I.

INTRODUCTION

a. brief discussion of the disease

The kidneys are located retroperitoneal, in the posterior aspect of the
abdomen, on either side of the vertebral column. They lie between the twelfth
thoracic and the third lumbar vertebrae. The left kidney is usually positioned
slightly higher than the right because of the position of the liver.
The kidneys balance the urinary excretion of substances against the
accumulation within the body through ingestion or production. Consequently,
they are a major controller of fluid and electrolyte homeostasis. The kidneys also
have several non-excretory metabolic and endocrine functions, including blood
pressure regulation, erythropoietin production, insulin degradation, prostaglandin
synthesis, and vitamin D metabolism.
Chronic kidney disease (CKD), also known as chronic renal disease, is a
progressive loss of renal function over a period of months or years. The
symptoms of worsening kidney function are unspecific, and might include feeling
generally unwell and experiencing a reduced appetite. Often, chronic kidney
disease is diagnosed as a result of screening of people known to be at risk of
kidney problems, such as those with high blood pressure or diabetes and those
with a blood relative with chronic kidney disease. Chronic kidney disease may
also be identified when it leads to one of its recognized complications, such as
cardiovascular disease, anemia or pericarditis. Creatinine levels may be normal
in the early stages of CKD, and the condition is discovered if urinalysis (testing of
a urine sample) shows that the kidney is allowing the loss of protein or red blood
cells into the urine. CKD is initially without specific symptoms and can only be
detected as an increase in serum creatinine or protein in the urine.
 As the kidney function decreases blood pressure is increased due to fluid
overload and production of vasoactive hormones, Erythropoietin synthesis is
decreased (potentially leading to anemia, which causes fatigue). People with
chronic kidney disease suffer from accelerated atherosclerosis and are more
likely to develop cardiovascular disease than the general population. Urinary tract
infection (UTI) is a bacterial infection that affects any part of the urinary tract. The
main etiologic agent is Escherichia coli. Although urine contains a variety of
fluids, salts, and waste products, it does not usually have bacteria in it. [1] When
bacteria gets into the bladder or kidney and multiply in the urine, they may cause
an UTI. Symptoms include frequent feeling and/or need to urinate, pain during
urination, and cloudy urine.[3]
The most common symptoms of a bladder infection are burning with urination
(dysuria), frequency of urination, an urge to urinate. Nephropathy refers to
damage to or disease of the kidney. An older term for this is nephrosis.
b. Reasons for choosing the case
As student nurses, we chose CKD as our case because we want to

have an in depth understanding of the disease in order to improve our

knowledge as a basis of health teachings to our future patient having

the same illness. Also, we have chosen this study because we want to

provide more information about this disease since there are a lot of things left

unexplained about it. Through this, we will make people aware of the

complications and other underlying disease condition that may occur if

left untreated.
c. Statistics

Mean level of GFR by age group:

Philippine vs. US data.

Age Group NNHeS 2003 NHANES III

in Years Philippines U.S.A.

20-29 119 116

30-39 109 107

40-49 103 99

50-59 100 93

60-69 86 85

70+ 77 75

The population of Filipinos aged 20 years and above in 2005 was 46,627,172
A prevalence of 2.6% means that 1,212,306 adult Filipinos have CKD.

Morbidity
• Number of noninstitutionalized adults with diagnosed kidney
disease: 3.7 million
• Percent of noninstitutionalized adults with diagnosed kidney
disease: 1.7%
Mortality

• Number of deaths from nephritis, nephrotic syndrome, and

nephrosis: 45,344

• Deaths per 100,000 population: 15.1

• Cause of death rank: 9

d. Nurse-Centered Objectives
1. To gather enough data and information upon assessment.

2. To understand chronic kidney disease, its causes and

pathophysiology.

3. To familiarize with the possible complications, signs and

symptoms of the problem

4. To design a plan of care for patient with CKD.

5. To have a thorough understanding of the case of the patient,

the medical management and the necessary health teachings
to the patient

6. To be able to formulate those data into nursing diagnosis that

may aid in the patient’s current conditions.

7. To be able to set priorities and goal outcomes in collaboration

with the patient.

I. Nursing History

1. Personal History

• Demographic Data

Purple, 65 years of age, was born on April 13, 1945 in a government hospital, a
Roman Catholic, and a natural born Filipino citizen. Her husband Blue died at the age
of 65 years old because of vehicular accident. She is currently residing at Angeles
City. She has 4 children, namely Black (eldest), Yellow, (25 years old), Green (20
years old) and Red (19 years old). However, her eldest son Black died at the age of 27
years old due to lung collapse. Purple was brought in one of the private hospitals in
Angeles City last July 6, 2010 with a diagnosis of Chronic Kidney disease secondary to
urinary tract infection and non-obstructive nephropathy.

• Socio-economic and Cultural Factors

 Purple manages their sari-sari store. According to her, she earns an average of
P 7, 000 a month. Her daughter Yellow works as a call center agent and earns P10,
000. On the other hand, her son Green works as a computer technician in one of the
companies at Clark. He earns at around P8, 000 on a monthly basis. Her youngest
daughter is unemployed. Most of the income is allotted for food and monthly bills.
When it comes to dietary habits, the patient is fond of eating spicy foods, and junk
foods, and sweets. She is also fond of drinking sodas. Purple had been smoking for 20
years. She consumes an average of 2 sticks a day.
Purple does not believe on “herbularyos” and faith healers. She buys
over-the-counter drugs if a family member catches colds, cough or fever. When any of
the family members get seriously sick, she consults the doctor.
 2. Family-Health Illness History
Schematic diagram
Grey White
HPN, DM RF, ARTH

