End-stage renal disease

2o hypertensive
nephrosclerosis

Presented by: Christelle Queen S. Bacalla

INTRODUCTION
End-stage renal disease (ESRD) represents a clinical state or
condition in which there has been an irreversible loss of renal
function in which the bodys ability to maintain metabolic and
fluid and electrolyte balance fails, resulting in uremia or
azotemia (retention of urea and other nitrogenous wastes in
the blood), and these patients usually need to accept renal
replacement therapy (dialysis or kidney transplantation) in
order to avoid life-threatening uremia. Itis the final stage
(stage 5) of chronic kidney disease (CKD). This means
kidneys are only functioning at 10 to 15 percentof their
normal or not functioning at all. Kidney disease is usually
progressive. It typically does not reach the end stage until 10
to 20 years after you are diagnosed with chronic kidney
disease, which may also develop slowly.

INTRODUCTION
Most cases of ESRD are caused by diabetesor
highblood pressure.Chronic Kidney disease (CKD)
is an umbrella term that describes kidney damage
or a decrease in glomerular filtration rate (GFR) for
3 or more months. Untreated CKD can result in endstage renal disease (ESRD) and necessitate renal
replacement therapy (dialysis or kidney
transplantation). Chronic kidney disease is identified
by a blood test for creatinine. Higher levels of
creatinine indicate a falling glomerular filtration rate
and as a result a decreased capability of
thekidneys to excrete waste products.

INTRODUCTION
Creatinine
levels may be normal in the early stages ofCKD, and the

condition is discovered ifurinalysis shows that the kidney is allowing the

loss ofproteinor red blood cells into theurine. To fully investigatethe
underlying cause of kidney damage, various forms ofmedical imaging,
blood tests and often renal biopsy are employed to find out if there is a
reversible cause for the kidney malfunction.
The five stages of CKD are based on the glomerular filtration rate (GFR)
wherein the normal GFR is 125 mL/min/1.73m2. Stage 1 is when there is
kidney damage with normal or GFR 90mL/min/1.73m 2. Stage 2 is when
the GFR is ranging from 60-89. Stage 3 has a GFR of 30-59. Stage 4 has a
severe decrease in GFR ranging from 15-29. The final stage is considered
Kidney failure or End-stage renal disease with a GFR of <15mL/1.73m 2.
Hypertensive nephrosclerosis is a medical condition referring to damage
to thekidneydue to chronichigh blood pressure. It is a progressive
disease that results from sclerosis (hardening) of the small blood vessels
in the kidneys which can lead tokidney failure. Nephrosclerosis is
classified as either benign or malignant:

INTRODUCTION

Benign nephrosclerosisis a gradual and prolonged deterioration of the

renal arteries. First the inner layer of the walls of smaller vessels
thickens, and gradually this thickening spreads to the whole wall,
sometimes closing the central channel of the vessel. Fat then becomes
deposited in the degenerated wall tissue. The larger arteries gain an
excess of elastic tissue, which may block their channels. Both of these
conditions cause the blood supply to the vital kidney areas to be
blocked, and tissue deterioration ensues.

Inmalignant nephrosclerosisa similar process occurs but at a much

faster rate. Thediseasemay develop so rapidly that there is little time
for gross kidney changes to occur. The surface of the kidney, however, is
nearly always covered with large red blotches at points where bleeding
has occurred. In the malignant disease the arteriole walls thicken and
may be closed off by rapid cell growth. The nuclei of these cells die, and
the elastic fibers disappear. With the loss of the elastic fibres, the walls
of the vessels become much more fragile and easily distended. Severe
ruptures and hemorrhages are frequent. The arterioles often suffer
spasms that can force blood through lesions in the vessel walls; the
tissues become swollen as a result.

INTRODUCTION
According to the 2011US Renal Data
System(USRDS) data, in the year 2009,
hypertensive nephrosclerosis (HN)
accounted for 28% of patients
reachingend-stage renal disease(ESRD).
The rate of ESRD attributed to hypertension
has grown 8.7% since the year 2000.
Hypertensive nephrosclerosis is reportedly
the second most common cause of ESRD in
white people (23%) and is the leading
cause of ESRD in black people (46%).

INTRODUCTION
I chose this case because I want to gain
comprehensive knowledge about the disease.
Objectives of my case study are the following:
To understand the nature and pathophysiology of
the disease.
To identify signs and symptoms exhibited by the
patient with ESRD.
To assess the patient, find out need of patient and
come up with appropriate interventions utilizing
the nursing process.
To provide discharge plan to the patient with
ESRD.

DEMOGRAPHIC PROFILE

Name: Patient M.
Age: 43 years old
Sex: Male
Civil Status: Married
Religion: Seventh day Adventist
Address: P-4 Cantugas, Mainit, SDN
Date of Birth: 04/06/1972
Final Diagnosis: ESRD 2o Hypertensive
Nephrosclerosis

PAST MEDICAL HISTORY

The patient was diagnosed with Hypertension as early as 31
years of age but did not comply with his treatment regimen. He
would usually buy Captopril whenever he feels like his blood
pressure is elevated.
He was admitted at Surigao Medical Center on December 2013
due to vomiting and diarrhea. The patients doctor suggested
him to undergo Hemodialysis for the reason that his serum
creatinine was elevated amounting to 32mg/dl. However, the
patient refused, thinking that hemodialysis was just a waste of
money and that sooner or later he will die. On April 2014, he was
brought to CRH by his daughter because he had an altered
sensorium, vomiting, and peripheral edema. According to him,
his creatinine increased to 112 and his BUN was very elevated,
he cannot recall the rest of the history. He was then diagnosed
with ESRD secondary to Hypertensive Nephrosclerosis.
Arteriovenous Fistula was created at his left arm on April 06,
2014 by Dr.Ycong. The patient also verbalized that his doctor
explained to him the result of his sonography that both of his
kidneys shrunk.

