: preservation of
renal function, delay for as long as possible the need for dialysis or transplant,
improvement of of blood chemistry levels, alleviation, as much as possible, of extrarenal
manifestations, and providing an optimal quality of life for the patient.
Nursing Care for Patients with Chronic Renal Failure
Disease Stage Nursing Plan of Patient Care

Stage 1
o Identify and treat specific causes of chronic kidney
disease
o Assess for cardiovascular risk factors, which might
cause rapid decline in eGFR
o Vigilant monitoring of blood pressure
o Good glucose control
o Monitor weight and instigate weight management
plans
o Monitor cholesterol levels
o Annual eGFR
Stage 2
o Good glucose control
o Monitor and treat blood pressure
o Encourage patients with self-management strategies
o Encourage patients with lifestyle modifications
o Monitor cholesterol levels
o Annual eGFR
o Concordance with medications
Disease Stage Nursing Plan of Patient Care
Stage 3
o Good blood pressure control
o Blood tests for eGFR, hemoglobin, potassium,
calcium and phosphate
o Routine referral to nephrology services if progressive
fall in eGFR, microscopic hematuria present,
uncontrolled blood pressure
o Immunize against influenza and pneumococcus
o Review all medications – ensure correct dose
o Avoid nephrotoxic drugs, for example, non-steroidal
anti-inflammatory drugs
o Provide information to enable patients to make
informed choice about renal replacement therapy and
conservative management
o Dietary advice to prevent malnutrition
Stage 4
o Psychological support
o Blood tests as stage 3, also bicarbonate and
parathyroid hormone level
o Immunization against hepatitis B
o Assist patients to prepare for renal replacement
therapy or conservative management
o Liaise effectively between primary and secondary care
o Provide timely access for dialysis treatments
o More intensive management of cardiovascular
complications and bone disease
o Treat symptoms associated with established renal
failure, that is, altered sleep pattern, itching, fatigue
and loss of appetite
o Refer to dietician, social worker and pharmacist
o Manage and treat renal anemia and renal bone
disease
Stage 5
o As in stage 4
o Commence renal replacement therapy or conservative
management approach
o Prevent malnutrition
o Maintain adequacy of dialysis
In summary, a general overview of chronic renal failure has been presented in
Part C of the module. It is essential for patients with renal insufficiency to be assessed
and followed up by the health care team in an attempt to reduce morbidity and mortality.
Chronic renal failure patients need to understand the importance of following their
medical regime to prevent or treat possible controllable factors that can affect morbidity
and mortality such as, anemia, acidosis, and hypertension. As nurses, we need to be
aware of risk factors for chronic renal failure, assess and educate our patients about the
problem to prevent its development as much as possible. In addition, we also need to
be able to intervene to stop or slow its progress in our patients.
Good work on the completion of this module!
Now move on to the Post Test!
REFERENCES
American Nephrology Nurses Association. Partnering for quality care: Module 3: Stages
1 & 2, chronic kidney disease. Retrieved December 2007 from
www.ananurse.org
American Nephrology Nurses Association. Partnering for quality care: Module 2:
Stages 3 & 4 chronic kidney disease. Retrieved December 2007 from
www.ananurse.org
Black, J., & Matassarin-Jacobs, J. (1997). Medical surgical nursing: Clinical managment
for continuity of care (5th ed. ed., Vol. Volume 2). Philadelphia: W.B. Saunders
Co.
Broscious, S. K. , & Castagnola, J. (2006). Chronic kidney disease: Acute
manifestations and role of critical care nurses. Critical Care Nurse,26 (4), 17-28.
Burrows-Hudson, S. (2005). Chronic kidney disease: An overview. American Journal of
Nursing, 105 (2), 40-49.
Holcomb, S. S. (September/October 2004). Keeping kidney function flowing. Nursing
Made Incredibly Easy, 30-41.
Kidd, P., & Wagner, K.D. (2001). High acuity nursing (3rd ed.). Upper Saddle River,
New Jersey: Prentice-Hall Inc.
Morton, P., Fontaine, D., Hudak, C., &. Gallo, B.M. (2005). Critical care nursing: A
holistic approach (8th ed.). Philadelphia, PA: Lippencott Williams & Wilkins.
Polzien, G. (2007). Chronic kidney disease and kidney failure: Important numbers to
know. Home Healthcare Nurse, 25(10), 655-660.
Ward, K. ( March/April 2005). Kidneys don't fail me now! Nursing Made Incredibly Easy,
18-27.
POST TEST
1. Match the following conditions and characteristics with their associated causes of
acute renal failure. (Answers can be used more than once).
a. Decreased cardiac output 1. Prerenal

