Nephrotic syndrome (Nephrosis)

DEFINITION: • Nephrotic syndrome is a group of symptoms including protein in the urine (more than 3.5
grams per day), low blood protein levels, high cholesterol levels, high triglyceride levels, andsw elling.

• Autoimmune process leading to structural alteration of glomerular membrane that results in increased
permeability to plasma proteins, particulary albumin.

• Nephrotic syndrome is a disorder of the glomeruli (clusters of microscopic blood vessels in the kidneys
that have small pores through which blood is filtered) in which excessive amounts of protein are
excreted in the urine. This typically leads to accumulation of fluid in the body (edema) and low levels of
the protein albumin and high levels of fats in the blood.

• Nephrotic syndrome is not a specific glomerular disease but a cluster of clinical findings,
including:Marked increase in protein (particularly albumin) in the urine (proteinuria), Decrease in
albumin in the blood (hypoalbuminemia), Edema, High serum cholesterol and low-density lipoproteins
(hyperlipidemia).

ANATOMY AND PHYSIOLOGY:

The organs, tubes, muscles, and nerves that work together to create, store, and carry urine are the
urinary system. The urinary system includes two kidneys, two ureters, the bladder, two sphincter
muscles, and the urethra. Your body takes nutrients from food and uses them to maintain all bodily
functions including energy and self-repair. After your body has taken what it needs from the food, waste
products are left behind in the blood and in the bowel. The urinary system works with the lungs, skin,
and intestines—all of which also excrete wastes—to keep the chemicals and water in your body
balanced. Adults eliminate about a quart and a half of urine each day. The amount depends on many
factors, especially the amounts of fluid and food a person consumes and how much fluid is lost through
sweat and breathing. Certain types of medications can also affect the amount of urine eliminated. The
urinary system removes a type of waste called urea from your blood. Urea is produced when foods
containing protein, such as meat, poultry, and certain vegetables, are broken down in the body. Urea is
carried in the bloodstream to the kidneys. The kidneys are bean-shaped organs about the size of your
fists. They are near the middle of the back, just below the rib cage. The kidneys remove urea from the
blood through tiny filtering units called nephrons. Each nephron consists of a ball formed of small blood
capillaries, called a glomerulus, and a small tube called a renal tubule. Urea, together with water and
other waste substances, forms the urine as it passes through the nephrons and down the renal tubules
of the kidney

From the kidneys, urine travels down two thin tubes called ureters to the bladder. The ureters are about
8 to 10 inches long. Muscles in the ureter walls constantly tighten and relax to force urine downward
away from the kidneys. If urine is allowed to stand still, or back up, a kidney infection can develop. Small
amounts of urine are emptied into the bladder from the ureters about every 10 to 15 seconds. The
bladder is a hollow muscular organ shaped like a balloon. It sits in your pelvis and is held in place by
ligaments attached to other organs and the pelvic bones. The bladder stores urine until you are ready to
go to the bathroom to empty it. It swells into a round shape when it is full and gets smaller when empty.
If the urinary system is healthy, the bladder can hold up to 16 ounces (2 cups) of urine comfortably for 2
to 5 hours. Circular muscles called sphincters help keep urine from leaking. The sphincter muscles close
tightly like a rubber band around the opening of the bladder into the urethra, the tube that allows urine
to pass outside the body. Nerves in the bladder tell you when it is time to urinate, or empty your
bladder. As the bladder first fills with urine, you may notice a feeling that you need to urinate. The
sensation to urinate becomes stronger as the bladder continues to fill and reaches its limit. At that point,
nerves from the bladder send a message to the brain that the bladder is full, and your urge to empty
your bladder intensifies. When you urinate, the brain signals the bladder muscles to tighten, squeezing
urine out of the bladder. At the same time, the brain signals the sphincter muscles to relax. As these
muscles relax, urine exits the bladder through the urethra. When all the signals occur in the correct
order, normal urination occurs. Problems in the urinary system can be caused by aging, illness, or injury.
As you get older, changes in the kidneys’ structure cause them to lose some of their ability to remove
wastes from the blood. Also, the muscles in your ureters, bladder, and urethra tend to lose some of their
strength. You may have more urinary infections because the bladder muscles do not tighten enough to
empty your bladder completely. A decrease in strength of muscles of the sphincters and the pelvis can
also cause incontinence, the unwanted leakage of urine. Illness or injury can also prevent the kidneys
from filtering the blood completely or block the passage of urine