SOCIAL HISTORY
The patient lives in P-4 Cantugas, Mat-I, SDN. He has 3
children, two of them have their own family, and the
youngest is currently living with him and his wife at
their residence. Before he was diagnosed with ESRD,
he was living only with his youngest daughter who is
studying in High School because his wife worked
abroad. After his hospitalization, his wife went home
to take care of him. He formerly worked as a treasurer
in their municipality and stopped when he was already
diagnosed with ESRD because he easily gets tired and
has to go on hemodialysis twice a week. The patient
does not smoke, and only drinks liquors occasionally.
He has a good relationship with his neighbors.

FAMILY HISTORY OF ILLNESS

The patient verbalized that his parents

have a history of HPN.

PHYSICAL ASSESSMENT
VITAL SIGNS:
BP: 160/100 mmHg 180/110 mmHg
TEMPERATURE: 36.4oC
PULSE RATE: 86 bpm
RESPIRATORY RATE: 21 bpm

SKIN:
Color: Dark brown
Integrity: Intact
Moisture: Dry flaky skin
(+)pruritus @ arms and back
HAIR:
Color: Black
Thickness: Thick and dry hair

NAILS:
Shape: Normal; symmetrical
Texture: Smooth
Nailbed color: Pale
Capillary Refill: Normal
Appearance: Dirty
FACE:
Symmetry of Movements: Symmetrical
Appearance: puffy cheeks
EYES:
Color: White
Hollowness: Sunken
Pale conjunctiva

PUPILS:
Color: Brown
Shape: Circular
Symmetry: Symmetrical
AURICLES:
Normal and symmetrical
Texture, elasticity, tenderness: Firm; non-tender
Skin lesions: No skin lesions
NOSE:
Symmetrical; (-)flaring

MOUTH:
(-)halitosis; without dentures
Teeth color: light yellow
Appearance: pale
LUNGS:
Breath sounds: (+)crackles on both lung fields
ABDOMEN:
Distended
ARMS:
Symmetrical, with AVF @ L arm
LEGS:
Symmetrical, with scar @ posterior L calf, edema (1+)
on both feet

GORDONS TYPOLOGY OF HEALTH PATTERN

HEALTH PERCEPTION HEALTH MANAGEMENT

The patient rarely seeks medical attention whenever he has

an illness because he believes that it is just a waste of
money. Before he was diagnosed with ESRD, he does not
take any vitamins and only buys Captopril whenever he
feels dizzy and his BP becomes elevated. But now he is
already compliant to his prescribed medications with the
help of his wife by reminding him to take his meds. He
undergoes hemodialysis twice a week, and undergoes blood
transfusion of PRBC whenever his RBC count becomes very
low usually every 3 months. The wife verbalized that the
patient is very hard headed because the patient often times
wont listen to him and his diet is still salty and high in fat.
The patient maintains a weight of 54.5kg pre-HD and
weight goal post-HD is 51kg.

NUTRITIONAL METABOLIC PATTERN

His usual water intake is 4-6 times a day. His diet is usually
salty and high in fat. He often drinks soda and Cobra energy
drink for 2-3 times a day before he was diagnosed. He
drinks liquors occasionally and never smoke. The patient
does not have food allergies. He often has no appetite and
his wife usually has to bring him to restaurants to eat; he
verbalized that his appetite depends on the smell and
appearance of the food. However, he still eats salty foods
even though hes already diagnosed with ESRD. He does
not limit his fluid intake though his doctor advised him to
limit fluid intake to 1L per day. The patient also verbalized
that after eating salty foods or drinking soda, he will
experience swelling of the feet and bone pains just hours
later.

ELIMINATION PATTERN
The patient usually voids 5-7 times a day in
scanty-minimal amount, dark yellow in color or
colorless. His bowel movement is usually once
every 2 days.
ACTIVITY,
LEISURE,
AND
RECREATIONAL
ACTIVITIES
He previously worked as a treasurer in their
Municipal office. The patient did not engage in
exercises before and until now. He watches
television more often and does not usually go out
for a walk. The patient does not do household
chores because he gets easily tired.

SLEEP AND REST PATTERN

The patient usually sleeps at 10pm and woke up at

4am. Often times he experienced waking up at
night to void. He verbalized karon nga naingani
nako, naa rako pirmi sa balay kaon katulog kay dili
man ko pa trabahuon sakong asawa.

COGNITIVE-PERCEPTUAL PATTERN

The patient is a college graduate. He has difficulty

seeing near objects. He even holds his cellphone
away while reading a text message. He is very
sensitive in the smell and appearance of food which
affects his appetite.

SELF PERCEPTION-SELF CONCEPT PATTERN

The patient likes to socialize with his workmates before.
He thought that he was healthy and does not have any
problem about his hypertension. He verbalized in an
inappropriate affect Wala gyud ko nag tuo nga muabut
sa ingani, nga maingani ko, karon nghulat nalang ko knusa mamatay.

ROLE RELATIONSHIP
His primary dialect is Surigaonon. He is married, with 3
children who he is well-supported and loved. The patient
is currently living with his wife and youngest child. His
eldest daughter who is a nurse abroad is the only one
who supports him on his treatments.

SEXUALITY-REPRODUCTIVE PATTERN

Unavailable.

COPING AND STRESS TOLERANCE

Whenever he has problems, he does not usually tell it to his family

especially now because he does not want to be a burden in the
family.

