RENAL

FAILURE

Melissa Greer, Ylise Dobson,

Megan Stacey, Melissa Terpstra,
& Emily Peterson
The Radical Renal Team
Dr. McCurly
The Radical Renal Team

The Nurses
McTall & McShorty
The Radical Renal Team

The Nurses
McSmall & McGiant
 Case Study
Tia Smith is a 26 year old female patient who is 10 hours post-
partum following an emergency C-section for twins. She was 33.5
weeks pregnant and had a difficult pregnancy with PIH (pregnancy
induced hypertension) and frequent urinary tract infections. On
admission Tia was diagnosed with HELLP syndrome (hemolysis,
elevated liver enzymes, low platelets) which necessitated immediate
delivery of her babies. During the C-section Tia became
hypovolemic resulting from massive hemorrhaging and required
blood products and fluid replacements. Tia eventually developed
hypovolemic shock and remained unstable for 2 hours. For the past
nursing shift Tia has been hypotensive with blood pressures ranging
from 59/47 to 95/52. Tia’s urinary output has been 2-12cc/hr of
brown cloudy foul smelling urine. During your morning assessment
you discover the following:
 Case cont’d
• VS: T: 37.4 P: 125bpm R: 33 BP: 96/62

• Respiratory: Chest is clear fine crackles heard throughout all lung fields,
there is diminished A/E at the bottom of the R & L lobes
• CV: S1, S2 audible with pericardial friction, bounding rapid pulse
• Mental Status: drowsy and with assistance will orient slowly to PPT, pt c/o
persistent hiccups
• Neurovascular: edema, skin cool & pale, bruises observed throughout
extremities, skin turgor poor, bilateral decreased sensation in feet
• GI: pt c/o N&V
• Genitourinary: pt has foley catheter draining brown cloudy foul smelling
urine at 2-12cc/hr
• Psychosocial: pt very emotional and crying at times because she cannot be
with her newborn babies and is unable to breastfeed, she is concerned for
their health, and does not understand how this happened to her
So… What is Tia’s diagnosis?

Acute Renal Failure

Anatomy of the Kidney

http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html
 Nephron

http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html
 10 Functions of the Kidney’s
• Urine Formation: Formed in the nephrons through a
complex three-step process: GF, tubular reabsorption, and
tubular secretion
• Excretion of waste products: eliminates the body’s
metabolic waste products (urea, creatinine, phosphates,
sulfates)
• Regulation of electrolytes: volume of electrolytes
excreted per day is exactly equal to the volume ingested
– Na – allows the kidney to regulate the volume of body fluids,
dependent on aldosterone (fosters renal reabsorption of Na)
– K – kidneys are responsible for excreting more than 90% of total
daily intake
• RETENTION OF K IS THE MOST LIFE-THREATENING
EFFECT OF RENAL FAILURE
 Renin-Angiotensin System

http://en.wikipedia.org/wiki/Image:Renin-angiotensin-aldosterone_system.png
 Kidney Function con’td
• Regulation of acid-base balance: elimination
of sulphuric and phosphoric acid
 Kidney function cont’d
• Control of water balance: Normal ingestion of water
daily is 1-2L and normally all but 400-500mL is excreted
in the urine
– Osmolality: degree of dilution or concentration of urine
(#particles dissolved/kg urine (glucose & proteins are osmotically
active agents)
– Specific Gravity: measurement of the kidney’s ability to
concentrate urine (weight of particles to the weight of distilled
water)
– ADH: vasopressin – regulates water excretion and urine
concentration in the tubule by varying the amount of water
reabsorbed.
 Still talking about kidney
function…
• Control of blood pressure: BP monitored by the vasa
recta.
– Juxtaglomerular cells, afferent arteriole, distal tubule,
efferent arteriole http://www.wisc-online.com/objects/AP2204/AP2204.swf
• Renal clearance: ability to clear solutes from plasma
– Dependent on… rate of filtration across the
glomerulus, amount reabsorbed in the tubules,
amount secreted into the tubules
– CREATININE
• Regulation of red blood cell production:
Erythropoeitin is released in response to decreased
oxygen tension in renal blood flow. This stimulates the
productions of RBCs (increases amount of hemoglobin
available to carry oxygen)
 Kidney function cont’d
• Synthesis of vitamin D to active form: final conversion
of vit D into active form to maintain Ca balance
• Secretion of prostaglandins: important in maintaining
renal blood flow (PGE & PGI). They have a vasodilatory
effect
 Timeline of Events

PIH HELLP EMERGENCY

C-SECTION HEMORRHAGE

HYPOVOLEMIC HYPOVOLEMIA
SHOCK

ACUTE RENAL FAILURE

 HELLP SYNDROME
• A syndrome featuring a combination of "H" for hemolysis (breakage
of red blood cells), "EL" for elevated liver enzymes, and "LP" for low
platelet count (an essential blood clotting element).
• PREGNANCY COMPLICATION - occurring in 25% of pregnancies
with toxemia or pre-eclampsia.
• Symptoms include-
– Shortness of breath
– H/A
– Dimmed vision
– Nausea
– Dizziness & Fainting
– Edema
– Pain in the upper abdomen
Effects of HELLP on Mom & Baby