PREDISPOSING

FACTOR RATIONALE
Age Children ages 11⁄2 and 4 yr are predisposed in having nephrotic syndrome
Sex Males are more predisposed than males in acquiring nephrotic syndrome
Genetics People with family history of nephrotic syndrome increases likelihood of
developing nephrotic syndrome
Focal segmental Most common cause of idiopathic NS among adults. May be secondary to
glomerulosclerosis HIV/AIDS infection or loss of nephrons.
> HIV/AIDS
> Nephrectomy

Membranous Deposition of immune complexes on the glomerular basement membrane

nephropathy causing it to thicken. It can be secondary to certain cancers, Hepatitis B
>Hepatitis B infection infections and autoimmune disorders such as SLE.
> SLE
> Cancer
Minimal change disease Causes 80 to 90% of childhood nephrotic syndrome in children 4 to 8
years of age idiopathic in nature.
Diabetes Mellitus Prolonged elevated blood glucose levels alters glomerular base membranes
thereby causing impaired renal function
SYMPTOMS

LEGEND SYMPTOM RATIONALE

S1 Albuminuria In nephrotic syndrome the podocytes are damaged and very
permeable allowing albumin from the blood to escape and be
excreted out the body along with urine.
S2 Edema Edema is the result of fluid shifting from the intravascular space to
the interstitial space due to the decrease intravascular pressure.
S3 Hyperlipidemia Results due to the increased production of lipoproteins by the liver
in response to the low levels of albumin in the blood.
S4 HypoalbuminemiaIn nephrotic syndrome the podocytes are damaged and very
permeable allowing albumin from the blood to escape and be
excreted out the body along with urine

MEDICAL MANAGEMENT

1. fluid and sodium restriction, oral or intravenous diuretics, and angiotensin-converting enzyme
inhibitors.
• Fluid and sodium restrictions
Creating a negative sodium balance will help reduce edema, presumably as the underlying illness is
treated or as renal inflammation slowly resolves. Patients should limit their sodium intake to 3 g per
day, and may need to restrict fluid intake (to less than approximately 1.5 L per day). Large
doses (e.g., 80 to 120 mg of furosemide) are often required,14 and these drugs typically must be
given intravenously because of the poor absorption of oral drugs caused by intestinal edema.3 Low
serum albumin levels also limit diuretic effectiveness and necessitate higher doses. Thiazide
diuretics, potassium-sparing diuretics, or metolazone (Zaroxolyn) may be useful as adjunctive or
synergistic diuretics.
• Diuretics
"Diuretics are the mainstay of medical management; however, there is no evidence to guide drug
selection or dosage," Dr. Kodner writes. "Based on expert opinion, diuresis should aim for a target
weight loss of 1 to 2 lb (0.5 to 1 kg) per day to avoid acute renal failure or electrolyte disorders.
Loop diuretics, such as furosemide (Lasix) or bumetanide, are most commonly used."