b. Mechanical outflow obstruction 2. Intrarenal
c. Initial cause of most acute renal failure 3. Post-renal
d. Prostate cancer
e. Tubular obstruction by myoglobin
f. Hypovolemia
g. Renal Stones
h. Nephrotoxic Drugs
i. Bladder cancer
j. Renal vascular obstruction
k. Acute glomerulonephritis
l. Anaphylaxis
2. The nurse determines that a client with oliguria has prerenal oliguria when
a. urine testing reveals a low specific gravity.
b. the causative factor is malignant hypertension.
c. urine testing reveals a high sodium concentration.
d. reversal of the oliguria occurs with fluid replacement.
3. Metabolic acidosis occurs in the oliguric phase of acute renal failure as a result of
impaired
a. ammonia synthesis.
b. Excretion of sodium.
c. Excretion of bicarbonate.
d. Conservation of potassium.
4. The nurse determines that a patient is in the recovery phase of acute renal failure
when the patient experiences
a. a return to normal weight.
b. a urine output of 3700mLs/day.
c. decreasing BUN and creatinine levels.
d. decreasing sodium and potassium levels.
5. A client with acute renal failure has a serum potassium level of 6.8 mmol/L (6.8
mEq/L) and the following arterial blood gas results: pH 7.28, PaCO2 30mmHg, PaO2
86mmHg, HCO3_ 18mmol/L (18mEq/L). The nurse recognizes that treatment of the
acid-base problem would cause a decrease in the
a. pH.
b. potassium level.
c. bicarbonate level.
d. carbon dioxide level.
6. In replying to a patient’s questions about the seriousness of her chronic renal failure,
the nurse knows that the stage of chronic renal failure is based on
a. the total daily urine output.
b. the glomerular filtration rate.
c. serum creatinine and BUN.
d. the degree of altered mental status.
7. List 2 clinical manifestations and their pathophysiological causes that can be noted by
the nurse when performing physical assessment of the following systems on the patient
with chronic renal failure.
Findings Cause
a. Skin
b. Cardiovascular
Findings Cause
c. Respiratory
d. GI
e. Neurological
8. Match the following drugs with their use in chronic renal failure (answers may be
used more than once).
___________ a. Erythropoietin 1. Treatment of hyperkalemia
___________b. IV glucose and insulin 2. Treatment of hyperphosphatemia
___________c. Nifedipine 3. Treatment of anemia
___________d. Sodium polystyrene 4. Treatment of hypertension
Sulfonate( Kayexalate)
___________e. Furosemide
___________f. 10% Calcium gluconate
9. During the assessment of a patient with renal insufficiency, the nurse asks the patient
specifically about a history of
a. angina.
b. asthma.
c. hypertension.
d. rheumatoid arthritis.
10. A patient returns from her initial hemodialysis appointment with nausea, confusion,
twitching, and jerking. The pathophysiological mechanism of dialysis responsible for
these signs and symptoms is a
a. loss of blood into the dialyzer by heparin use.
b. rapid removal of vascular volume causing hypovolemia
c. high osmotic gradient in the brain causing cerebral edema.
d. neuromuscular hypersensitivity resulting from fluid and sodium loss.
ANSWER KEY
PRETEST ANSWERS
1. a
2. b
3. b
4. c
5. d
6. c
7. c
8.b
9. c
10. b
Time Out Answers