• Mothers with HELLP are at increased risk

for:
– Liver rupture, DIC, abruptio placentae, and acute renal
failure, stroke, seizure, ARD, pulmonary edema
– 1st order of tx is management of blood clotting issues
– Women with a hx of HELLP are considered at risk for
future pregnancies
– After delivery, mothers vitals are CLOSELY
monitored to observe for complications
Acute Renal Failure
 Definition
• Acute renal failure (ARF) is an abrupt and
sudden reduction in renal function resulting in the
inability to excrete metabolic wastes and
maintain proper fluid & electrolyte balance
• It is usually associated with oliguria (urine output
<30cc/hr or <400cc/day), although urine output
may be normal or increased
• BUN & creatinine values are elevated
 Statistics of ARF
• Frequency: condition develops in 5% of
hospitalized patients and 0.5% patients
require dialysis
– Elderly are at high risk
– Post-op patients
• Mortality: the mortality rate estimates
vary from 25-90%
• Race: no racial predilection is recognized
 Pathophysiology
• ARF may occur in 3 clinical settings:
– As an adaptive response to severe volume
depletion and hypotension, with structurally
and functionally intact nephrons (Prerenal)
– In response to cytotoxic or ischemic insults to
the kidney, with structural and functional
damage (Intrinsic or Intrarenal)
– Obstruction to the passage of urine (Postrenal)
 Phases of Acute Renal Failure
• Clinical progression of reversible RF occurs in four phases:
– Initiation phase
• Begins with initial insult and ends when oliguria develops
– Oliguric phase
• Accompanied by rise in serum concentrations of substances usually excreted
by kidneys (urea, creatinine, ua, organic acids, intracellular cations [K+ &
Mg])
• urinary output <400cc/day
• May last 1-3 weeks
– Diuretic phase
• The kidneys begin to recover
• Initially produce hypotonie urine d/t increase in GFR
– Recovery phase
• Tubular function restored
• Diuresis subsides and kidney begins to function normally again
 Prerenal acute renal failure
• Is the most common cause of ARF occurring in
60-70% of cases
• It is caused by impaired blood flow as a result of
intravascular depletion, which leads to decreased
effective circulating volume to the kidneys
• In patients with prerenal ARF, the parenchymal is
undamaged, and the kidneys respond as if
volume depletion has occurred.
 Prerenal ARF
• Causes include:
– Secondary to renal hypoperfusion which occurs in setting of
extracellular fluid loss
• Diarrhea
• Vomiting
• Diuretics
– Impaired/inadequate cardiac output
– Drugs
• NSAIDs
• ACE Inhibitors
– Hypovolemia
– Hemorrhage
– Renal vasoconstriction
 Intrinsic acute renal failure
• Is the result of actual parenchymal damage to the
glomeruli or kidney tubules
• A physiologic hallmark is failure to maximally
concentrate urine
• Is divided into 4 categories:
– Acute tubular disease
– Glomerular disease
– Vascular disease
– Interstitial disease
 Intrinsic ARF
• Acute Tubular Necrosis
– most common type of ARF, a more ischemic insult to the
kidneys, usually induced by ischemia or toxins
– Caused by:
• Burns, and crush injuries – myoglobin & hemoglobin are liberated
causing renal toxicity or ischemia
• Drugs – NSAIDs, ACE inhibitors, aminoglycosides
• Infections
• Nephrotoxic agents – contrast agent
• Glomerulonephritis
– uncommon cause, most associated with CRF
– Caused by:
• Can be a primary disorder or can occur secondary to systemic
disease
• Systemic lupus erythematosus
 Intrinsic ARF
• Acute Interstitial Nephritis
– Interstitial disturbance that leads to ARF
– Caused by:
• Allergic reaction to drugs
• Vascular Disease
– Can occur on microvascular and macrovascular
– Caused by:
• Microvascular
– Hemolytic anemia
– ARF secondary to small vessel thrombosis or occlusion
• Macrovascular
– Suspected in elderly
– Renal artery stenosis or thrombosis
– Atheroembolism secondary to atrial fibrillation and aortic disease
 Postrenal acute renal failure
• Is rare and occurs with urinary tract
obstruction that affects the kidneys
bilaterally
• Pressure rises in the kidney tubules,
eventually the GFR decreases
 Postrenal ARF
• Causes include:
– Bladder tract obstruction
– Prostatic hypertrophy
– Catheters
– Neurogenic bladder
• Postrenal causes are typically reversible
 Assessment
• History
– Observe for disorder that predisposes pt to ARF
– Ask questions about recent illness, infections, or
injuries
– Medication history
– Urinary patterns
– History of GI problems
• Psychosocial
– Anxious
– Family members
 Clinical Manifestations of ARF
• Cardiovascular • Genitourinary
– Arrhythmias – Oliguria
– BP, N, high or low – Anuria
– Anemia – abN urine colour, clarity, smell
– P, rapid, bounding, or N
• GI
– Pericardial-type chest pain
– Moist tongue & increased saliva
• Respiratory – Dry tongue & mucous membranes
– Dyspnea – N&V
– Crackles
• Integumentary
– Tachypnea
– Moist, warm skin & pitting edema
– Kussmaul’s respirations
– Decreased skin turgor
• Mental Status – bruises
– Lethargy – Pallor
– Tremors – Thin, brittle hair & nails
– Memory loss
– Confusion
• Musculoskeletal
– Muscle spasms
– Weakness
 Nursing Care Plan
• Fluid volume deficit related to hemorrhage
(hypovolemic shock)
– Priority to restore fluid balance and circulation
• The patient will:
– show stable vital signs
– have adequate urine output >30cc/hr
– have strong peripheral pulses indicating tissue
perfusion
– display LOC normal for patient
 Nursing Care Plan
• Interventions
– Bleeding reduction, fluid
resuscitation, blood product
administration, IV therapy
– Monitor VS q2h
– Monitor weight daily
– Skin & tongue turgor
– Monitor and document I&O
– Monitor CBC, ABG,
urinalysis, ECG
• Rationales
– Early intervention can prevent
progression of hypovolemia to
hypovolemic shock that may
result in renal damage
– S&S correlate with the
approximate percentage of
volume loss
• Medullary vasomotor center
stimulation via the
baroreceptor reflex
• ADH
– Foley catheter facilitates
monitoring of urine output
– Shock pt hemodynamically
unstable with compromised
compensatory mechanisms,
volume admin may cause fld
overload
 Nursing Care Plan
• Electrolyte imbalance related to decreased
electrolyte excretion, and metabolic acidosis
– Priority to prevent complications of electrolyte
imbalance
• Within 24h of admission and then continuously,
the pt will:
– Maintain serum electrolyte levels within acceptable
limits
– Have normal sinus rhythm
 Nursing Care Plan
• Interventions
– Monitor & document
electrolyte levels q8-12h,
especially:
• K+, P, Ca, Mg
– Monitor ABG
– Monitor ECG especially:
• High tented T waves,
prolonged PR interval or
widened QRS complex
– Limit dietary & drug intake of
potassium
• Rationales
– Kidneys’ ability to regulate
electrolyte excretion &
reabsorption may result in
high K+ & P, low Ca, &
high/low Mg levels.
– ARF causes metabolic
acidosis which may increase
the release of K+ from cells in
exchange for H+ ions
– Electrolyte abN can trigger
arrhythmias & cardiac arrest
– When kidneys cannot excrete
K+, excess intake can increase
serum K+ to dangerous levels
 Nursing Care Plan
• Knowledge deficit of acute renal failure related
to lack of exposure to information on
management of complex condition
– Priority to provide in depth information on acute renal
failure
• Upon discharge the patient will:
– Be able to identify signs and symptoms to report to
nurse or physician
– Commitment to comply with treatments, including
dialysis, dietary modifications, and activity restrictions
 Nursing Care Plan
• Interventions
– Provide as appropriate
information on the severity of
ARF & dialysis
• Stages of ARF
• Medications including action
and adverse effects
• S&S
• Procedures such as dialysis
including schedule and
adverse effects
• Dietary modifications
including limitations of
proteins (catabolism),
electrolytes and fluids
• Rest and activity restrictions
• Rationales
– The patient and family need
assistance, explanation, and
support during this time.
– Teaching may decrease
anxiety and fear, and enhance
recovery to patient and family
members.
– Continued assessment of the
patient for complications of
ARF and of its precipitating
cause is essential.
Acute Renal Failure