• Angiotensin-converting enzyme
In persons with nephrotic syndrome, angiotensin-converting enzyme inhibitors have been shown to
decrease proteinuria and lower the risk for progression to renal disease. Angiotensin-converting
enzyme (ACE) inhibitors have been shown to reduce pro-teinuria and reduce the risk of progression
to renal disease in persons with nephrotic syndrome.15,16 One study found no improvement in
response when corticosteroid treatment was added to treatment with ACE inhibitors.17 The
recommended dosage is unclear, and enalapril (Vasotec) dosages from 2.5 to 20 mg per day were
used. Most persons with nephrotic syndrome should be started on ACE inhibitor treatment to
reduce protein-uria, regardless of blood pressure.
* Although corticosteroid treatment may benefit some adults with nephrotic syndrome, research
evidence supporting this therapy is limited. At present, intravenous albumin, prophylactic
antibiotics, and prophylactic anticoagulation are not advised.

ALBUMIN
Intravenous albumin has been proposed to aid diuresis, because edema may be caused by
hypoalbuminemia and resulting oncotic pressures. However, there is no evidence to indicate benefit
from treatment with albumin,18 and adverse effects, such as hypertension or pulmonary edema, as
well as high cost, limit its use.

CORTICOSTEROIDS
Treatment with corticosteroids remains controversial in the management of nephrotic syndrome in
adults. It has no proven benefit, but is recommended in some persons who do not respond to
conservative treatment.19,20 Treatment of children with nephrotic syndrome is different, and it is
more clearly established that children respond well to corticosteroid treatment.21 Classically,
minimal change disease responds better to corticosteroids than FSGS; however, this difference
isfound primarily in children with nephrotic syndrome. One older study found that corticosteroid
treatment improved proteinuria and renal function in persons with minimal change disease, but not
membranous nephropathy or proliferative glomerulonephritis.22 Another small older study found
that persons with less severe glomerular changes responded well to corticosteroids.23 One case
series in black persons with FSGS found no benefit from corti-costeroid treatment.19 Two Cochrane
reviews on the treatment of nephrotic syndrome in adults found no benefit for mortality or need for
dialysis with corticosteroid therapy for membranous nephropathy or minimal change disease, but
found a weak benefit for disease remission and proteinuria in persons with membranous
nephropathy.20,24 However, the findings for minimal change disease were based on only one
randomized trial, and the role of corticosteroid treatment remains unclear. Many experts
recommend the use of corticosteroids, particularly for persons with minimal change disease1;
however, adverse effects from corticosteroids often lead to discontinuation.

Family physicians should discuss with patients and consulting nephrologists whether treatment with
corticosteroids is advisable, weighing the uncertain benefits and possibility of adverse effects.
Alkylating agents (e.g., cyclophosphamide [Cytoxan]) also have weak evidence for improving disease
remission and reducing proteinuria, but may be considered for persons with severe or resistant
disease who do not respond to corticosteroids.
LIPID-LOWERING TREATMENT

A Cochrane review is underway to investigate the benefits and harms of lipid-lowering agents in
nephrotic syndrome.25 Some evidence suggests an increased risk of athero-genesis or myocardial
infarction in persons with nephrotic syndrome, possibly related to increased lipid levels.25
However, the role of treatment for increased lipids is unknown and, at present, the decision to start
lipid-lowering therapy in persons with nephrotic syndrome should be made on the same basis as in
other patients. ANTIBIOTICS There are no data from prospective clinical trials about treatment and
prevention of infection in adults with nephrotic syndrome. Given the uncertain risks of infection in
adults with nephrotic syndrome in the United States, there are currently no indications for
antibiotics or other interventions to prevent infection in this population. Persons who are
appropriate candidates should receive pneumococcal vaccination.

ANTICOAGULATION THERAPY

There are currently no recommendations for prophylactic anticoagulation to prevent

thromboembolic events in persons with nephrotic syndrome who have not had previous thrombotic
events, and clinical practice varies. A Cochrane review is in process.26 Physicians should remain
alert for signs or symptoms suggesting thromboembolism and, if it is diagnosed, these events
should be treated as in other patients. Persons who are otherwise at high risk of thromboembolism
(e.g., based on previous events, known coag-ulopathy) should be considered for prophy-lactic
anticoagulation while they have active nephrotic syndrome

LABORATORY EXAM

1.Proteinuria (predominately albumin) exceeding 3.5 g/day is the hallmark of the diagnosis of
nephrotic syndrome.
2.A needle biopsy of the kidney may be performed for histologic examination of renal tissue to
confirm the diagnosis.
3.Recent studies have confirmed the usefulness of serum markers as a means of assessing the
disease process. Anti-C1q antibodies are the most reliable markers for assessing disease activity.