VALUES-BELIEF PATTERN
The patients religion is Seventh Day Adventist. He does not
regularly go to Church but he always pray to God. He realized that
promoting good health is really important than to regret later in
your life particularly in his condition in which he has to undergo
hemodialysis for a lifetime. However, even though he is already on
hemodialysis, he does not change his lifestyle and diet because he
believes that it is okay to eat salty foods and drink soda since hes
already on hemodialysis which functions now as his kidneys, and
besides, he will still die in the end.

REVIEW OF ANATOMY AND

PHYSIOLOGY
Location
The kidneys are a pair of organs
found along the posterior muscular
wall of the abdominal cavity. The
left kidney is located slightly more
superior than the right kidney due
to the larger size of the liver on the
right side of the body. Unlike the
other abdominal organs, the
kidneys lie behind the peritoneum
that lines the abdominal cavity and
are thus considered to be
retroperitoneal organs. The ribs
and muscles of the back protect
the kidneys from external damage.
Adipose tissue known as perirenal
fat surrounds the kidneys and acts
as protective padding.

Structure
The kidneys are bean-shaped with the
convex side of each organ located
laterally and the concave side medial.
The indentation on the concave side of
the kidney, known as the renal hilus,
provides a space for the renal artery,
renal vein, and ureter to enter the
kidney.
A thin layer of fibrous connective tissue
forms the renal capsule surrounding
each kidney. The renal capsule provides
a stiff outer shell to maintain the shape
of the soft inner tissues.
Deep to the renal capsule is the
soft,dense,
vascularrenal
cortex.
Seven cone-shaped renal pyramids form
the renal medulla deep to the renal
cortex. Therenal pyramids are aligned
with their bases facing outward toward
the renal cortex and their apexes point
inward toward the center of the kidney.
Each apex connects to a minor calyx, a
small hollow tube that collects urine. The
minor calyces merge to form 3 larger
major calyces, which further merge to
form the hollow renal pelvis at the
center of the kidney. The renal pelvis
exits the kidney at the renal hilus, where

The Nephron
Each kidney contains
around 1 million
individual nephrons,
the kidneys
microscopic functional
units that filter blood
to produce urine. The
nephron is made of 2
main parts: the renal
corpuscle and the
renal tubule.

Responsible forfiltering the blood, our renal corpuscle is

formed by the capillaries of the glomerulus and the
glomerular capsule (also known as Bowmans capsule).
The glomerulus is a bundled network of capillaries that
increases the surface area of blood in contact the blood
vessel walls. Surrounding the glomerulus is the glomerular
capsule, a cup-shaped double layer of simple squamous
epithelium with a hollow space between the layers.
Special epithelial cells known as podocytes form the layer
of the glomerular capsule surrounding the capillaries of
the glomerulus. Podocytes work with the endothelium of
the capillaries to form a thin filter to separate urine from
blood passing through the glomerulus. The outer layer of
the glomerular capsule holds the urine separated from the
blood within the capsule. At the far end of the glomerular
capsule, opposite the glomerulus, is the mouth of the
renal tubule.
A series of tubes called the renal tubule concentrate urine
and recover non-waste solutes from the urine. The renal
tubule carries urine from the glomerular capsule to the
renal pelvis.

The curvy first section of the renal

tubule is known as the proximal
convoluted tubule. The tubule cells
that line the proximal convoluted
tubule reabsorb much of the water and
nutrients initially filtered into the urine.
Urine next passes through the loop of
Henle, a long straight tubule that
carries urine into the renal medulla
before making a hairpin turn and
returning to the renal cortex.
Following the loop of Henle is the distal
convoluted tubule.
Finally,
urine
from
the
distal
convoluted
tubules
of
several
nephrons enters the collecting duct,
which carries the concentrated urine
through the renal medulla and into the
renal pelvis.
From the renal pelvis urine from many
collecting ducts combines and flows
out of the kidneys and into the ureters.

The main function of the kidneys is to filter

water, impurities and wastes from the blood.
The blood from the body enters the kidneys
through the renal arteries. Once in the kidney,
the blood passes through the nephrons, where
waste products and extra water are removed.
The clean blood is returned to the body through
the renal veins. The waste products filtered
from the blood are then concentrated into urine.
The urine is collected in the renal pelvis. The
ureters move the urine to the bladder, where it
is stored. Urine is passed out of the bladder and
the body through the urethra.

Water Homeostasis

The kidneys are able to control the volume ofwater in the

bodyby changing the reabsorption of water by the tubules of
the nephron. Under normal conditions, the tubule cells of the
nephron tubules reabsorb (via osmosis) nearly all of the water
that is filtered into urine by the glomerulus.
Water reabsorption leads to very concentrated urine and the
conservation of water in the body. The hormones antidiuretic
hormone (ADH) and aldosterone both increase the
reabsorption of water until almost 100% of the water filtered
by the nephron is returned to the blood. ADH stimulates the
formation of water channel proteins in the collecting ducts of
the nephrons that permit water to pass from urine into the
tubule cells and on to the blood. Aldosterone functions by
increasing the reabsorption of Na+ and Cl- ions, causing more
water to move into the blood via osmosis.

Acid/Base Homeostasis

The kidneys regulate the pH level of the blood by controlling the

excretion of hydrogen ions (H+) and bicarbonate ions (HCO3-).
Hydrogen ions accumulate when proteins are metabolized in the
liver and when carbon dioxide in the blood reacts with water to form
carbonic acid (H2CO3). Carbonic acid is a weak acid that partially
dissociates in water to form hydrogen ions and bicarbonate ions.
Both ions are filtered out of the blood in the glomerulus of the
kidney, but the tubule cells lining the nephron selectively reabsorb
bicarbonate ions while leaving hydrogen ions as a waste product in
urine. The tubule cells may also actively secrete additional hydrogen
ions into the urine when the blood becomes extremely acidic.