Violet Indigo Purple Magenta Lavender

ARTH, RF DM, HPN ARTH, HPN, DM, HPN DM, RF
CKD 2˚ UTI

Legends:
= female

= male

= deceased

DM = diabetes

RF = renal failure

ARTH = arthritis

UTI = urinary tract infection

CKD = chronic kidney disease

Purple’s father, Grey, had hypertension and diabetes. He died at the age of 70.
Her mother, White, had arthritis and died at an age of 55 years old because of renal
failure.
 Purple’s eldest sister, Violet, had arthritis and died at the age of 40 due to
renal failure. Indigo has diabetes and hypertension. Magenta, like her brother Indigo,
has diabetes and hypertension. The youngest among the 5 siblings, Lavender, had
diabetes and died at an age of 32 years old due to renal failure.
History of past illness
According to Purple, during the first month of June 2010, she
experienced urgency to urinate accompanied by flank pain, burning sensation
on urination and fever. She also experienced joint pains wherein she sometimes
finds difficulty to walk and perform activities of daily living such as doing
household chores. She did not consulted the physician immediately because she
thought that it is just normal because of old age, and that her difficulty in
urinating is only brought about menopause. She took paracetamol to relieve
fever, and drank "buko juice" to releive the burning sensation during
micturation. Her daughter adviced her to drink 8 glass of water everyday, but
Purple said she can only consume an average of 4 glasses a day. After 5 days,
her fever has subsided, however, she still experience pain when voiding. Also,
despite of her feeling that her bladder is full, she only voids little amount of
urine. In addition, she said that her urine is dark yellow in color. On June 8,she
consulted the doctor. She had her urine and blood tested. The physician told
her that her urine has pus, RBCs and protein. She was then diagnosed of having
UTI. The physician prescribed her antibiotics and adviced her to return after a
week for follow-up check up.
History of Present Illness
On June 13, 2010, Purple said that she still experiences pain when
urinating. She felt weak. Her daughter noticed that she appears pale so she
brought her to the hospital. Her vital signs were taken and results revealed a
blood pressure of 140/90 mmHg and her temperature was 38.5C. Purple said
that she could not believe it since her usual blood pressure is 120/80mmHg.
Urinalysis, stool exam and CBC was done. She was then admitted with a
diagnosis of Chronic Kidney Disease, UTI, non-obstructive nephropathy. On
June 15, foley catheter was inserted and her fever subsided. She was
discharged on June 17, 2010 and was advised to return after a month to
remove the foley catheter. According to her, the catheter was changed every 2
weeks.
Purple went back on July 11, 2010. She still feels weak and her daughter
said she looks a bit pale. Her urine is yellow in color, but somewhat appears
lighter than her previous urine. She was then admitted for monitoring and
follow-up care. She was discharged on July 15, 2010.

III. PHYSICAL ASSESSMENT

Physical Examination (IPPA- Cephalocaudal Approach)

Upon admission (July 11, 2010): Lifted from the chart.

Vital Signs:

T: 37.7 °C

PR: 92 bpm

RR: 22 cpm

1st Nurse-Patient Interaction

July 14, 2010

Received lying on bed awake and coherent with Vital Signs of:

T: 37.5° C

PR: 86 bpm

RR: 17 cpm

Integumentary

 Skin warm to touch

 pallor
 thin brittle nails
 coarse thinning hair

Skull
  Generally round

 absence of nodule

 No tenderness noted upon palpation

Scalp

 No scars noted

 No lesions noted

 No tenderness or masses upon palpation.

Hair

 Hair is black in color

 Evenly distributed covers the whole scalp

 With dry coarse short hair

Face

 Face is oval in shape

 with symmetrical facial structures

Eyes

 Evenly placed and in line with each other

 Non-protruding

Ears
  The ear lobes are bean shaped, parallel, and symmetrical auricle

is higher that the outer cantus of the eye, mobile, firm and

tender

 Skin is same in color as in the complexion

 No lesions noted on inspection

Nose

 No Discharges

 No nasal flaring noted

 Both nares are patent

 No tenderness and no lesions

Mouth

 Lips are dark, dry with no lesions

 With brownish gums

 With yellowish discolored teeth

Neck

 No palpable and visible mass or lumps

 No palpable lymph nodes

Abdomen

 Skin color is uniform, no lesions

 rounded and symmetrical with no masses

Urinary

 urine is light yellow in color

 190ml in a 8hr shift

Extremities

 Trimmed fingernails and toenails with no clubbing on both hands

and feet

 Nail beds are pink and with capillary refill of 2 seconds

 No involuntary movements

 Edema noted on left upper extremity and bipedal edema

July 15, 2010

Received lying on bed awake and coherent with Vital Signs of:

T: 36.9° C
 PR: 91 bpm

RR: 21 cpm

Integumentary

 Skin warm to touch

 thin brittle nails
 coarse thinning hair

Skull

 Generally round

 absence of nodule

 No tenderness noted upon palpation

Scalp

 No scars noted

 No lesions noted

 No tenderness or masses upon palpation.

Hair

 Hair is black in color

 Evenly distributed covers the whole scalp

 With dry coarse short hair

Face
  Face is oval in shape

 with symmetrical facial structures

Eyes

 Evenly placed and in line with each other

 Non-protruding

Ears

 The ear lobes are bean shaped, parallel, and symmetrical auricle

is higher that the outer cantus of the eye, mobile, firm and

tender

 Skin is same in color as in the complexion

 No lesions noted on inspection

Nose

 No Discharges

 No nasal flaring noted

 Both nares are patent

 No tenderness and no lesions

Mouth

 Lips are dark, dry with no lesions

  With brownish gums

 With yellowish discolored teeth

Neck

 No palpable and visible mass or lumps

 No palpable lymph nodes

Abdomen

 Skin color is uniform, no lesions

 rounded and symmetrical with no masses

Extremities

 Trimmed fingernails and toenails with no clubbing on both hands

and feet

 Nail beds are pink and with capillary refill of 2 seconds

 No involuntary movements

 Edema noted on left upper extremity and bipedal edema

 II. Diagnostic And Laboratory Procedures

DATE NORMAL
ORDERED/ VALUES
ANALYSIS AND
DIAGNOSTIC/LABORATORY DATE (UNITS
INDICATION/PURPOSE RESULTS INTERPRETATION
PROCEDURE RESULTS USED IN
RESULTS
WERE THE
RELEASED HOSPITAL)
Hematology