LAB VALUES
 Medications for ARF
Pharmacologic treatment of ARF has been
attempted on an empirical basis, with varying
success rates. Several promising experimental
therapies in animal models are awaiting human
trials
It is critical to adjust (decrease or discontinue)
medication dosages for patient in acute renal
failure. Administering the average dose to patient
in renal failure can kill a patient.
 Medications for ARF continued
Immediate goal is to retain fluid volume deficit through use
of blood products and crystalloids
• Normal Saline (0.9% Na) – only one that is compatible
with blood transfusions
– Restores fluid loss
– Provides electrolytes resembling those of plasma
• Packed RBC
– To increase blood volume
– To restore blood to kidneys
 Medications for ARF continued
•Diuretics
–Furosemide (Lasix) only given with severe fluid
overload
•Increases excretion of water by interfering with chloride-binding
cotransport system, which, in turn, inhibits sodium and chloride
reabsorption in the thick ascending loop of Henle and the distal
renal tubule
–Adult dose: 20-80 mg PO/IV once; repeat 6-8h prn or
dose may be increased by 20-40 mg no sooner than 6- 8h
after previous dose until desired effect
–Nursing Assessments: Watch for hypokalemia, assess BP
before and during therapy can cause hypotension
 Medications for ARF continued
• Vasodilators
– Dopamine
• In small doses causes selective dilatation of the renal
vasculature, enhancing renal perfusion.
• Reduces sodium absorption, thereby decreasing the energy
requirement of the tubules. This enhances urine flow, which,
in turn, helps prevent tubular cast obstruction.
– Adult dose: 2-5 mcg/kg/min
– Nursing Assessments: Monitor BP during
administration, stop infusion if BP drops 30mm Hg,
Monitor I&O
 Medications for ARF continued
• Alkalinizer
– Sodium Bicarbonate
– Increases plasma bicarbonate, which buffers Hydrogen ion
concentration; reverses acidosis
– Adult Dose: Initial dose IV bolus 1 mEq/kg, then infuse 2-5
mEq/kg over 4-8 hr depending on CO2, pH
• Dilute with equal amounts of NS, 2-5 mEq/kg
– Nursing assessments: Assess resp. and pulse rate,
rhythm, depth, lung sounds, monitor I&O,
electrolytes, blood pH, PO2, HCO3, monitor urine pH,
and UO during beginning of treatment, monitor for
alkalosis, monitor ABGs and blood studies
 13 have passed and now Tia is
diagnosed with…
Chronic Renal Failure
• 13 years have passed  Tia is now 39 years of age and
has been experiencing declining renal function over the
past 13 years. Tia has lost 15lbs on her already small
frame, she feels generally ill most of the time with
frequent N&V, she suffers from fatigue, muscle twitching
& cramps decreased sensation in her hands and feet and
generalized puritus. The Physician has diagnosed Tia
with ESRD and has determined that long term dialysis
will be required.
Chronic Renal Failure
ESRF
 Definition
• Also known as End-Stage Renal Failure (ESRF),
is a progressive deterioration in renal function in
which the body’s ability to maintain metabolic
and fluid and electrolyte balance fails, resulting
in uremia (retention of urea and other
nitrogenous wastes in the blood).
• decreased kidney glomerular filtration rate (GFR)
of <60 mL/min/1.73 m2 for 3 or more months
 Statistics
• In the U.S. The US Renal Data System (USRDS) has
shown a dramatic increase in patients with CRF who
require chronic dialysis or transplantation. In 1999, there
were 340,000 such patients, but, by 2010, this number is
projected to reach 651,000.
• Internationally: The incidence rates of end-stage
renal disease (ESRD) have increased steadily
internationally since 1989. The United States has the
highest incident rate of ESRD, followed by Japan. Japan
has the highest prevalence per million population, with
the United States taking second place.
 Statistics Cont’d
• Mortality /Morbidity: CRF is a major cause of
morbidity and mortality, particularly at the later stages.
The 5-year survival rate for a patient undergoing chronic
dialysis is approximately 35%. This is approximately
25% in patients with diabetes. The most common cause
of death in the dialysis population is cardiovascular
disease.
• Race: Affects all races
 Pathophysiology