The reabsorbed bicarbonate ions enter the bloodstream where

they can neutralize hydrogen ions by forming new molecules of
carbonic acid. Carbonic acid passing through the capillaries of
thelungsdissociates into carbon dioxide and water, allowing us to
exhale the carbon dioxide.

Blood Pressure Homeostasis

The kidneys help to control blood pressure in the body by regulating the excretion
of sodium ions and water and by producing the enzyme renin. Because blood is
mostly made of water, an increased volume of water in the body results in an
increase in the volume of blood in the blood vessels. Increased blood volume
means that the heart has to pump harder than usual to push blood into vessels
that are crowded with excess blood. Thus, increased blood volume leads to
increased blood pressure. On the other hand, when the body is dehydrated, the
volume of blood and blood pressure decrease.
The kidneys are able to control blood pressure by either reabsorbing water to
maintain blood pressure or by allowing more water than usual to be excreted into
urine and thus reduce blood volume and pressure. Sodium ions in the body help to
manage the bodys osmotic pressure by drawing water towards areas of high
sodium concentration. To lower blood pressure, the kidneys can excrete extra
sodium ions that draw water out of the body with them. Conversely, the kidneys
may reabsorb additional sodium ions to help retain water in the body.
Finally, the kidneys produce the enzyme renin to prevent the bodys blood
pressure from becoming too low. The kidneys rely on a certain amount of blood
pressure to force blood plasma through the capillaries in the glomerulus. If blood
pressure becomes too low, cells of the kidneys release renin into the blood. Renin
starts a complex process that results in the release of the hormone aldosterone by
the adrenal glands. Aldosterone stimulates the cells of the kidney to increase their
reabsorption of sodium and water to maintain blood volume and pressure.

Hormones

The kidneys maintain a small but important endocrine function by

producing the hormones calcitriol and erythropoietin.

Calcitriol is the active form of vitamin D in the body. Tubule

cells of the proximal convoluted tubule produce calcitriol from
inactive vitamin D molecules. At that point, calcitriol travels
from the kidneys through the bloodstream to the intestines,
where it increases the absorption of calcium from food in the
intestinal lumen.

Erythropoietin (EPO) is a hormone produced by cells of the

peritubular capillaries in response to hypoxia (a low level of
oxygen in the blood). EPO stimulates the cells of redbone
marrowto increase their output of red blood cells. Oxygen
levels in the blood increase as more red blood cells mature and
enter the bloodstream. Once oxygen levels return to normal,
the cells of the peritubular capillaries stop producing EPO.

PATHOPHYSIOLOGY

LABORATORY RESULTS
May 8, 2015

COMPONENT

RESULTS

NORMAL
VALUES

ANALYSIS

RBC

2.7

4.5-5.2 x 109/L

Decreased

Hemoglobin

8.4

13.5-17.5g/dL

Decreased

Hematocrit

25.7%

40-52%

Decreased

WBC

9.0

4.5-10.5 x 109

Within normal range

Platelet

293

159-400

Within normal range

The patients RBC is below normal. This indicates alteration in

erythropoietin production secondary to renal malfunction.
Hemoglobin and hematocrit were below normal, thus showing
anemia related to insufficient RBC production. The patients
doctor ordered for blood transfusion of PRBC 280ml.

COMPONENT

RESULTS

NORMAL
VALUES

ANALYSIS

BUN

57

7-18mg/dL

Indicates renal problem

Creatinine

32

0.7-1.3mg/dL

Indicates renal problem

The BUN and Creatinine were below their normal range thus
showing inability of the kidney to excrete nitrogenous waste.

Aug. 28, 2015

COMPONENT

RESULTS

NORMAL VALUES

ANALYSIS

RBC

2.4

4.5-5.2 x 109/L

Decreased

Hemoglobin

6.9

13.5-17.5g/dL

Decreased

Hematocrit

23.3%

40-52%

Decreased

WBC

9.0

4.5-10.5 x 109

Within normal range

Platelet

301

159-400

Within normal range

The patients RBC is below normal. This indicates alteration in

erythropoietin production secondary to renal malfunction.
Hemoglobin and hematocrit were below normal, thus showing
anemia related to insufficient RBC production. The patients doctor
ordered for blood transfusion of PRBC 280ml.

COMPONENT

RESULTS

NORMAL VALUES

ANALYSIS

Creatinine

13

0.7-1.3mg/dL

Indicates
problem

renal

The Creatinine was below normal range thus showing inability of the
kidney to excrete nitrogenous waste.

COURSE IN THE WARD

The patient arrived in the dialysis unit at around 7am.
The patient was well-groomed. He had a pre-HD weight
of 54.5kg. He was calm, cooperative, and had
spontaneous speech throughout the interview.
However, when discussing self perception-self concept
pattern, the patient displayed behavior suggestive of
altered self-concept such as avoidance of eye contact
during such discussion, and speaking in an
inappropriate affect. His vital signs throughout the
dialysis period were as follows: BP: 160-180/100110mmHg, PR: 85-91bpm, RR: 21-24bpm, T: 36.236.4oC. He frequently scratched his arm and asked his
wife to scratch his back. The patient also chatted with
the other patients.