Hemoglobin To determine the amount D.O.: 9.3 d/dl 11.6 - 15.5 The hemoglobin that
of oxygen carried by June 8, 2010 g/dl is present in the
RBC’s. D.R: blood is slightly
June 8, 2010 lower than the
normal level. This
indicates disruption
in the production of
erythropoietin in the
body, a special cells
in the kidney that
monitor the oxygen
concentration in
blood resulting from
chronic kidney
disease.
Hematocrit To measure the D.O.: 27.9 % 36.47% The level of
concentration of RBC June 8, 2010 hematocrit is lower
within the blood volume D.R: than the normal
 and evaluate hydation June 8, 2010 level. Thus,
status. It also indicates indicating lower
presence of anemia which RBC concentration
is one of the common in the blood due to
complication of chronic decreased ability of
kidney disease. the kidneys to
produce
erythropoietin, a
hormone that
stimulates the
production of RBC.
Red Blood Cells To determine amount of D.O.: 3.0 x 1012/L 4.2 – 5.4/L The level of RBC is
Red blood cells, the blood June 8, 2010 lower than the
cell that carries oxygen. D.R: normal level. This
June 8, 2010 indicates decreased
erythropoietin
production which
stimulates the bone
marrow to produce
RBC due to chronic
kidney disease.
White Blood Cells To determine the D.O.: 11.08 x 4.8 – 10.8 x The level of WBC is
presence of infection. It June 8, 2010 109/liter 109/liter higher than the
was also use to monitor D.R: normal level, this
the body’s response to June 8, 2010 might be due to
treatment and monitor Increased levels of
bone marrow function uremic toxins
and immune response. resulting from CKD
that could impaired
the immune and
inflammatory
 response causing
infection.
Neutrophils To determine the D.O.: 91 40 – 74 The level of
neutrophils, a June 8, 2010 neutrophils is higher
polymorphonuclear D.R: than the normal
leukocytes that help the June 8, 2010 level. Thus,
body fight infections and indicating presence
other diseases. of infection in the
body due to the
presence of uremia
in the blood.
Lymphocytes This measured to D.O.: 4.9 19 - 48 The lymphocyte
determine if there’s a June 8, 2010 level in the blood is
lowered immune status in D.R: lower than the
the patient. June 8, 2010 normal level. This
indicates lowered
immune status of the
patient.
A. HEMATOLOGY

Nursing Responsibilities

BEFORE:

 Check the doctor’s order.

 Identify the patient.

 Inform the patient and/or SO before doing the procedure and adequately explain the importance and
purpose of doing such procedure.

 Inform that there is no food/fluid restriction before the test.

 Inform that the test requires blood sample and that she may experience transient discomfort from
needle puncture.

DURING:
 Adhere to standard precautions which include:

• Applying sterile technique.

• Make sure to have patient’s pertinent information in the container.

AFTER:
 Apply direct pressure on the venipuncture site.

 Send the specimen immediately to the laboratory and fill-out laboratory forms properly and adequately.
  Chart all procedures done.

B. URINALYSIS

Nursing Responsibilities

BEFORE:

 Explain to the patient what test to be done, it’s purpose and how it is done.

 Inform the patient that the test require a urine specimen.

 Instruct the patient how is the proper way to collect urine specimen.

 Provide a clear container for the specimen.

DURING:
 Adhere to standard precautions which include:
 • Applying sterile technique.

• Collect the specimen properly.

AFTER:
 Label properly together with the laboratory slip.

 Send the specimen to the laboratory.

 Chart time of collection and attach results to chart as soon as they are available.
 DATE NORMAL
ORDERED/ VALUES
ANALYSIS AND
DIAGNOSTIC/LABORATORY DATE (UNITS
INDICATION/PURPOSE RESULTS INTERPRETATION
PROCEDURE RESULTS USED IN
RESULTS
WERE THE
RELEASED HOSPITAL)
Hematology

Hemoglobin To determine the amount D.O.: 11.1 d/dl 11.6 - 15.5 The hemoglobin that
of oxygen carried by June 13, 2010 g/dl is present in the
RBC’s. D.R: blood is slightly
June 13, 2010 lower than the
normal level. This
indicates disruption
in the production of
erythropoietin in the
body, a special cells
in the kidney that
monitor the oxygen
concentration in
blood resulting from
chronic kidney
disease.
Hematocrit To measure the D.O.: 33.9 % 36.47% The level of
concentration of RBC June13, 2010 hematocrit is lower
within the blood volume D.R: than the normal
and evaluate hydation June 13, 2010 level. Thus,
status. It also indicates indicating lower
presence of anemia which RBC concentration
is one of the common in the blood due to
complication of chronic decreased ability of
 kidney disease. the kidneys to
produce
erythropoietin, a
hormone that
stimulates the
production of RBC.
Red Blood Cells To determine amount of D.O.: 3.0 x 1012/L 4.2 – 5.4/L The level of RBC is
Red blood cells, the blood June 13, 2010 lower than the
cell that carries oxygen. D.R: normal level. This
June 13, 2010 indicates decreased
erythropoietin
production which
stimulates the bone
marrow to produce
RBC due to chronic
kidney disease.
White Blood Cells To determine the D.O.: 11.08 x 4.8 – 10.8 x The level of WBC is
presence of infection. It June 13, 2010 109/liter 109/liter higher than the
was also use to monitor D.R: normal level, this
the body’s response to June 13, 2010 might be due to
treatment and monitor Increased levels of
bone marrow function uremic toxins
and immune response. resulting from CKD
that could impaired
the immune and
inflammatory
response causing
infection.
Neutrophils To determine the D.O.: 91 40 – 74 The level of
neutrophils, a June 13, 2010 neutrophils is higher
polymorphonuclear D.R: than the normal
 leukocytes that help the June 13, 2010 level. Thus,
body fight infections and indicating presence
other diseases. of infection in the
body due to the
presence of uremia
in the blood.
Lymphocytes This measured to D.O.: 4.9 19 - 48 The lymphocyte
determine if there’s a June 13, 2010 level in the blood is
lowered immune status in D.R: lower than the
the patient. June 13, 2010 normal level. This
indicates lowered
immune status of the
patient.
 DATE NORMAL
ORDERED/ VALUES
ANALYSIS AND
DIAGNOSTIC/LABORATORY DATE (UNITS
INDICATION/PURPOSE RESULTS INTERPRETATION
PROCEDURE RESULTS USED IN
RESULTS
WERE THE
RELEASED HOSPITAL)
Hematology