• As renal function declines, the end products of protein metabolism

(which are normally excreted in the urine), accumulate in the blood.
Uremia develops and adversely effects every system in the body.
• The greater the buildup of waste products, the more severe the
symptoms.
• Approximately 1 million nephrons are present in each kidney, each
contributing to the total GFR. Regardless of the etiology of renal
injury, with progressive destruction of nephrons, the kidney has an
innate ability to maintain GFR by hyperfiltration and compensatory
hypertrophy of the remaining healthy nephrons.
• This nephron adaptability allows for continued normal clearance of
plasma solutes such that substances such as urea and creatinine start
to show significant increases in plasma levels only after total GFR
has decreased to 50%, when the renal reserve has been exhausted.
The plasma creatinine value will double with a 50% reduction in
GFR.
 Stages of Chronic Renal Disease
• 3 stages in nephron function

• Stage 1: Reduced Renal Reserve

 Characterized by a 40%-75% loss of nephron
funtion. The patient is usually asymptomatic
because the remaining nephrons are able to carry
out normal function of the kidney
 Stage 2 of Renal Disease
• Stage 2: Renal Insufficiency
 Occurs when 75%-90% of nephron function is
lost. At this point, the serum creatinine and BUN
rise, the kidney loses its ability to concentrate
urine and anemia develops. The patient may
report polyuria and nocturia
 Stage 3 of Renal Disease
• Stage 3: End-Stage Renal Disease
 The final stage, occurs when there is less than
10% of nephron function remaining. All normal
regulatory, excretory, and hormonal functions of
the kidneys are severely impaired. ESRD is
evidenced by elevated creatinine and BUN levels
as well as electrolyte imbalances.
 Dialysis is usually indicated at this point.
 Glomular Filtration Rate
• GFR: a Kidney function
test in which results can
be determined from
amount of ultrafiltrate
formed by plasma
flowing through the
glomeruli of the kidney.
• As glomular filtration
decreases, the serum
creatinine and BUN
levels increase.
 Causes
 Type 1 and type 2 diabetes
mellitus cause a condition called
diabetic nephropathy, which is the
leading cause of kidney disease in
the United States.

 High Blood Pressure

(hypertension), if not controlled,
can damage the kidneys over time.

 Glomerulonephritis is the
inflammation and damage of the
filtration system of the kidney and
can cause kidney failure.
Postinfectious conditions and
Lupus are among the many causes
of glomerulonephritis.
 More Causes
 Polycystic Kidney Disease is an example of a hereditary cause
of chronic kidney disease wherein both kidneys have multiple
cysts

 Use of analgesics such as acetaminophen (Tylenol) and

ibuprophen regularly over long durations of time can cause
analgesic nephropathy, another cause of kidney disease. Certain
other medications can also damage the kidneys.

 Clogging and hardening of the arteries (atherosclerosis) leading

to the kidneys causes a condition called ischemic nephropathy,
which is another cause of progressive kidney damage.

 Obstruction of the flow of urine such as by stones, an enlarged

prostate, strictures (narrowings), or cancers may also cause
kidney disease
 Clinical Manifestation
• Patients with CRF stage 3 or lower (GFR >30
mL/min) generally are asymptomatic and do not
experience clinically evident disturbances in
water or electrolyte balance or
endocrine/metabolic disturbances.
• Generally, these disturbances clinically manifest
with CRF stages 4 and 5 (GFR <30 mL/min).
 Clinical Manifestations
• Hyperkalemia usually develops when GFR
falls to less than 20-25 mL/min because of
the decreased ability of the kidneys to
excrete potassium.