DRUG
NAME

MoA

Clonidine
stimulates
Clonidine alpha2receptors in
Antihypertens brainstem
which results
ive
in reduced

sympathetic
outflow from
the CNS and
a decrease
in peripheral
resistance
leading to
reduced BP
and pulse
rate. It does
not alter
normal
hemodynami
c response
to exercise
at
recommende
d dosages.

DRUG STUDY

INDICATION

CONTRAINDICATION

Hypertensio
n, used
alone or as
part of
combination
therapy.

Hypersensitivity.
Disorders of cardiac
pacemaker activity
and conduction.
Pregnancy and
lactation.

SIDE
EFFECTS

INTERVENTIONS

dry mouth,
drowsiness,
dizziness,
irritability,
mood
changes, sleep
problems
(insomnia or
nightmares),
headache, ear
pain, fever,
feeling hot,
constipation,
diarrhea,
stomach pain,
increased
thirst,
decrease
libido,
impotence,
cold symptoms
such as runny
or stuffy nose,
sneezing,
cough, or sore
throat

WARNING:
Do not discontinue
abruptly; discontinue
therapy by reducing the
dosage gradually over
24 days to avoid
rebound hypertension,
tachycardia, flushing,
nausea, vomiting,
cardiac arrhythmias
(hypertensive
encephalopathy and
death have occurred
after abrupt cessation
of clonidine).

Do not discontinue
transdermal therapy
prior to surgery;
monitor BP carefully
during surgery; have
other BP-controlling
drugs readily available.

Continue oral clonidine

therapy within 4hr. of
surgery then resume as
soon as possible
thereafter.

DRUG
NAME

Mechanism
of Action

INDICATION

CONTRAINDICA
TION

SIDE
EFFECTS

INTERVENTIONS

Amlodipine

Amlodipine
decreases
arterial smooth
muscle
contractility
and
subsequent
vasoconstrictio
n by inhibiting
the influx of
calcium ions
through
calcium
channels.
Inhibition of
the initial influx
of calcium
decreases the
contractile
activity of
arterial smooth
muscle cells
and results in
vasodilation.
The
vasodilatory
effects of
amlodipine
result in an
overall
decrease in
blood pressure.

Treatment for
hypertension or
in combination
with other
antihypertensive
s.

Hypersensitivit
y to the drug.

Blood pressure
less than 90
mmHg.

Patients with
hepatic
impairment,
aortic stenosis,
CHF.

Headache,
dizziness,
drowsiness,
tired
feeling,
gastric
upset, dry
mouth,
flushing.

Monitor
blood
pressure and
pulse before
therapy,
during dose
titration, and
periodically
during
therapy.

Use
cautiously in
severe
hepatic
impairment,
history of
CHF, aortic
stenosis.

-Calcium
Channel
blocker

DRUG
NAME

Twynsta

MoA
Twynsta
contains a
combination
of
Amlodipine
and
Telmisartan.
Amlodipine
is a calcium
channel
blocker.
Amlodipine
relaxes
(widens)
blood
vessels and
improves
blood flow.

INDICATION

This product
is used to
treat
hypertension.

These
medications
are used
together
when one
drug is not
controlling
the blood
pressure. The
doctor may
Telmisartan
is an
direct the
angiotensin
patient to
II receptor
start taking
antagonist.
Telmisartan
the individual
keeps blood
vessels from medications
first, and
narrowing,
which lowers then switch
blood
pressure and to this
combination
improves
blood flow.
product if it is
the best dose

CONTRAINDICATION

Hypersensitivity to
Amlodipine and
Telmisartan.

Check with the

physician first if the
patient has any of
the following:
Severe Narrowing of
the Aortic Heart
Valve, Renal Artery
Stenosis, Abnormally
Low Blood Pressure,
Liver Problems,
Severe Liver Disease,
Kidney Disease,
Pregnancy,
Decreased Blood
Volume, Extreme
Loss of Body Water,
High Amount of
Potassium in the
Blood.

SIDE
EFFECTS
Signs of an
allergic
reaction to
Twynsta:hives
; difficulty
breathing;
swelling of
your face,
lips, tongue,
or throat.

Common
Twynsta side
effects may
include:
swelling in the
hands or feet,
fast
heartbeats,
dizziness,
drowsiness,
tired feeling;
flushing
(warmth,
redness, or
tingly feeling);
back pain; or
nausea,
diarrhea,
stomach
pain.

INTERVENTIONS

Check blood
pressure before
and after giving
the drug.

Instruct patient to
avoid getting up
too fast from a
sitting or lying
position, or he
may feel dizzy.

DRUG
NAME

Terraferr
on

INDICATION

MoA

Consists of
Folic Acid,

Iron (Ferrous
-Vit. and
Sulfate),Vita
minerals
suppleme min
B1,Vitamin
nt;
Antianemi B12,Vitamin
c
B2,Vitamin

B3,
Vitamin B6,
Vitamin C.

Stimulates
the
hematopoieti
c system.

Prevention
and
treatment
of iron
deficiency
anemia.

CONTRAINDICATION

SIDE
EFFECTS

INTERVENTIONS

Thromboembolism,
erythremia,
erythrocytosis,
increased sensitivity
to cyanocobalamin.

Nausea
Vomiting

Allergic
reaction:
Urticaria.

Drink with
orange juice to
improve
absorption and
to minimize
nausea.

Do not take with

milk, tea or
coffee.

DRUG
NAME

Clopidogr
el

MoA

Inhibits
platelet
activation

and
antiplatelet aggregati

on
through
the
irreversibl
e binding
of its
active
metabolit
e to ADP
receptors
on
platelets.