Hemoglobin To determine the amount D.O.: 9.3 d/dl 11.6 - 15.5 The hemoglobin that
of oxygen carried by June 13, 2010 g/dl is present in the
RBC’s. D.R: blood is slightly
June 13, 2010 lower than the
normal level. This
indicates disruption
in the production of
erythropoietin in the
body, a special cells
in the kidney that
monitor the oxygen
concentration in
blood resulting from
chronic kidney
disease.
Hematocrit To measure the D.O.: 27.9 % 36.47% The level of
concentration of RBC June 13, 2010 hematocrit is lower
within the blood volume D.R: than the normal
and evaluate hydation June 13, 2010 level. Thus,
status. It also indicates indicating lower
presence of anemia which RBC concentration
is one of the common in the blood due to
 complication of chronic decreased ability of
kidney disease. the kidneys to
produce
erythropoietin,a
hormone that
stimulates the
production of RBC.
Red Blood Cells To determine amount of D.O.: 3.0 x 1012/L 4.2 – 5.4/L The level of RBC is
Red blood cells, the blood June 13, 2010 lower than the
cell that carries oxygen. D.R: normal level. This
June 13, 2010 indicates decreased
erythropoietin
production which
stimulates the bone
marrow to produce
RBC due to chronic
kidney disease.
White Blood Cells To determine the D.O.: 11.08 x 4.8 – 10.8 x The level of WBC is
presence of infection. It June 13, 2010 109/liter 109/liter higher than the
was also use to monitor D.R: normal level, this
the body’s response to June 13, 2010 might be due to
treatment and monitor Increased levels of
bone marrow function uremic toxins
and immune response. resulting from CKD
that could impaired
the immune and
inflammatory
response causing
infection.
Neutrophils To determine the D.O.: 91 40 – 74 The level of
neutrophils,a June 13, 2010 neutrophils is higher
 polymorphonuclear D.R: than the normal
leukocytes that help the June 13, 2010 level. Thus,
body fight infections and indicating presence
other diseases. of infection in the
body due to the
presence of uremia
in the blood.
Lymphocytes This measured to D.O.: 4.9 19 - 48 The lymphocyte
determine if there’s a June 13, 2010 level in the blood is
lowered immune status in D.R: lower than the
the patient. June 13, 2010 normal level. This
indicates lowered
immune status of the
patient.
 DATE NORMAL
ORDERED/ VALUES
ANALYSIS AND
DIAGNOSTIC/LABORATORY DATE (UNITS
INDICATION/PURPOSE RESULTS INTERPRETATION
PROCEDURE RESULTS USED IN
RESULTS
WERE THE
RELEASED HOSPITAL)
Urinalysis This is used as a D.O.: Color: dark the presence of pus
screening and/or June 13, 2010 yellow cells is due to
diagnostic tool which can D.R: Slightly infection brought
help detect if the patient June 13, 2010 turbid about by the
is experiencing any Pus cells: 10- 0-5 HPF invasion of
genitourinary problems 13 HPF microorganism on
like UTI or detect if Red cells : 1- absent the urinary tract.
patient has DM or co- 2 HPF
morbid conditions whic Presence of RBC is
affect in the client’s CRCL: brought about
treatment and diganosis. 65ml/min 87-107ml/min impaired glomerular
function secondary
Protein: 0.8 mg/dl to tubular necrosis
11 mg/dL leading to scarring of
nephrons.

Proteinuria results
from the impaired
function of the
glomerulus, wherein
protein is excreted in
the urine.

Low creatinine
clearance results
from decrease in
GFR.
 DATE
NORMAL
ORDERED/
VALUES ANALYSIS AND
DIAGNOSTIC/LABORATORY DATE
INDICATION/PURPOSE RESULTS (UNITS USED INTERPRETATION
PROCEDURE RESULTS
IN THE RESULTS
WERE
HOSPITAL)
RELEASED
Creatinine Use to measure GFR. D.O.: 18.3 mg/dl 0.5-7 mg/dl The result is above
To measure kidney June 13, the normal limit.
function. 2010 An increase in the
D.R: level of Creatinine
June 13, indicates impaired
2010 kidney function to
excrete excessive
creatinine
therefore, it
accumulates on
the blood.
BUN Measures the renal D.O.: 100 mg/dl 10-20mg/dl An increase in
excretion of urea June 13, level of BUN
nitrogen, which is a by- 2010 signifies that the
product of protein D.R: kidney is unable to
metabolism. It June 13, excrete waste
indicates extent of 2010 product from
renal clearance of this metabolism due to
nitrogenous waste impaired
product. glomerular
function.
K D.O.: 7mmol/L 3.5-5mmol/L Hyperkalemia
June 13, results from
2010 decrease
D.R: glomerular
June 13, filtration rate
2010 wherein excess
potassium is not
excreted in the
urine.
ABG
6/14/10
Results Normal Values
pH 7.367 7.35-7.45
pCO2 16.7 35-45mmHg
pO2 101.01 80-100 mmHg
HCO3 9.4 22-26mEq/L

ABG Impression: Metabolic acidosis

X-Ray 6/14/10
-No abnormal densities seen in the parenchyma of both lungs. Heart enlarged. Aorta is calcified;
Impression: Cardiomegaly
UTZ 6/14/10
Kidneys and urinary bladder- both kidneys are small in sizes exhibiting diffuse increased parenchyma echogenecity. The
consticomedullary differentiation. Both kidneys are well distinct. The renal parenchyma thickness are within normal limits. No solid
mass aptic lesion or calculus noted.
The right kidney measures about 8.2x3.1x3.2 cm with cortical thickness of 1.5cm while the left kidney measures about 7.6x2.8x3.2cm
with cortical thickness of 1cm.
The urinary bladder is well distended with smooth mucosal lining. Intraluminal mass or calculus seen. The wall is not thickened. Post
void volume is 1046ml. The patient hard urinated 64 the ultrasound study.
Impression:
-Small sized kidney with diffuse parenchymal disease; bilateral.
-Mild hydronephrosis, Right kidney, urinary retention.
V. Anatomy and Physiology

The Kidney

The urinary system functions to

create urine, store it, and carry it
out of the body. It is made up of
two kidneys, two ureters, the
bladder, two sphincter muscles,
and the urethra. Illustration
adapted from drawing of kidney
from the Nat'l Istitute of
Diabetes and Digestive and
Kidney Diseas, National Institute
of Health

The kidneys are bean-shaped

organs, each about the size of
your fist. They are located near the middle of your back, just below the rib cage.