NURSING DIAGNOSIS

• Excess fluid volume related to compromised regulatory mechanism with changes in hydrostatic or
oncotic vascular pressure and increased activation of RAAS

• Imbalanced nutrition: Less than body requirements related to anorexia, nausea, vomiting, protein
catabolism, dietary restrictions and altered oral mucous membranes
• Decreased cardiac output related to fluid imbalances affecting circulating volume, myocardial
workload and systemic vascular resistance
• Risk for infection depression of immunologic defenses
• Disturbed body image related to changes in physical appearance
• Risk for injury

NURSING MANAGEMENT
• Assess and document the location and character of the patient's edema.
• Weigh the patient each morning after he voids and before he eats, make sure he's wearing the
same amount of clothing each time you weigh him.
• Measure blood pressure with the patient lying down and standing. Immediately report a decrease
in systolic or diastolic pressure exceeding 20 mm Hg.
• Monitor intake and output
• Ask the dietitian to plan a low-sodium diet with moderate amounts of protein.
• Frequently check urine for protein
• Provide meticulous skin care to combat the edema that usually occurs with nephrotic syndrome
• Use a reduced-pressure mattress or padding to help prevent pressure ulcers.
• To prevent the occurrence of thrombophlebitis, encourage activity and exercise, and provide
antiembolism stockings as ordered
• Give the patient and family reassurance and support, especially during the acute phase, when
edema is severe and the patient's body image changes

PROGNOSIS
The prognosis varies depending on the cause of the nephrotic syndrome, the person's age, and the
type and degree of kidney damage. Symptoms may disappear completely if the nephrotic syndrome
is caused by a treatable disorder, such as an infection, cancer, or drugs. This situation occurs in
about half the cases in children but less often in adults. If the underlying disorder responds to
corticosteroids, sometimes progression of the disease is halted, and less often the condition
partially or, rarely, completely reverses. When the syndrome is caused by HIV infection, it usually
progresses relentlessly, often resulting in complete kidney failure in 3 or 4 months. Children born
with the nephrotic syndrome rarely live beyond their first birthday, although a few have survived by
means of dialysis treatments or a kidney transplant. When the cause is systemic lupus
erythematosus or diabetes mellitus, drug treatment often stabilizes or decreases the amount of
protein in the urine. However, some people do not respond to drug treatment and develop
progressive kidney failure within a few years. In cases of nephrotic syndrome resulting from
conditions such as an infection, allergy, or intravenous heroin use, the prognosis varies, depending
on how early and effectively the underlying condition is treated. Nephrotic syndrome may go away
once the underlying cause, if known, has been treated. In children, 80 percent of nephrotic
syndrome cases are caused by minimal change disease, which can be successfully treated with
prednisone. However, in adults most of the time a kidney disease is the underlying cause, and these
diseases cannot be cured.
Good – Fair – Poor Prognosis
Pathophysiology RAAS – Renin Angiotensin Aldosterone System
ARF – Acute Renal Failure
CRF – Chronic Renal Failure
ESRD – End Stage Renal Disease
CAD – Coronary Artery Disease
CVD – CardioVascular Disease