• Metabolic acidosis because the kidney

cannot excrete increased loads of acid.
 Clinical Manifestations
• Extracellular volume expansion and total-body
volume overload results from failure of sodium
and free water excretion.
• Anemia principally develops from decreased
renal synthesis of erythropoietin, the hormone
responsible for bone marrow stimulation for red
blood cell (RBC).
• Calcium and Phosphorus imbalance occurs
because of a disorder in metabolism. They have a
reciprocal relationship in the body; as one rises,
the other decreases.
 Signs and Symptoms
• Neurologic
weakness, fatigue, confusion,
disorientation, tremors,
seizures, restlessness of legs,
burning of soles of feet,
behavioral changes.
• Integumentary
Gray-bronze skin colour, dry, flaky
skin, pruritus, ecchymosis, thin
brittle nails, coarse, thinning
hair
• Pulmonary
Crackles, thick tenacious sputum,
depressed cough reflex,
pleuritic pain, shortness of
breath, engorged neck veins,
tachypnea, uremic
pneumonitis, “uremic lung”
• Gastrointestinal
Ammonia odour to breath,
metallic taste, mouth
ulcerations and bleeding,
anorexia, N&V, hiccups,
constipation or diarrhea,
bleeding from GI tract.
• Hematologic
Anemia, thrombocytopenia
• Musculoskeletal
Muscle cramps, loss of muscle
strength, renal osteodystrophy,
bone pain, bone fractures, foot
drop
 Nursing Care Plan
 Excess fluid volume r/t decreased
urine output, and retention of
sodium and water
Goal is maintenance of ideal body
weight without access fluid
• Nursing Interventions
 Assess fluid Status
 Daily weight
 I&O
 Skin turgour & edema
 Distention of neck veins
 BP, P, R
 Limit fluid intake to prescribed
volume
 Explain to pt and family rationale
for restriction of food
 Provide or encourage frequent oral
care
 Rationale
 Assessment provides baseline and
ongoing database for monitoring
changes and evaluating interventions
 Fluid restriction will determine on the
basis of weight, urine output, and
response of therapy
 Understanding promotes pt and family
cooperation with fluid restrictions
 Oral hygiene minimizes dryness of
oral mucous membranes
 Expected Outcomes
 Demonstrates no rapid weight changes
 Maintains dietary and fluid restrictions
 Exhibits normal skin turgour without
edema
 Normal vitals
 Reports no difficulty breathing or
shortness of breath
 Reports decrease dryness of oral
mucous membranes.
 Nursing Care Plan
 Hyperkalemia, pericarditis,
pericardial effusion and
temponade, hypertension,
anemia, bone disease
• Goal: Patient experiences and
absence of complications
 Nursing Interventions
 Hyperkalemia
 Monitor serum K levels and
notify physician if greater than
5.5 mEq/L.
 Assess patient for muscle
weakness, diarrhea, ECG
changes( tall tented Twaves,
widened QRS).
• Rationale
 Hyperkalemia causes
potentially life-threatening
changes to the body
 Cardiovascular S & S are
characteristic of hyperkalemia
 Expected Outcomes
 Pt has normal K level
 Experiences no muscle
weakness or diarrhea,
 Exhibits normal ECG pattern
 Vital signs are within normal
limits
• Pericarditis, Pericardial
effusion, tamponade
 Assess for fever, chills,
chest pain and pericardial
friction rub (signs of
pericarditis).
 If pt has pericarditis, ax q
4 hrs
• Extreme hypotension
• Weak of absent peripheral
pulses, altered level of
consciousness, bulging
neck veins.
• Rationale
 About 30-50% of CRF pts develop
pericarditis due to uremia; fever
,chest pain, and pericardial friction
rub are classic signs
 Pericardial effusion is common
following pericarditis. Signs of
effsusion: paradoxical pulse (> 10
mm drop in BPduring inspiration)
and signs of shock d/t compression
of the heart by a lg effusion.
 Cardiac tamponade exists when
the pt is severely compromised
hemodynamically
 Outcomes
 Has strong and equal peripheral
pulse
 Absence of paradoxical pulse
 Absence of pericardial effusion, or
tamponade
• Hypertension
 Monitor and record blood
pressure
 Administer antihypertensives
as prescribes
 Encourage compliance with
dietary and fluid restriction
therapy
 Teach pt report signs of fluid
overload, vision changes,
headaches, edema, seizures
• Rationale
 Antihypertensives play a key role
in tx of hypertension associated
with CRF.
 Adherence to diet and fluid
restrictions prevents excess fluid
and sodium accumulation
 These are indications of
inadequate control of
hypertension, and need to alter
therapy
 Outcomes
 BP is within normal limits
 No headaches, visual problems or
seizures
 No edema
 Demonstrates compliance with
dietary and fluid restrictions
• Anemia
 Monitor RBC count, Hg, and
HCT levels
 Administer prescribes meds:
iron and folic acid
 Avoid drawing unnecessary
blood specimens
 Teach pt to prevent bleeding;
avoid vigorous nose blowing
 Administer blood component
therapy
• Rationale
 Provides Ax of degree of
anemia
 RBCs need iron and folic acid
to be produced.
 Anemia is worsened by
drawing numerous specimens
 Blood component therapy may
be needed if pt has symptoms
 Outcomes
 Pt has normal colour without
pallor
 Hematology values are within
acceptable limits
 Experiences not bleeding form
any site.
• Bone Disease  Rationale
 CRF causes numerous physiologic
 Administer the following changes affecting calcium,
meds as prescribed: phosphorus and vit D metabolism.
phosphate binders,  Hyperphophatemia, hypocalcemia,
calcium supplements, vit and excess aluminum
accumulation are common
D supplements  Bone demineraliztion decreases
 Monitor serum lab values with immobility.
( calcium, phosphorus,  Outcomes
aluminum)  Serum calcium, phosphorus, and
aluminum levels are within
 Assist pt with exercise acceptable ranges.
program  Has no bone demineralization
 Discuss importance of maintaining
activity level and exercise
program.
 Diet
• Protein restriction b/c urea, uric acid and organic acids- the
breakdown product of dietary and tissue proteins- accumulate
rapidly in the blood when there is impaired renal clearance.
• The allowed protein must be of high biologic value (diary
products, eggs, meats). These proteins are those that are
complete proteins and supply the essential amino acids
necessary for cell growth and repair; also maintenance of fluid
balance, healing and skin integrity, and maintenance of
immune function.
• Fluid restrictions: fluid allowance is usually 500-600 ml more
than the previous day’s 24 hr output.
• Calories are supplied by carbs and fats to prevent wasting and
malnutrition
• Vitamin supplementation because a protein restricted diet does
provide the necessary amounts of vitamins and the pt on
dialysis may lose water soluble vitamins from the blood during
treatment.
Chronic Renal Failure