Kidneys remove wastes and extra water from the blood to form urine. About 2 quarts of
urine is made each day from filtering about 200 quarts of blood through the kidneys. If
your kidneys did not remove these wastes, the wastes would build up in the blood and
you would eventually die. Some people have serious health problems if they have less
than 25 percent of their renal function. If renal function drops below 10 to 15 percent, a
person cannot live long without some form of
renal replacement therapy—either dialysis or
transplantation.Urine flows from the kidneys,
through the ureters, and empties into the
bladder. The urethral sphinctor (a valve that
seals off the bladder outlet through the
urethra) remains closed, during this time,
allowing the bladder to fill.

The urinary bladder is composed of smooth

muscle which is normally relaxed at rest.

The bladder first signals an urge to empty

when it is about half full.
Urination normally begins voluntarily, by muscle contraction, pushing the urine out of
the bladder, causing the sphinctor to open. Once urination begins, the urine flows from
the bladder, past the now open urethral spinctor, and out of the body through the urethra.

Cardiovascular System Anatomy & Physiology

The heart is the pump responsible for maintaining adequate circulation of

oxygenated blood around the vascular network of the body. It is a four-chamber pump,
with the right side receiving deoxygenated blood from the body at low presure and
pumping it to the lungs (the pulmonary circulation) and the left side receiving oxygenated
blood from the lungs and pumping it at high pressure around the body (the systemic
circulation).

The myocardium (cardiac muscle) is a specialised form of muscle, consisting of

individual cells joined by electrical connections. The contraction of each cell is produced
by a rise in intracellular calcium concentration leading to spontaneous depolarisation, and
as each cell is electrically connected to its neighbour, contraction of one cell leads to a
wave of depolarisation and contraction across the myocardium.

This depolarisation and contraction of the heart is controlled by a specialised

group of cells localised in the sino-atrial node in the right atrium- the pacemaker cells.

1. These cells generate a rhythmical depolarisation, which then

spreads out over the atria to the atrio-ventricular node.
2. The atria then contract, pushing blood into the ventricles.
3. The electrical conduction passes via the Atrio-ventricular
node to the bundle of His, which divides into right and left
branches and then spreads out from the base of the ventricles
across the myocardium.
4. This leads to a 'bottom-up' contraction of the ventricles, forcing
blood up and out into the pulmonary artery (right) and aorta
(left).

5. The atria then re-fill as the myocardium relaxes.

The 'squeeze' is called systole and normally lasts for about 250ms. The relaxation
period, when the atria and ventricles re-fill, is called diastole; the time given for diastole
depends on the heart rate.
 The ECG

The Electrocardiograph (ECG) is clinically very useful, as it shows the electrical

activity within the heart, simply by placing electrodes at various points on the body
surface. This enables clinicians to determine the state of the conducting system and of the
myocardium itself, as damage to the myocardium alters the way the impulses travel
through it.

When looking at an ECG, it is often helpful to remember that an upward

deflection on the ECG represents depolarisation moving towards the viewing electrode,
and a downward deflection represents depolarisation moving away from the viewing
electrode. Below is a normal lead II ECG.

• The P wave represents atrial depolarisation- there is

little muscle in the atrium so the deflection is small.
• The Q wave represents depolarisation at the bundle of
His; again, this is small as there is little muscle there.
• The R wave represents the main spread of
depolarisation, from the inside out, through the base of
the ventricles. This involves large ammounts of
muscle so the deflection is large.
• The S wave shows the subsequent depolarisation of
the rest of the ventricles upwards from the base of the
ventricles.

• The T wave represents repolarisation of the

myocardium after systole is complete. This is a
relatively slow process- hence the smooth curved
deflection.

The Coronary Circulation

 The heart needs its own reliable blood supply in order to keep beating- the
coronary circulation. There are two main coronary arteries, the left and right coronary
arteries, and these branch further to form several major branches (see image). The
coronary arteries lie in grooves (sulci) running over the surface of the myocardium,
covered over by the epicardium, and have many branches which terminate in arterioles
supplying the vast capillary network of the myocardium. Even though these vessels have
multiple anastomoses, significant obstruction to one or other of the main branches will
lead to ischaemia in the area supplied by that branch.
 Precipitating factors:
Allergies
Pathophysiology: CKD UTI non-obstructive nephropathy Diet
Book-based Hygiene
Sexual activity
Predisposing factors: Instrumentation
Gender Pregnancy
Age Rheumatic Heart Disease
Hereditary Frequent sore throat
Autoimmune disorders Obstruction
Neurogenic bladder Kidney/ urinary tract stones
Vesiculoureteral reflux
DM
DHN

Bacteria gains access to blood and Intestinal, exogenous or genito-

goes to the kidney through systemic urinary m.o goes to the kidney
circulation through ureters and bladder

Urinary freq.,
Bacteria triggers inflammatory response Cloudy urine

Edema and swelling Tubular cell Fever Infection

of involved tissues necrosis
Dysuria Increase WBC
anemia Fibrosis/scar tissue
Flank pain formation Produces antigen-
antibody complex
Weakness,
Nausea, pallor, Impaired tubular
vomiting reabsorption/secretion; Trapped in
dizziness glomerulus
Damage in glomeruli

Inflammatory
Decrease GFR damage which
impedes
glomerular fxn
 hyperkale oliguria
More urea is hematuria proteinuria mia Activation
absorbed; decrease of RAAS
excretion of uric
acid P and Ca
imbalance Edema
Na and water vasoconstriction
retention
Increase Deposition of
BUN, and uric acid on oliguria
Respiratory and
CREA level joints or soft cardiac Increase in
tissue (gouty manifestations blood pressure
arthritis)

Confusion, Cardiomegaly
difficulty due to LVH
concentrating,
seizure, coma
IV. THE PATIENT’S ILLNESS
SYNTHESIS OF THE DISEASE
Pyelonephritis is a Bacterial infection of the kidney. Pyelonephritis can be
acute (sudden) or chronic (slow, subtle, and stubborn). It is most often due to
the ascent of bacteria from the bladder up the ureters to infect the kidneys.