YOU MAY WONDER >>> Q. HOW DOES RAAS LEAD TO ARF??? A. RAAS will eventually be exhausted.
Moreover, the RAAS cannot increase vascular volume since there is no albumin to hold the water
within the vascular space. Thus the water and sodium reabsorbed will shift into the interstitial
space. RAAS will only exacerbate the edema and make the patient more edematous. xD If left
untreated then the blood flow to the kidneys(due to decreased intravascular volume) will be
compromised causing acute trauma and injury to the nephrons ultimately causing ARF. =) hope this
helps
Nephrotic syndrome is a nonspecific disorder in which the , kidneys are damagedcausing them to
leak large amounts of ( . . proteinproteinuria at least 35 grams per day per 173 m2 ) . body surface
areafrom the blood into the urineOther
( symptoms includehypoalbuminemiadecrease in albumin in ), ,
( the bloodedemahypercholesterolemiahigh serum ), . cholesterol and normal renal function * .
The most common sign is excess fluid in the body This may : take several forms  , o Puffiness
around the eyescharacteristically in . the morning  ( . ., o Edema over the legs which is
pittingieleaves a , little pit when the fluid is pressed outwhich resolves ). over a few seconds  o
Fluid in the pleural cavity causing pleural . effusion More commonly associated with excess fluid is .
pulmonary edema  . o Fluid in the peritoneal cavity causing ascites

 , The following are baseline essential investigations

 *Urine sample shows proteinuria (> . . ). 35g per 173 m2 per 24 hour 
* () Comprehensive metabolic panelCMP : shows Hypoalbuminemiaalbumin level ≤. / ( =.- / ). 2 5g
dLnormal3 5 5g dL 
*High levels of cholesterol ( ), hypercholesterolemia specifically , elevated LDLusually with
concomitantly elevated VLDL 
* , Electrolytesurea and creatinine ( ): . EUCsto evaluate renal function

CAUSES
Nephrotic syndrome has many causes and may either
cell diseasediabetes mellitus and malignancy. such as leukemia  Secondary causes of nephrotic
syndrome occurs, after an infectious disease such as infection
- ,with group A betahemolytic streptococci, syphilis malaria tuberculosis orviral infections including
varicella hepatitis B HIV. and infectious mononucleosis

CASE STUDY FORMAT

I. PATIENT DEMOGRAPHIC DATA

Name: Rose Nina Francisco
Age/Sex: 14/Female
Status: Single Religion: Roman Catholic
Home Address: Cogon, Pardo Nationality:
Filipino Occupation: N/A
 II. HEALTH HISTORY PROFILE

A. Past Medical History

1. Pediatric and Adult Illness

Date Illness Medication Remarks

NONE NONE NONE NONE

2. Immunization

Immunization Doses Immunization Dates Remarks

BCG 1 Can’t Recall Complete
DPT 3 Can’t Recall Complete
OPV 3 Can’t Recall Complete

3. Hospitalization
Date/Year Hospital Diagnosis Duration
2007 2008 Cebu City Medical Center Nephrotic Syndrome 1 week
Cebu City Medical Center Nephrotic Syndrome 1 week

4. Injuries and Accidents

The patient did not experience any injuries and accidents.

5. Transfusions- The patient did not undergo any transfusions such as blood transfusion.

6. Allergies(specify)- The patient has no any allergies

B. Family History

C. Social and Personal History

•1.Occupation-N/A
2.Number of Children-N/A
3.Military experiences, foreign travel-N/A
4.Habits (tobacco, alcohol, non-prescription drugs, others)-N/A
5.Diet-fruits, vegetables, pork chop, dried fish
6.Type of Family-Extended Family
7.Cultural and Religious Beliefs-N/A
8.Brief description of average day:

5:30 am-wake up
6:00 am-breakfast
7:00-9:00 am-class hours
9:15-9:30 am-recess
9:30-12:00 am-class hours
12:00-1:00 pm-lunch
1:00-5:00 pm-class hours
5:30 pm-do homework
6:00 pm-dinner
7:00-8:00 pm-watch T.V
8:00 pm-sleeping time

D. Review System (for the past 6 months).

Physical Assessment

General Weight loss Fatigue Anorexia Night sweats Chills Fever Weakness

The patient experienced fever due to cough and colds.