LAB VALUES
 Medications for CRF
• Diuretics
– Furosemide (Lasix) only given with severe fluid
overload
• Increases excretion of water by interfering with chloride-
binding cotransport system, which, in turn, inhibits sodium
and chloride reabsorption in the thick ascending loop of Henle
and the distal renal tubule
– Adult dose: 20-80 mg PO/IV once; repeat 6-8h
prn or dose may be increased by 20-40 mg no
sooner than 6-8h after previous dose until
desired effect
– Nursing Assessments: Watch for hypokalemia,
assess BP before and during therapy can cause
hypotension
 Medications for CRF continued
• Phosphate-lowering agents
– Calcium acetate (Calphron, PhosLo)
• Combines with dietary phosphorus to form insoluble calcium
phosphate, which is excreted in feces.
– Adult dose: 1-2 g PO bid-tid with each meal; increase
to bring serum phosphate value to 6 mg/dL as long as
hypercalcemia does not develop;
– Calcium carbonate (Caltrate, Apo-Cal, Tums)
• Successfully normalizes phosphate concentrations
• Neutralizes gastric acidity, increase serum Ca
– Adult dose: 1-2 g PO divided bid-tid; with meals as a
phosphorous binder; between meals as a calcium
supplement
Phosphate-lowering agents
– Calcitriol (Rocaltrol, Calcijex)
• Increases intestinal absorption of calcium for treatment of
hypocalcemia and increases renal tubular resorption of
phosphate
– Adult dose for hypocalcemia during chronic dialysis:
• 0.25 mcg/day or every other day, may require 0.5-1 mcg/day
PO
– Sevelamer (Renagel)
• Indicated for the reduction of serum phosphorous in patients
with ESRD.
– Adult dose: Initial: 800-1600 mg PO tid with meals
Maintenance: Increase or decrease by 400-800 mg per
meal q2wk to maintain serum phosphorous at 6 mg/dL
or less
 Phosphate-lowering agents
• Lanthanum carbonate
(Fosrenal)
– for reduction of high
phosphorus levels in
patients with ESRD
– Adult dose: Initial:
250-500 mg PO tid pc
(chewable tabs); adjust
dose q2-3wk to target
serum phosphorus
level
Maintenance: 500-
1000 mg PO tid pc
Phosphate-lowering agents
– Doxercalciferol (Hectorol)
• To lower parathyroid hormone levels in patients undergoing
chronic kidney dialysis. Increases serum Ca
– Adult dose: 10 mcg PO 3 times/wk at dialysis;
increase dose by 2.5 mcg/8 wk if iPTH is not lowered
by 50% and fails to reach the target range; not to
exceed 20 mcg/3 times/wk
Alternatively, 4 mcg IV 3 times/wk; may adjust dose
by 1-2 mcg/8 wk to maintain iPTH levels
– Nursing Assessment for all phosphate lowering
agents: Monitor BUN, creatinine, chloride,
electrolytes, urine pH, urinary calcium, mg,
phosphate, urinalysis urinary Ca should be 9-10mg/dl,
assess for hypocalcemia: headache, N/V, confusion
Medications for CRF continued
• Anemia
– Epoetin alfa (Epogen, Procrit)
• Stimulates RBC production
– Adult dose: 50 -150 U/kg IV/SC 3 times per week,
then adjust dose by 25 U/kg/dose to maintain
appropriate Hct; maintenance 12.5-25 U/kg, titrate to
target Hct,
– Nursing Assessment: Monitor renal studies: urinalysis,
protein, blood, BUN, creatinine; I&O. Monitor blood
studies, Hgb, Hct, RBC, WBC, INR, PTT
Medications for CRF continued
– Darbepoetin (Aranesp)
• Stimulates erythropoiesis
– Adult dose: 0.45 ug/kg IV/SC as a single
injection, titrate not to exceed a target Hgb of
12 g/dl
– Has a longer half-life than epoetin alfa
– Nursing Assessments: Assess blood studies,
renal studies; assess BP, check for rising BP as
Hct rises
 Medications for CRF continued
• Iron Salts
– To treat anemia
– Ferrous sulfate (Feosol, Feratab, Slow FE)
• Replaces iron stores need for RBC development
– Adult dose: 100-200mg tid
– Iron sucrose (Venofer)
• Used to treat iron deficiency dute to chronic hemodialysis
– Adult dose: IV 5ml (100mg of elemental iron) given
during dialysis, most will need 1000mg of elemental
iron over 10 dialysis
• Nursing Assessments: Monitor blood studies,
Hct, Hgb, total Fe, monthly. Assess bowel
elimination for constipation
Dialysis
 What is Dialysis?
• Dialysis is a type of renal replacement therapy which is used to
provide artificial replacement for lost kidney function due to acute or
chronic kidney failure
• It is a life support treatment, it does not cure acute or chronic renal
failure
• May be used for very sick clients who have suddenly lost kidney
function
• May be used for stable clients who have permanently lost kidney
function
• Healthy kidneys remove waste products (potassium, acid, urea) from
the blood and they also remove excess fluid in the form of urine
• Dialysis has to duplicate both of these functions
 Dialysis – waste removal
 Ultrafiltration – fluid removal
 Principle of Dialysis
• Dialysis works on the principle of diffusion of
solutes along a concentration gradient across a
semipermiable membrane
• Blood passes on one side of the semipermeable
membrane, and a dialysis fluid is passed on the
other side
• By altering the composition of the dialysis fluid,
the concentrations of the undesired solutes
(potassium, urea) in the fluid are low, but the
desired solutes (sodium) are at their natural
concentration found in healthy blood
 Prescription for Dialysis
• A prescription for dialysis is given by a
physician who specializes in the kidney
(nephrologist)
• The MD will set various parameters for the
treatment
Time and duration of the dialysis sessions
Size of the dialyzer
Rate of blood flow
 2 Main Types of Dialysis
• Hemodialysis
• Peritoneal Dialysis
 Hemodialysis

Adapted from National Institute of Diabetes and Digestive and Kidney Diseases.