The symptoms of pyelonephritis include flank (side) pain, fever, shaking chills,
sometimes foul-smelling urine, urgency (to urinate), frequency (urinating), and
general malaise. Tenderness is elicited on gently tapping over the kidney with
a fist (percussion).

Glomerulonephritis is the term used to describe a group of diseases that

damage the part of the kidney that filters blood. When the kidney is damaged,
it cannot get rid of wastes and extra fluid in the body. If the illness continues,
the kidneys may stop working completely. Some other terms you may hear used
are nephritis and nephrotic syndrome. Glomerular diseases damage the
glomeruli, letting protein and sometimes red blood cells leak into the urine.
Sometimes a glomerular disease also interferes with the clearance of waste
products by the kidney, so they begin to build up in the blood. Furthermore,
loss of blood proteins like albumin in the urine can result in a fall in their level
in the bloodstream. In normal blood, albumin acts like a sponge, drawing extra
fluid from the body into the bloodstream, where it remains until the kidneys
remove it. But when albumin leaks into the urine, the blood loses its capacity
to absorb extra fluid from the body. Fluid can accumulate outside the
circulatory system in the face, hands, feet, or ankles and cause swelling.

Body Water Regulation

Fluid volume is altered when the kidney loses its ability to excrete water
because of damaged nephrons and the resultant decreased GFR. Other factors
that contribute to the development of fluid volume overload are proteinuria
and increased renin. Proteinuria occurs in response to damage of the glomeruli.
High blood pressure can cause sclerotic changes in the glomeruli with a
resultant loss of protein, especially albumin in the urine. This damage to the
kidneys from hypertension is also known as hypertensive nephrosclerosis and
may cause damage not only to the glomueruli but also to the arteriolar walls.
The loss of albumin in the urine contributes to fluid shifting from the
intravascular space to the interstitial space because of decreased oncotic
pressure. As a response to decreased GFR, aldosterone is released from the
adrenal cortex, causing the kidneys to reabsorb sodium and water. Fluid
retention in turn results in the development of respiratory and cardiovascular
clinical manifestations

Acid-Base Balance
Metabolic acidosis is associated with CKD because the tubules cannot excrete
hydrogen ions (H+), resulting in the use of bicarbonate (HCO3–) anions to
maintain acid-base balance. Two other buffering systems are in place that
assist in compensating for the acidosis. Hydrogen ions combine with ammonia
produced in the renal tubule cells to form ammonium, which combines with
chloride and is excreted in the urine. This mechanism helps to remove H+ while
generating HCO3–. However, because of impaired nephron function, excretion of
ammonium is decreased. The third mechanism involved with acid-base balance
results in H+ combining with phosphate (one of the body’s buffering systems).
Metabolic acidosis also contributes to a shift of calcium from the bone, allowing
H+ to enter and be buffered in the bone.

Electrolyte Balance
Multiple electrolyte levels are altered in patients with CKD. Potassium levels
may be normal until late in ESRD, and elevated potassium levels are often
associated with CKD because of the inability of the kidney to excrete potassium
as a result of decreased GFR. In addition, when metabolic acidosis is present,
potassium ions shift from the intracellular compartment to the extracellular
space in exchange for H+, in an effort to maintain extra-cellular acid-base
balance.

The third mechanism that affects serum levels of calcium is the endocrine
system. When the serum level of calcium decreases, the parathyroid gland
increases its secretion of parathyroid hormone, causing calcium to be released
from the bone and compensating for the decreased serum level of calcium.

In CKD, nitrogenous waste products from protein metabolism are retained in

the body, resulting in azotemia, as evidenced by the increased serum levels of
urea nitrogen and creatinine. The tubules, which are permeable to urea,
normally reabsorb little urea. However, as GFR decreases, more urea is
reabsorbed. Although elevated serum levels of urea nitrogen alone can indicate
other abnormalities, such as dehydration, elevation of serum levels of both
urea nitrogen and creatinine indicates kidney failure. The serum urea nitrogen–
creatinine ratio (normal 10:1 to 20:1) was once used to assess kidney function,
but the ratio is not considered as an important indicator today.
Anemia results from several factors in patients with CKD. The peritubular
capillary endothelium in the kidneys produces erythropoietin, which is needed
to stimulate bone marrow to release red blood cells. In addition, uremia
inactivates erythropoietin. Failure of this mechanism results in a
normochromic, normocytic anemia. Uremia can also contribute to anemia by
shortening the life span of the red blood cells. Finally, the low hemoglobin
level contributes to acidosis, because less hemoglobin is available in the body
to buffer acids.

Cardiovascular
Hypertension is a result of increased fluid retention and stimulation of the
renin-angiotensin-aldosterone system. In addition, hypertension can lead to the
development of CKD..

Respiratory
An increased respiratory rate may result from fluid overload, as a compensatory
mechanism for metabolic acidosis, or from decreased PaO2. Although not
identified as Kussmaul respirations, deep breaths associated with metabolic
acidosis occur as a compensatory mechanism to eliminate carbon dioxide.

Gastrointestinal
Anorexia, weight loss, nausea, and vomiting are frequent findings in patients
with CKD, Gastrointestinal bleeding from altered platelet function and
increased gastric acid secretion from increased release of parathyroid hormone
may occur. The focus of the nursing assessment includes inspecting oral mucous
membranes, monitoring weight, checking stool for occult blood, and noting
breath odor.

Neurological
Central nervous system findings in patients with CKD can range from confusion
and difficulty concentrating to seizures and coma. These findings are described
as uremic encephalopathy. Impaired thinking processes are sometimes
described as "BUN [blood urea nitrogen] blunting." The effects of CKD on the
peripheral nervous system result in peripheral neuropathy, particularly
affecting the lower extremities. The cause of these neurological effects is
thought to be atrophy and demeylination of the nerves as a result of uremic
toxins and electrolyte imbalances.

Integumentary
Pruritus often occurs in patients with CKD because of the excretion of waste
products and phosphate through the skin.

Musculoskeletal
Renal osteodystrophy results from the loss of calcium in the bones and
ineffective conversion of vitamin D to allow absorption of calcium. Three bone
changes are associated with this syndrome: (1) osteomalacia due to inadequate
absorption of calcium from the gastrointestinal tract, (2) osteitis fibrosa or
bone demineralization due to increased parathyroid hormone, and (3)
osteosclerosis, which is manifested as bands of increased and decreased bone
density in the vertebrae.