Time Out 1 Answer --b.
Time Out 2 Answer –prerenal
Time Out 3:
Nursing diagnoses that apply to the patient with acute renal failure:
Fluid volume excess

Decreased cardiac output
Altered nutrition: less than body requirements
Potential complication: GI bleeding
Fluid volume excess
Potential complication: electrolyte imbalance
Anxiety
Knowledge Deficit
Time Out 4 Answer 1. False. Diabetes mellitus is the leading cause of ESRD followed
by hypertension and glomerulonephritis. Other causes include polycystic kidney
disease, immunologic disorders, acute renal failure, and trauma.
Answer 2. False. Actually, these levels are generally low in patients with ESRD. Factors
contributing to anemia include reduced production of erythropoietin (the hormone that
stimulates production of red blood cells in the bone marrow), blood loss through
hemodialysis, and a shortened life span of red blood cells.
POST TEST ANSWERS

1.a. 1; b. 3; c. 1; d. 3; e. 2; f. 1; g. 3; h. 2; i. 3; j. 1; k. 2; l. 1
2. d. Rationale: In prerenal oliguria, the oliguria is caused by a decrease in

circulating blood volume—and there is no damage yet to the renal tissue. It can be
potentially reversed by correcting the precipitating factor—such as fluid replacement
for hypovolemia. Prerenal oliguria is characterized by urine with a high specific
gravity and a low sodium concentration, while oliguria of intrarenal failure is
characterized by urine with a low specific gravity and a high sodium concentration.
Malignant hypertension causes damage to renal tissue and intrarenal oliguria.
3. a. Rationale: Metabolic acidosis occurs in ARF because the kidneys cannot

synthesize ammonia needed to excrete H+, resulting in an increased acid load.
Sodium is lost in urine because the kidneys cannot conserve sodium, and impaired
excretion of potassium results in hyperkalemia. Bicarbonate is normally generated
and reabsorbed by the functioning kidney to maintain acid-base balance.
4. c. Rationale: The BUN and creatinine levels remain high during oliguric and
diuretic phases of acute renal failure. The recovery phase begins when the
glomerular filtration returns to a rate at which BUN and creatinine stabilize and then
decrease. Urinary output of 3-5 L/day, decreasing sodium and potassium levels, and
fluid weight loss are characteristics of the diuretic phase of ARF>
5. b. Rationale: During acidosis, potassium moves out of the cell in exchange for H +
ions, increasing the serum potassium level. Correction of the acidosis with sodium
bicarbonate will help lower potassium levels. A decrease in pH and bicarbonate and
PaCO2 levels would indicate worsening acidosis.
6. b. Rationale: Stages of chronic renal failure are based on the glomerular filtration
rate and/or the presence of kidney damage over a period of 3 months. No specific
markers of urine output or azotemia classify the degree of chronic renal failure.
7. a. Skin.
Yellowish discoloration, retention of urinary chromogens
Pallor; anemia of decreased erythropoiesis, folic acid deficiency
Uremic frost; urea crystallization on skin with very high BUN levels.
Excoriations; pruritus caused by scratching from calcium- phosphate deposition
on the skin.
b. Cardiovascular.
Hypertension; sodium and fluid overload, increasing rennin production
Pericardial friction rub; uremic pericarditis
Peripheral edema; sodium and fluid retention.
c. Respiratory
Kussmaul’s respirations; respiratory compensation of metabolic acidosis
Dyspnea; pulmonary edema of congestive heart failure and fluid overload
Pleural friction rub; uremic pleuritis.
d. GI
Mucosal ulcerations; increased ammonia from bacterial breakdown of urea
Anorexia; nausea, vomiting; irritation of the GI tract from urea
Diarrhea; hyperkalemia and hypocalcemia
Urine odour of breath; high urea content of the blood.
e. Neurological
General CNS depression; high urea content of the blood
Coma and convulsions; high urea content of the blood.
8. a. 3; b. 1; c. 4; d. 1; e. 4; g. 1
9. c. Rationale: The most common causes of chronic renal failure in Canada are
hypertension and diabetes mellitus. The nurse should obtain information on long
term health problems that are related to kidney disease. The other disorders are not
closely associated with renal disease.
10. c. Rationale: A complication of hemodialysis especially in initial treatment, is