National Institute of Diabetes and Digestive and Kidney Diseases. End-stage renal disease: choosing a treatment that's right for
you. Available at: http://www.niddk.nih.gov/health/kidney/pubs/esrd/esrd.htm. Accessed May 10, 2000.
 What is Hemodialysis (HD)?
• Client’s blood is passed through a system of tubing
(dialysis circuit) via a machine to a semipermeable
membrane (dialyzer) which has the dialysis fluid running
on the other side
• The cleansed blood is then returned via the circuit back to
the body
• The dialysis process is very efficient (much higher than in
the natural kidneys), which allows treatments to take
place intermittently (usually 3 times a week), but fairly
large volumes of fluid must be removed in a single
treatment which can be very demanding on a client
 Side Effects of HD
• The side effects are proportionate to the amount of fluid
being removed
• Decreased blood pressure
• Fatigue
• Chest pains
• Leg cramps
• Headaches
• Electrolyte imbalance
• N&V
• Reaction to the dialyzer
• Air embolism
 Complications of HD
• Because HD requires access to the circulatory system,
clients have a portal of entry for microbes, which could
lead to infection
 The risk of infection depends on the type of access used
• Bleeding may also occur at the access site
• Blood clotting was a serious problem in the past, but the
incidence of this has decreased with the routine use of
anticoagulants (Heparin is the most common)
 Anticoagulants also come with their own risk of side effects and
complications
 Rare Complication of HD
• On the rare occasion, a client may have a severe
anaphylactic reaction
 Sneezing
 Wheezing
 SOB
 Back pain
 Chest pain
 Sudden death
• This can be caused by the sterilant in the dialyzer
or the material in the membrane itself
 Three Types of Access for HD
• IV catheter
• Arteriovenous (AV) fistula
• Synthetic graft
• The type of access is influenced by factors such
as expected time course of the clients renal
failure and the condition of the clients
vasculature
• Some clients may have multiple accesses, usually
because an AV fistula or a graft is maturing and
an IV catheter is still being used
 IV Catheter
(Central Venous Catheter)
• Consists of a plastic catheter with two lumens which is inserted into a
large vein (vena cava via the internal jugular vein) to allow large
flows of blood to be withdrawn from the first lumen
• The blood goes into the dialysis circuit, and is returned to the body
via the second lumen
 Non-tunneled
 Tunneled
• This type of access is used for clients who need rapid access for
immediate dialysis
 Clients who are likely to recover from ARF
 Client with end-stage renal failure
 Clients waiting for other sites to mature
• This type of access is very popular for clients because it doesn’t
involve needles for each treatment
Complications of an IV Catheter
• Venous Stenosis
This is the abnormal narrowing of the blood
vessel
Because the catheter is a foreign body in the
vessel, it often provokes an inflammatory
reaction in the vein wall
This results in scarring and narrowing of the
vein, often to the point where the vein
occludes
 AV Fistula
• This access is recognized as the preferred access method
• To create a fistula a vascular surgeon joins an artery and a
vein together
• Since this bypasses the capillaries, blood flows at a very
high rate through the fistula
 This can be felt by placing a finger over a mature fistula (thrill)
• Usually created in the non-dominant hand
• It can be situated on the hand, forearm or the elbow
• It will take approximately 4-6 weeks to mature
• During treatment, 2 needles are inserted, one to draw
blood out of the body and the other to return blood to the
body
 Advantages of an AV Fistula
• Decreased infection rate
• Increased blood flow rates, therefore a
more effective dialysis treatment
• Decreased incidence of thrombosis
 Complications of an AV Fistula
• If an AV fistula has a very high flow rate and the
vasculature that supplies the rest of the limb is poor, than
a ‘steal syndrome’ can occur
 Blood that enters the limb is drawn into the fistula and returned to
the general circulation without entering the capillaries of the limb
 This results in cool extremities of the limb, cramping pains and
possible tissue damage
• Long term complications can be the development of a
bulging in the wall of the vein (aneurysm)
 The vessel wall is weakened by the repeated insertion of needles
over time
 Can be reduced by careful needling technique
 AV Graft
• This is much like a fistula, except an
artificial vessel is used to join the artery
and the vein
• Grafts are used when client’s own
vasculature does not permit a fistula
• An AV graft will mature much faster than
an AV fistula, and it could be ready to use
within days after formation
 Complications of an AV Graft
• AV grafts are at high risk for narrowing
where the graft is sewn to the vein
As a result clotting or thrombosis may occur
• As a foreign material is being placed in the
body, there is a greater risk of infection
 Equipment Needed for HD
• The HD machine performs the function of
pumping the patient's blood and the dialysate
through the dialyzer.
• The newest dialysis machines on the market are
highly computerized and continuously monitor an
array of safety-critical parameters, including
blood and dialysate flow rates, blood pressure,
heart rate, conductivity, pH, etc.
• If any reading is out of normal range, an audible
alarm will sound to alert the patient-care
technician who is monitoring the patient.
 Equipment – Water System
• An extensive water purification system is absolutely
critical for HD
• Since dialysis patients are exposed to vast quantities of
water, which is mixed with the acid bath to form the
dialysate, even trace mineral contaminants or bacterial
endotoxins can filter into the patient's blood.
• Because the damaged kidneys are not able to perform