The patient experienced fatigue due to illness and lack of sleep.
The patient experienced weakness due to fatigue.

Skin Itch
Rash
Lesions
Bruising
Bleeding Color change NONE

Eyes Pain
Discharge
Itch
Vision loss
Diplopia
Excessive tearing
Glasses/Contact lens
Date of last exam NONE

Ears Earaches Discharges Tinnitus Hearing loss NONE

 Nose Obstruction Discharges Epistaxis NONE

Throat and MouthSore throats Bleeding gums Toothache Dentures NONE

Neck and Head Swelling Dysphagia Hoarseness
NONE

Chest Cough Sputum Amount and Character Hemoptysis Wheeze Pain

on respiration Dyspnea The patient experienced
dyspnea due to obstruction of the airway

Cardiovascular Precordialpain Palpitation Dyspneaon exertion

Orthopnea Dyspnea Paroxysmal nocturnal Edema
Heart murmur Claudication Thrombophlebitis
NONE

Gastrointestinal Heartburn Nausea Vomiting Diarrhea Food

intolerance Excessive gas or indication
Constipation Jaundice Bloating Change in Bowel
movement Melena Hemorrhoids Hernia NONE

Genitourinary Heartburn Nausea Vomiting Diarrhea Food

intolerance Excessive gas or indication
Constipation Jaundice Bloating Change in Bowel
movement Melena Hemorrhoids Hernia NONE

Extremities Joint pains Varicose veins Claudication Back pain

Edema Stiffness Deformities
The patient experienced edema due to illness
which is nephrotic syndrome.
Endocrine Hot flashes Hair loss Temperature intolerance
Polydipsia Goiter NONE
Neurology Numbness Tingling Tremor Fainting Headaches
Muscle weakness Ataxia Seizure Unconsciousness
Paralysis/Paresis Memory loss Dizziness

The patient experienced headaches due to fever.

III. CURRENT HEALTH PROFILE

A.Presenting complaints and medical diagnosis to include intervention done prior to

hospitalization.

Rosa Nina Francisco was diagnosed for Nephrotic Syndrome. She Complain of difficulty in breathing.

B. Application of the Nursing Process 1. Assessment Finding (Head –to-Toe)

Skin Uniform skin color, no jaundice, cyanosis

Skin intact Skin warm and dry

Hair Hair is evenly distributed over scalp

Hair color black and thin
No lesions or pediculosis
Nails Color pink, well groomed ad convex, smooth and
firm
Head Normocephallic, erect and midline Head
symmetrical, no masses, nontende

Face Facial expression appropriate, no abnormal

movements or lesions Facial bones smooth,
intact,symmetrical,nontender
Ears Ears aligned with eyes, symmetrical, no redness,
lesions or drainage Eyes Eyes clear and bright,
equal parallel alignment
Eyelids color consistent with clients complexion
Eyelashes evenly distributed, no excessive tearing
or dryness
Nose Nose midline, symmetrical, no deviation, no flaring
No deformities or nasal tenderness Sinuses Sinuses
clear, nontender

Mouth Lips pink, moist, no lesions Oral mucosa pink,

moist, no lesions, intact
Teeth complete
Tongue pink, moist,midline

Neck Neck symmetrical, skin intact, no masses Upper

Extremities Skin color uniform; no erythema,
edema Abdomen Skin color consistent, no lesions,
rashes, scars or discoloration. Hair distribution
appropriate for client’s age and gender

Abdomen flat and symmetrical, no bulges or hernias

Umbilicus midline
Abdomen soft, nontender, no masses
 Lower Extremities Leg hair evenly distributed; color uniform; no
edema or lesion

Laboratory/Diagnostic Results

Date Lab Exam Patient Results Normal Findings Interpretation/Significant

09-01-09 Protein to 1.55 5-0.9 Suggests the presence of
Creatinine ratio nephrotic range
proteinuria.
Serum albumin 0.9g/dl 0. 3.4-5.4g/dl Hypoalbuminemia can be
caused by Excess
excretion by the kidneys.