Hematological
Decreased erythropoietin levels result in anemia.

Immunological
Increased levels of uremic toxins can lead to impaired immune and
inflammatory responses with resultant defects in granulocytes, impaired B- and
T-cell functioning, and impaired phagocytosis.The focus of the nursing
assessment is examination for signs or symptoms of an impaired inflammatory
and infectious response. Infection is a common occurrence in patients with CKD
that often results in hospitalization and death.

Renal
In patients with CKD, urinary signs and symptoms are related to fluid balance;
as GFR decreases, urine output decreases. Retention of waste products such as
urea nitrogen and creatinine leads to azotemia, whereas uric acid retention
may lead to gout. Proteinuria and hematuria were discussed previously. The
focus of the nursing assessment is fluid balance (intake and output, daily
weight, edema) and monitoring of laboratory results.
 Pathophysiology: CKD UTI non-obstructive nephropathy

Client-centered
Predisposing factors:
Female
65 yrs. old (menopause) Precipitating factors:
Mother had RF Eats spicy foods, junk foods,
and drinks sodas
Catheter for 1 month

Bacteria gains access to blood and Intestinal, exogenous or genito-

goes to the kidney through systemic urinary m.o goes to the kidney
circulation through ureters and bladder

Pus Cells
Bacteria triggers inflammatory response 10-13 HPF, June
13

Edema and swelling Tubular cell Fever Infection

of involved tissues necrosis 38.5 June 13
Increase WBC
Anemia Fibrosis/scar tissue 11.08 x 109/liter
Flank pain Hgb level = 9.3 g/dl formation Dysuria June 13, 2010
June 1-5 Hct= 27.9 % June 1-7, 2010
June 13, 2010
Produces antigen-
Impaired tubular antibody complex
reabsorption/secretion;
Pallor Damage in glomeruli Trapped in
June 13 Weakness glomerulus
June 13, July
11 Decrease GFR
CRCL= 65ml/min Inflammatory
June 13, 2010 damage which
impedes
glomerular fxn
 Oliguria
190ml on
8 hour
Hyperkalemia shift
Urea not decrease Hematuria Proteinuria 7mmol/L Activation of June 14
excreted excretion 1-2 HPF 11 mg/dL RAAS
of uric June 13 June 13,
acid
Na and water vasoconstriction
Edema on left upper retention
extremity, bipedal
BUN= 100mg/dl edema, june 14
CREA=
18.3mg/dl Increase BP
June 13, 2010 Deposition of 140/90 mmHg
uric acid on June 13, 14
joints or soft
tissue

Joint pain, Cardiomegaly

swelling on due to LVH
great toe June 14
June 1-5
SYNTHESIS OF THE DISEASE
Pyelonephritis is a Bacterial infection of the kidney. Pyelonephritis can be
acute (sudden) or chronic (slow, subtle, and stubborn). It is most often due to
the ascent of bacteria from the bladder up the ureters to infect the kidneys.

The symptoms of pyelonephritis include flank (side) pain, fever, shaking chills,
sometimes foul-smelling urine, urgency (to urinate), frequency (urinating), and
general malaise. Tenderness is elicited on gently tapping over the kidney with
a fist (percussion).

Glomerulonephritis is the term used to describe a group of diseases that

damage the part of the kidney that filters blood. When the kidney is damaged,
it cannot get rid of wastes and extra fluid in the body. If the illness continues,
the kidneys may stop working completely. Some other terms you may hear used
are nephritis and nephrotic syndrome. Glomerular diseases damage the
glomeruli, letting protein and sometimes red blood cells leak into the urine.
Sometimes a glomerular disease also interferes with the clearance of waste
products by the kidney, so they begin to build up in the blood. Furthermore,
loss of blood proteins like albumin in the urine can result in a fall in their level
in the bloodstream. In normal blood, albumin acts like a sponge, drawing extra
fluid from the body into the bloodstream, where it remains until the kidneys
remove it. But when albumin leaks into the urine, the blood loses its capacity
to absorb extra fluid from the body. Fluid can accumulate outside the
circulatory system in the face, hands, feet, or ankles and cause swelling.

Body Water Regulation

Fluid volume is altered when the kidney loses its ability to excrete water
because of damaged nephrons and the resultant decreased GFR. Other factors
that contribute to the development of fluid volume overload are proteinuria
and increased renin. Proteinuria occurs in response to damage of the glomeruli.
High blood pressure can cause sclerotic changes in the glomeruli with a
resultant loss of protein, especially albumin in the urine. This damage to the
kidneys from hypertension is also known as hypertensive nephrosclerosis and
may cause damage not only to the glomueruli but also to the arteriolar walls.
The loss of albumin in the urine contributes to fluid shifting from the
intravascular space to the interstitial space because of decreased oncotic
pressure. As a response to decreased GFR, aldosterone is released from the
adrenal cortex, causing the kidneys to reabsorb sodium and water. Fluid
retention in turn results in the development of respiratory and cardiovascular
clinical manifestations

Acid-Base Balance
Metabolic acidosis is associated with CKD because the tubules cannot excrete
hydrogen ions (H+), resulting in the use of bicarbonate (HCO3–) anions to
maintain acid-base balance. Two other buffering systems are in place that
assist in compensating for the acidosis. Hydrogen ions combine with ammonia
produced in the renal tubule cells to form ammonium, which combines with
chloride and is excreted in the urine. This mechanism helps to remove H+ while
generating HCO3–. However, because of impaired nephron function, excretion of
ammonium is decreased. The third mechanism involved with acid-base balance
results in H+ combining with phosphate (one of the body’s buffering systems).
Metabolic acidosis also contributes to a shift of calcium from the bone, allowing
H+ to enter and be buffered in the bone.

Electrolyte Balance
Multiple electrolyte levels are altered in patients with CKD. Potassium levels
may be normal until late in ESRD, and elevated potassium levels are often
associated with CKD because of the inability of the kidney to excrete potassium
as a result of decreased GFR. In addition, when metabolic acidosis is present,
potassium ions shift from the intracellular compartment to the extracellular
space in exchange for H+, in an effort to maintain extra-cellular acid-base
balance.