their intended function of removing impurities, ions that
are introduced into the blood stream via water can build
up to hazardous levels, causing numerous symptoms
including death
• For this reason, water used in HD is purified
 Equipment – The Dialyzer
• The dialyzer, or artificial kidney, is the piece of equipment that
actually filters the blood
• The blood is run through a bundle of very thin capillary-like
tubes, and the dialysate is pumped in a chamber bathing the fibers
• The process mimics the physiology of the glomerulus and the rest
of the nephron
• Dialyzers come in many different sizes. A larger dialyzer will
usually translate to an increased membrane area, and an increase
in the amount of undesired solutes removed from the patient's
blood.
• The nephrologist will prescribe the dialyzer to be used depending
on the patient
• Dialyzers are not shared between patients in the practice of reuse.
Peritoneal Dialysis
 What is Peritoneal Dialysis (PD)?
• Peritoneal dialysis works by using the body's peritoneal
membrane, which is inside the abdomen, as a semi-
permeable membrane.
• A specially formulated dialysis fluid is instilled around
the membrane, using an indwelling catheter, then dialysis
can occur, by diffusion
• Excess fluid can also be removed by osmosis, by altering
the concentration of glucose in the fluid.
• Dialysis fluid is instilled via a peritoneal dialysis catheter,
which is placed in the patient's abdomen, running from
the peritoneum out to the surface, near the navel
• Peritoneal dialysis is typically done in the patient's home
and workplace, but can be done almost anywhere
 Advantages of PD
• Can be done at home
• Relatively easy for the client to learn
• Easy to travel with, bags of solution are
easy to take on holiday
• Fluid balance is usually easier when the
client is on PD than if the client is on HD
 Disadvantage of PD
• Requires a degree of motivation and
attention to cleanliness while performing
PD
• There are a number of complications
 Complications of PD
• Peritoneal dialysis requires access to the peritoneum. As this
access breaks normal skin barriers, and as people with renal
failure generally have a slightly suppressed immune system,
infection is a relatively common problem
• Long term peritoneal dialysis can cause changes in the peritoneal
membrane, causing it to no longer act as a dialysis membrane as
well as it used to.
• This loss of function can manifest as a loss of dialysis adequacy,
or poorer fluid exchange (also known as ultrafiltration failure)
• Fluid may leak into surrounding soft tissue, often the scrotum in
males
• Hernias are another problem that can occur due to the abdominal
fluid load
 Nursing Assessments
• Before client is in the unit, look at the nurses notes from
the treatment before
 Any problems, will help nurse plan for the upcoming treatment
• Look at the client
 Strength
 Gait
 Whether client needs assistance
 Color
 Puffiness
 Could be caused by excess fluid, too much to drink, more fluid
should be taken off with each treatment, changes in voiding pattern
(are they voiding less than they did last month)
 Assessments Con’t
• Shortness of breath
 Could indicate fluid around the lungs
 Ask about SOB at night (does client have to sleep in a sitting
position?)
• Ask the client how they are feeling
 The client is usually the best source of information
 Clients are in 3 times a week, dialysis nurses really get to know their
clients
• Evaluate access
 Bruising, swollen, tender
 Bruit – listen with the stethoscope for a swishing sound of the blood,
listen all the way up the arm
 Thrill – felt with the fingers, tells the nurse if the blood is flowing in
the fistula (client’s are told to feel for this at home when a fistula is
first initiated)
 Assessments During Treatment
• Ask client how he/she feels
 Dizziness, diaphoretic,
• The machines automatically take BP and HR every 30 minutes
 Can program the machines to take it at whatever interval is
necessary (every min, 10 min, 15 min)
• Try to recognize a problem before it starts (ex. Hypovolemic
shock)
• Assess access site
 Watch trend of BP
 It usually gradually decreases throughout the course of the
treatment, but look for sudden or drastic drops
• Assess access site
 Bleeding, swelling, tenderness
 Nursing Interventions
• If client comes in with shortness of breath, offer
O2 which can be kept on for the full treatment if
necessary
• Comfort
 Client’s are sitting in the same chair for up to four
hours
 Offer extra pillows, some clients have special back
pillow they leave in the unit
 Ensure TV and audio is working properly
 Nursing Interventions Con’t
• If the blood pressure is dropping too quickly:
 Slow or stop fluid removal for a time period
 The machines are constantly being adjusted
throughout the course of the treatment depending on
the BP
 If the BP drops suddenly 200-300cc of normal saline
can be given to balance fluid levels
• Usually, more fluid will be taken off at the beginning of
the treatment, this will allow the client to feel better at the
end
• If the client is elderly, fluid removal starts slowly to ease
them into the treatment
 Responsibilities of Nursing Staff
Prior to Dialysis
• Ensure client is ready to sit for up to four
hours
Encourage client to use washroom before
arriving to the unit
Try to avoid laxatives if possible before
treatment
• Ensure client has eaten meal prior to
treatment
 Responsibilities of Nursing Staff
After Dialysis
• A dialysis nurse will give unit leader or primary nurse a
verbal report of treatment
 Any complications during treatment
 Check BP standing and sitting
 Assess access site
• Encourage client to rest
 Avoid treatments or physio for a couple of hours if possible
• Watch fluid intake
 Be aware if client is on fluid restriction
• Check thrill and bruit
• Do not take a BP on access arm
• Do not take blood from access arm
 Questions?
Thank you for listening.