INDICATION

CONTRAINDICATION

For prevention Hypersensitivity,

or treatment
Peptic ulcer or
of stroke and
intracranial
heart attack.

hemorrhage.

Use cautiously with

bleeding disorders,
recent surgery, renal
or hepatic
impairment,
pregnancy.

SIDE
EFFECTS
Dizziness,
easy
bruising, GI
upset,
headache.

Adverse
effects:
Rash, DOB,
chest
tightness,
confusion,
tarry stool.

INTERVENTIONS
Monitor blood
pressure.
Provide comfort
measures and
arrange for
analgesics if
headache occurs.
Provide small,
frequent meals if GI
upset occurs.

DRUG NAME

MoA

Montelukas
t+
Levocitirizi
ne

Binds to
cysteinyl
leukotrien
e type 1
(CysLT1)
receptor
in the
upper and
lower
airways to
prevent
leukotrien
emediated
effects
associated
with
allergic
rhinitis.

INDICATION CONTRAINDICATION

Prophylaxis
or
treatment
of allergic
reactions
such as
chronic
urticaria,
obstructive
airway
diseases
and rhinitis.

Hypersensitivity,
patients with
hepatic
impairment.

SIDE
EFFECTS
Nausea,
dry mouth,
drowsiness
,
dyspepsia,
headache.

INTERVENTIONS
Advise patients that
montelukast can be
taken without
regard to meals but
to take it with food
if stomach upset
occurs.
Advise patients with
known aspirin
sensitivity to
continue avoidance
of aspirin and
NSAIDs while taking
the drug.

DRUG
NAME

MoA

INDICATION

Nifedipin
e

Decreases
arterial
smooth
muscle
contractility
and
subsequent
vasoconstricti
on by
inhibiting the
influx of
calcium ions
through
calcium
channels.

For treatment
of
hypertension.

-calcium

channel
blocker

CONTRAINDICATION
Hypersensitivity to the
drug, CAD, history of
heart attack.

SIDE
EFFECTS

INTERVENTIONS

Dizziness,
urticaria,
flushing,
tremors,
nausea,
heartburn.

Monitor BP
carefully during
titration period.
Patient may
become severely
hypotensive,
especially if also
taking other drugs
known to lower BP.
Withhold drug and
notify physician if
systolic BP <90.

Instruct patient to
avoid getting up
too fast from a
sitting or lying
position, or he may
feel dizzy.

DRUG NAME

MoA

INDICATION

Exerts its Indicated as

NAcetylcystein mucolytic adjuvant
action
therapy for
e

-mucolytic

through
its free
sulfhydryl
group,
which
reduces
the
disulfide
bonds in
the
mucus
matrix
and
lowers
mucus
viscosity.

patients with
abnormal,
viscous or
thick
secretions.

CONTRAINDICATION
Drug hypersensitivity

SIDE
INTERVENTIONS
EFFECTS
Nausea,
Monitor patients VS
vomiting,
especially RR and
hypotension HR.
, diarrhea or
constipation
.

DRUG
NAME

CaCO3

phosphat
e binder
-dietary
suppleme
nt

MoA

INDICATION

As dietary
supplement,
used to
prevent or
treat
negative
calcium
balance; in
osteoporosis
, it helps to
prevent or
decrease
the rate of
bone loss.

Used for the

treatment of
hyperphosphatem
ia, normalizing
phosphate
concentrations in
patients with CKD.
It can also be
used as a calcium
supplement in
these patients.

Phosphate
binder:
Binds with
dietary
phosphate
to form
insoluble
calcium
phosphate,
which is
excreted in
feces.

CONTRAINDICATIO
N

Hypersensitivity,
patients with
hypercalcemia,
and
hypophatemia.

SIDE EFFECTS

Nausea,
flatulence,
constipation,
xerostomia,
vomiting.

INTERVENTIONS

Monitor serum
calcium and
phosphate levels.

Should be given
with meals to
increase
absorption. May
decrease iron
absorption, so
should be
administered 1-2
hours before or
after iron
supplementation;
limit intake of
with bran, foods
high in oxalates
or whole grain
cereals which
may decrease
calcium
absorption.

DRUG
NAME

MoA

INDICATION

Elevates
Used to treat
serum iron
iron deficiency

-iron
concentratio anemia.
supplement n which then
helps to form
High or
trapped in
the reticuloendothelial
cells for
storage and
eventual
conversion to
a usable
form of iron.

FeSO4

CONTRAINDICATION
Hypersensitivity,
severe hypotension.

SIDE
EFFECTS
Nausea,
vomiting,
dizziness.

INTERVENTIONS
Advise patient to
take medicine as
prescribed.
Caution patient to
make position
changes slowly to
minimize orthostatic
hypotension.

DRUG NAME

Sodium
Bicarbonate

MoA
Sodium
Bicarbo
nate
acts as
an
alkalini
zing
agent
by
releasin
g
bicarbo
nate
ions.

INDICATION
Used for the
treatment of
metabolic
acidosis
which may
occur in
severe renal
disease

CONTRAINDICATION

Metabolic or respi.
alkalosis,
hypocalcemia,
hypoventilation, and
hypersensitivity to
drug.

SIDE
EFFECTS

Headache,
anorexia,
unpleasant
taste, tired
feeling,
nausea,
and/or
vomiting.

INTERVENTIONS

Monitor urinary pH
and urine output as
guide for dosing.

Monitor patients VS
especially RR and
HR.

DRUG NAME

Hydroxizine

-antihistamine

MoA

INDICATION

Hydroxyzine
reduces
activity in
the central
nervous
system. It
also acts as
an
antihistamin
e that
reduces the
natural
chemical
histamine in
the body.