disequilibrium syndrome, which is caused by too-rapid removal of urea and other
solutes from the blood, leaving a high concentration of the solutes in the
cerebrospinal fluid and brain. The higher concentration pulls fluid into these areas,
causing cerebral edema and the related symptoms. Loss of blood can occur from
heparin use and loss into the dialyzer, and hypotension frequently occurs from fluid
loss during dialysis, but the symptoms relate to hypovolemia rather than increased
intracranial pressure. Muscle cramps result from neuromuscular hypersensitivity not
related to disequilibrium syndrome.
EVALUATION

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Abbotsford Regional Hospital
Education Resource
©2008

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PART A: ANATOMY & PHYSIOLOGY 7

PART B: ACUTE RENAL FAILURE 11

Nursing Care of Patients with ARF 25

PART C: CHRONIC RENAL FAILURE 29

Stages of Chronic Renal Failure 29

Causes of Chronic Renal Failure 30

Clinical Manifestations of Chronic Renal Failure 31

Nursing Care of Patients with Chronic Renal Failure 33

The purpose of this learning module is to provide you with:

At the completion of this learning package, you will be able to:

v. Understand treatment goals and relevant laboratory and diagnostic tests.

Now please take a few minutes to complete the Pretest.

a. Progressive irreversible destruction of the kidneys.

2. Prerenal causes of acute renal failure include

a. Prostate cancer and calculi formation.

a. Hypernatremia and CNS depression.

a. Hyperkalemia and hyponatremia.

7. Two major causes of intrarenal acute renal failure are

a. Dehydration and increased cardiac output.

8. During which phase of acute tubular necrosis are hyperkalemia, gastrointestinal

10. The causes of metabolic acidosis in renal failure include

a. Increased renal secretion and excretion of hydrogen ions.

The kidneys are two bean-shaped

Surrounding each glomerulus is a Bowman’s capsule, the initial structure of the

• Water (H2O), hydrogen ions(H+)

Functions of the Kidneys

If toxins build up I could stop

ACUTE RENAL FAILURE (ARF) is a sudden loss of kidney function with a

ARF represents a situation where prevention is undoubtedly better than

READ ON to learn more about how ARF

CAUSES OF ACUTE RENAL FAILURE

PRERENAL FAILURE INTRARENAL POSTRENAL

Cardiovascular Acute tubular Ureteral obstruction

Acute tubular necrosis

• Aminoglycosides (such as amikacin, gentamicin, tobramycin)

Hemodynamically mediated renal failure

• Angiotensin-converting enzyme inhibitors

While different causes of acute renal failure are easily

Stages of Acute Renal Failure

Early Diuretic Stage

Late (Recovery) Diuretic Stage

In the acutely ill patient, renal dysfunction often has an

• Recent use of nephrotoxic substances (nephrotoxic antibiotics, particularly

Neurologic Clinical Manifestations

Hypertension, pulmonary edema, peripheral edema, and arrhythmias are among

Cardiovascular and Pulmonary Clinical Manifestations

Pharmacotherapy to Treat Hyperkalemia

1. Regular Insulin Administration IV

4. Sodium Polystyrene Sulfonate (Kayexalate)

Hematopoietic Clinical Manifestations

Gastrointestinal Clinical Manifestations

Signs and Symptoms of ARF

Decreased urine output • Anuria or oliguria <400ml/day

Laboratory Tests Abnormal Trends

Nursing Care of Patients with ARF

In most cases of ARF, normal kidney function returns

Strategies for Prevention of ARF

Acute Renal Failure Treatment

Continuous Renal Replacement Therapy (Hemofiltration)