The third mechanism that affects serum levels of calcium is the endocrine
system. When the serum level of calcium decreases, the parathyroid gland
increases its secretion of parathyroid hormone, causing calcium to be released
from the bone and compensating for the decreased serum level of calcium.

In CKD, nitrogenous waste products from protein metabolism are retained in

the body, resulting in azotemia, as evidenced by the increased serum levels of
urea nitrogen and creatinine. The tubules, which are permeable to urea,
normally reabsorb little urea. However, as GFR decreases, more urea is
reabsorbed. Although elevated serum levels of urea nitrogen alone can indicate
other abnormalities, such as dehydration, elevation of serum levels of both
urea nitrogen and creatinine indicates kidney failure. The serum urea nitrogen–
creatinine ratio (normal 10:1 to 20:1) was once used to assess kidney function,
but the ratio is not considered as an important indicator today.

Anemia results from several factors in patients with CKD. The peritubular
capillary endothelium in the kidneys produces erythropoietin, which is needed
to stimulate bone marrow to release red blood cells. In addition, uremia
inactivates erythropoietin. Failure of this mechanism results in a
normochromic, normocytic anemia. Uremia can also contribute to anemia by
shortening the life span of the red blood cells. Finally, the low hemoglobin
level contributes to acidosis, because less hemoglobin is available in the body
to buffer acids.

Cardiovascular
Hypertension is a result of increased fluid retention and stimulation of the
renin-angiotensin-aldosterone system. In addition, hypertension can lead to the
development of CKD..

Respiratory
An increased respiratory rate may result from fluid overload, as a compensatory
mechanism for metabolic acidosis, or from decreased PaO2. Although not
identified as Kussmaul respirations, deep breaths associated with metabolic
acidosis occur as a compensatory mechanism to eliminate carbon dioxide.

Gastrointestinal
Anorexia, weight loss, nausea, and vomiting are frequent findings in patients
with CKD, Gastrointestinal bleeding from altered platelet function and
increased gastric acid secretion from increased release of parathyroid hormone
may occur. The focus of the nursing assessment includes inspecting oral mucous
membranes, monitoring weight, checking stool for occult blood, and noting
breath odor.

Neurological
Central nervous system findings in patients with CKD can range from confusion
and difficulty concentrating to seizures and coma. These findings are described
as uremic encephalopathy. Impaired thinking processes are sometimes
described as "BUN [blood urea nitrogen] blunting." The effects of CKD on the
peripheral nervous system result in peripheral neuropathy, particularly
affecting the lower extremities. The cause of these neurological effects is
thought to be atrophy and demeylination of the nerves as a result of uremic
toxins and electrolyte imbalances.

Integumentary
Pruritus often occurs in patients with CKD because of the excretion of waste
products and phosphate through the skin.

Musculoskeletal
Renal osteodystrophy results from the loss of calcium in the bones and
ineffective conversion of vitamin D to allow absorption of calcium. Three bone
changes are associated with this syndrome: (1) osteomalacia due to inadequate
absorption of calcium from the gastrointestinal tract, (2) osteitis fibrosa or
bone demineralization due to increased parathyroid hormone, and (3)
osteosclerosis, which is manifested as bands of increased and decreased bone
density in the vertebrae.

Hematological
Decreased erythropoietin levels result in anemia.

Immunological
Increased levels of uremic toxins can lead to impaired immune and
inflammatory responses with resultant defects in granulocytes, impaired B- and
T-cell functioning, and impaired phagocytosis.The focus of the nursing
assessment is examination for signs or symptoms of an impaired inflammatory
and infectious response. Infection is a common occurrence in patients with CKD
that often results in hospitalization and death.

Renal
In patients with CKD, urinary signs and symptoms are related to fluid balance;
as GFR decreases, urine output decreases. Retention of waste products such as
urea nitrogen and creatinine leads to azotemia, whereas uric acid retention
may lead to gout. Proteinuria and hematuria were discussed previously. The
focus of the nursing assessment is fluid balance (intake and output, daily
weight, edema) and monitoring of laboratory results.
A. IVF, BT, NGT feeding, Nebulization, TPN, Oxygen Therapy, etc.
 Medical General Description Date Ordered/ Indication/Purpose Clients Response to
Management Date Changed Treatment
1. IV fluid It is the giving of liquid Date Ordered: It is for rehydration The patient was
D5 03. substances directly into 7-13-10 (of fluids and supplied with
NaCl a vein. Date electrolytes) and adequate fluid. No
Changed: can be for adverse response
7-14-10 supplemental was noted.
nourishment, until
the patient TPN
(total parenteral
nutrition).

2. PNSS It is the giving of liquid Date Ordered: It is isotonic can be The patient was
substances directly into 7-14-10 used to replace supplied with
a vein. Which has the fluids in adequate fluid. No
same salt content as the dehydration, go adverse response
normal body fluid with blood was noted.
transfusions,
hyponatremia
(same osmolarity as
our body fluids)

3.BT (PRBC) Blood transfusion is the Date Ordered: Transfusions are The patient was
process of transferring 7-15-10 performed to supplied with
blood or blood-based replace a substantial adequate and
products from one loss of blood and as compatible blood.
person into the supportive No adverse
circulatory system of treatment in certain response was noted.
another. Blood diseases and blood
transfusions can be life- disorders.
saving in some
situations, such as
massive blood loss due
to trauma, or can be
used to replace blood
lost during surgery.

4. Foley A tube that are passed Date Ordered: To drain the urine The patient was
Catheterization through the urethra 7-15-10 in the urinary inserted a FC and
during urinary bladder. able to drain the
catheterization and into urine thru the
the bladder to drain straight FC.
urine.
 B. DIET

Type of Diet General Date Indcation/ Client’s

Description Ordered/date Purpose response to
Changed treatment

A low-protein Date Ordered: To sustain in The patient

Uremic Diet diet can help 7-16-10 the body with complied with
remove strain nutrients as the prescribed
from the needed and for diet.
kidneys, the condition of
improving the patients
condition. properly diet.

Nursing Responsibilities:

• Explain the purpose of food restriction or the prescribed diet to the patient.
• Mark the Kardex with “Uremic Diet”
• Inform the diet nutritionist about the diet status.
• Inform the patients and family about the diet status.