Commonly
used to treat
pruritus in
patients with
ESRD.

CONTRAINDICATION

Hypersensitivity,
glaucoma,

SIDE
EFFECTS
Dry mouth,
drowsiness,
nausea,
hypotensio
n.

INTERVENTIONS
Assess patients
alertness.
Instruct patient not
to drink alcohol.
Instruct patient to
increase fluid
intake.

ASSESSMENT

DIAGNOSIS

Objective data:

Crea:
32mg/dL
BUN:
57mg/dL
Oliguria
peripheral
edema
(grade 1)
Distended
abdomen
Puffy face
(+)crackles
in the lungs

BP: 160-180/
100-110mmHg
PR: 86bpm
RR: 21bpm
T: 36.4oC

Altered
renal tissue
perfusion
r/t glomerular
malfunction
AEB
increased
serum
creatinine
and BUN.

PLANNING

Short Term: After 4

hours of nursepatient
interaction, the
patient will
demonstrate
participation in his
recommended
treatment
program.

Long Term: After 3

days of rendering
nursing
interventions, the
patient will
establish behavior/
lifestyle
changesto
prevent
complications.

INTERVENTIONS

Note patients sensorium status and review

lab. results such as BUN and creatinine
levels. Increased serum creatinine can alter
patients sensorium.

Monitor VS especially BP, ascertain patients

usual range.

Observe for dependent generalized edema

to note renal impairment degree.

Instruct pt. to measure urine output on a

regular schedule and weigh daily to assess
renal perfusion and function.

Encourage patient to verbalize concerns

regarding his condition to decrease anxiety
and correct his wrong ideas about condition.

Instruct pt. to restrict sodium, fat, and

protein in diet as ordered. Protein increases
BUN level.

Administer medications as prescribed.

ASSESSMENT

PLANNING

DIAGNOSIS

Subjective data:
Usahay rako
makaihi nya
ginagmay ra
usahay mu tulo ra
gyud. Pag mukaon
ko ug parat
manghupong
dayon akong tiil.

Fluid volume
excess r/t
decreased
glomerular
filtration rate
and sodium
retention
secondary to
renal failure
AEB peripheral
edema,
distended
abdomen,
puffy cheeks,
oliguria,
presence of
crackles in the
lungs,
increased
serum
creatinine and
BUN.

Short Term

After 8 hours
ofnursing
interventions, the
patient will
demonstrate
behaviors to monitor
fluid status and
reduce recurrence
offluid excess.

Long Term

Within 3 days
ofnursing
interventions, the
patient will manifest
and maintain ideal
body weight without
excess fluid AEB
balanced I & O,
stable weight, and
free from signs of
edema.

Objective data:
Presence of
peripheral
edema (grade
1)

Distended
abdomen

Puffy face

Oliguria

(+)crackles in
the lungs

Crea: 32mg/dL

BUN: 57mg/dL

BP: 160-180/
100-110mmHg
PR: 86bpm
RR: 21bpm
T: 36.4oC

INTERVENTIONS

Monitor

and

monitoring

record

vital

signs

for

changes

and

evaluating

interventions.
-

Instruct patient to restrict sodium and

fluid to prescribed volume to lessen fluid
retention and overload.

Note amount/rate offluid intake from all

sources to monitor intake and output and
to avoid fluid overload.

Instruct patient to weigh self daily and

compare to previous weight to monitor
fluid retention.

Auscultate breath sounds for presence of

pulmonary congestion.

Note presence of edema and its grade.

Measure abdominal girth for changes.

Review lab. data like BUN, Creatinine,

serum
function

electrolytes
and

to

to

monitor

assess

for

kidney
fluid

electrolytes imbalance.

Administer diuretics as ordered by the

physician to promote diuresis.

Collaborate to a dietitian in making a diet

plan for the type of diet suited for the

ASSESSMENT
Objective data:

DIAGNOSIS

Impaired skin
peripheral
integrity r/t
edema
edema and
(grade 1)
pruritus AEB
Distended
peripheral
abdomen
edema,
Puffy face
distended
Frequent
scratching of abdomen,
frequent
the arms.
scratching on the
arms, puffy face.

PLANNING

Short Term: After 4

hours of nurse-patient
interaction, the patient
will establish behaviors
to prevent skin
damage.

Long Term: The patient

will maintain intact
skin.

INTERVENTIONS

Inspect patients skin for changes in

color, turgor, vascularity.

Assess patients peripheral edema,

elevate legs to promotes venous
return, limiting edema formation.

Provide soothing skin care to

patient, applying ointment or cream
to relieve dry and cracked skin.

Keep bed/chair linen dry and

wrinkle-free to reduce skin irritation.

Recommend patient to use cool,

moist compresses to apply pressure
rather than scratch pruritic areas to
prevent skin injury.

Instruct patient to keep fingernails

short.

ASSESSMENT

DIAGNOSIS

Deficient
Subjective data:
knowledge r/t
Mukaon gihapon information
kog mga parat
misinterpretatio
kay nag dialysis
n about dialysis
na bitaw ko para therapy.
ma puslan unya
mao ra gihapon
mamatay raman
gihapon. as
verbalized by the
patient.

PLANNING

INTERVENTIONS

Short Term

Within 4 hours ofnursing

interventions, the
patient will verbalize
understanding of
condition and potential
complications.

Long Term

The patient will initiate

necessary lifestyle
changes.

Review disease process and prognosis

and future expectations. This provides
knowledge base from which patient
can make informed choices.
Review patients diet and fluid
restriction as prescribed and explain to
the patient the advantage of eating
the ordered diet.
Educate patient that hemodialysis
treatment does not mean he can eat
whatever he likes. The pt. does not
receive dialysis treatment daily so he
needs to be careful of what he eats to
prevent complication such as lifethreatening uremia.

Inform patient that eating the

restricted diet can further increase the
patients blood pressure, and can also
precipitate bone pains and edema.

DIAGNOSIS
Risk for Injury
r/t infection.

PLANNING

Within 4 hours ofnursing

interventions, the patient will
have patent vascular access
and be free of infection.

INTERVENTIONS

Monitor internal AV shunt patency at frequent

intervals. Palpate skin around shunt for warmth.
Diminished blood flow results in coolness of
shunt.

Palpate for distal thrill. Thrill is caused by

turbulence of high-pressure arterial blood flow
entering low-pressure venous system and should
be palpable above venous exit site.

Note color of blood and/or obvious separation of

cells and serum. Change of color from uniform
medium red to dark purplish red suggests
sluggish blood flow and/or early clotting.
Separation in tubing is indicative of clotting. Very
dark reddish-black blood next to clear yellow fluid
indicates full clot formation.

Avoid trauma to shunt by handling tubing gently,

maintaining cannula alignment. Not taking BP or
drawing blood samples in shunt extremity. To
decrease risk of clotting or disconnection.

Instruct patient not to sleep on side with shunt or

carry packages, books, purse on affected
extremity.

Administer low-dose of Heparin if indicated to

ASSESSMENT

DIAGNOSIS
Risk for
Objective:
Ineffective

protection r/t
>fatigue
abnormal blood
>pale mucous
profile 2o
membranes
>pallor general suppressed
appearance
erythropoietin

production.
RBC: 2.4
Hgb: 6.9
Hct: 23.3%

PLANNING

INTERVENTIONS

Long Term

Within a month, the

patient will be able to
establish normal lab.
values and
demonstrate
improvement in normal
laboratory values.
-

Note reports of increasing fatigue, weakness

of the patient. Observe for tachycardia,
pallor of skin and mucous membranes,
dyspnea, and chest pain.
Monitor level of consciousness and behavior.
Anemia may cause cerebral hypoxia
manifested by changes in mentation, and
behavioral responses.
Evaluate response to activity, ability to
perform tasks. Assist as needed and
develop schedule for rest.

Instruct patient to take his iron supplements

as prescribed.

Limit vascular sampling, combine laboratory

tests when possible. Recurrent or excessive
blood sampling can worsen anemia.

RBCs, Hb and Hct. Uremia (elevated

ammonia, urea, other toxins) decreases
production of erythropoietin and depresses
RBC production and survival time. In CRF,
Hb and Hct are usually low but tolerated;
(patient may not be symptomatic until Hb is
below 7).

Administer PRBC and Erythropoietin as

ordered. This corrects many of the
symptoms of CRF resulting from anemia.

DISCHARGE PLAN

Instruct patient to strictly take medicines as directed

and to make a list of the medicines, vitamins, and
herbs that the patient is taking, including the amounts,
when and why the patient take them. Instruct also the
patient to bring the list to follow-up visits. Medicine list
should be carry by the patient in case of an emergency.
Instruct patient to weigh self daily, following the goal
weight ordered by his physician.
Involve and assist patient in making his exercise plan
as directed. Regular exercise can help the patient
manage high blood pressure.
Strongly advise patient to quit smoking and avoid
drinking alcohol.
Advice patient to avoid stress related factors and have
adequate rest.

Teach the patient to properly care his AVF or AVG by

following these steps:

Clean the skin over the fistula or graft every day with soap and
water.
Take the bandage off the fistula or graft 4 to 6 hours after dialysis.
Check the fistula or graft every day for good blood flow by
touching it with fingertips. The buzzing sensation means that it is
working.
Check for bleeding, pain, redness, or swelling. These may be signs
of infection or a clogged fistula or graft.
To prevent damage to the fistula or graft, no one should take
blood pressure or draw blood from the armwith the fistula or
graft.
Should not wear tight-fitting shirts, jewelry (such as bracelets)
that may restrict blood flow on the access arm.
making sure the straps or handles dont tighten around the fistula
when carrying things (groceries, bags, luggage),
Making sure that the patients body, pillow or cushion doesnt rest
on the arm with fistula when sitting or sleeping,

Instruct patient to ask his doctor if he need

vaccines.Infections
such
as
pneumonia,
influenza, and hepatitis can be more harmful
or more likely to occur when a person have
CKD. Vaccines reduce the risk of infection with
these viruses.
Instruct patient to follow up check-up regularly
with his physician as directed.
Instruct patient to eat foods directed by his
doctor. His doctor may advise him to eat food
low in sodium, potassium, phosphorus, or
protein. The patient may need to see a
dietitian if he needs help planning meals.

Instruct patient to discuss with his

physician regarding how much fluid he
has to drink every day and what fluids
the patient can and cannot drink.
Encourage patient to suck on hard candy
or chew gum to help keep mouth moist
without having to drink liquids.
Instruct patient to seek medical attention
immediately if the skin around the fistula
or graft is painful, hot, red, or swollen.

REALIZATION

High blood pressure can affect the kidneys and can

cause renal damage.
End-Stage Renal Disease brings many complications
to the body that causes the patient to suffer.
Renal disease is a progressive disease and is
asymptomatic at first; renal failure can be prevented
thru regular check-up and early intervention.
Having an ESRD is costly, hassle, and boring; you
have to spend money and 4-5hr. of your time per
dialysis session for the rest of your life. You have to
make changes such as modifying your lifestyle and
diet to avoid complications.
You will have an altered body image.