 NORMAL KIDNEY SIZE -The normal kidney size of an adult human is about 10 to -The normal
kidney size of an adult human is about 10 to 13 cm (4 to 5 inches) long and about 5 to 7.5 cm (2
to 3 13 cm (4 to 5 inches) long and about 5 to 7.5 cm (2 to 3 inches) wide. It is approximately the
size of inches) wide. It is approximately the size of a a conventional computer mouse
conventional computer mouse. .
 NORMAL KIDNEY COLOR NORMAL KIDNEY COLOR -The kidneys are dark-red, bean-shaped
organs. One side The kidneys are dark-red, bean-shaped organs. One side of the kidney bulges
 outward (convex) and the other of the kidney bulges outward (convex) and the other side is
indented (concave) side is indented (concave)

 NORMAL KIDNEY LOCATION NORMAL KIDNEY LOCATION - -towards the back of the abdominal
cavity, just towards the back of the abdominal cavity, just above the waist. One kidney is
normally located just above the waist. One kidney is normally located just below the liver, on
the right side of the abdomen and below the liver, on the right side of the abdomen and the
other is just below the spleen on the left side. the other is just below the spleen on the left side

 The most basic structures of the kidneys, are nephrons. They are responsible for filtering the
blood.

• The renal artery delivers blood to the kidneys each day. Over 180 liters (50 gallons) of blood pass
through the kidneys every day. When this blood enters the kidneys it is filtered and returned to
the heart via the renal vein.

• The process of separating wastes from the body fluids and eliminating them, is known as
excretion. The urinary system is one of the organ systems responsible for excretion. The kidneys
are the main organs of the urinary system.

 The kidney is full of blood vessels. Every function of the kidney involves blood, therefore, it
requires a lot of blood vessels to facilitate these functions.

• Together, the two kidneys contain about 160 km of blood vessels

Renal capsule

•is a tough fibrous layer surrounding the kidney and covered in a thick layer of adipose tissue. It
provides some protection from trauma and damage

•is the outer portion of the kidney between the renal capsule and the renal medulla. In the adult, it
forms a continuous smooth outer zone with a number of projections (cortical columns) that extend
down between the pyramids.

•ultra filtration occurs

Renal

•is the innermost part of the kidney

•split up into a number of sections, known as the renal pyramids

•contains the structures of the nephrons responsible for maintaining the salt and water balance of
the blood
•is hypertonic to the filtrate in the nephron and aids in the reabsorption of water.

 are cone-shaped tissues of the kidney

 made up of 8 to 18 of these conical subdivisions
 The broad of each pyramid faces the renal cortex, and its apex, or papilla, points internally
 The base of each pyramid originates at the corticomedullary border and the apexterminates in a
papilla, which lies within a minor calyx, made of parallel bundles of urine collecting tubules.
 surrounds the apex of the malpighian pyramids. Urine formed in the kidney passes through a
papilla at the apex into the minor calyx then into the major calyx.
 Peristalsis of the smooth muscle originating in pace-maker cells originating in the walls of the
calyces propels urine through the pelvis and ureters to the bladder.

Phatophysiology

Nephrotic syndrome results from damage to the kidney’s glomeruli, the tiny blood vessels that filter
waste and excess water from the blood and send them to the bladder as urine. They consist of
capillaries that are fenestrated, that is, have small openings, which allow fluid, salts, and other small
solutes to flow through but normally not proteins. Damage to the glomeruli from diabetes,
glomerulonephritis, or even prolonged hypertension, causes the membrane to become more porous, so
that small proteins, such as albumin, pass through the kidneys into urine. As protein continues to be
excreted, serum albumin is decreased, which in turn decreases the serum osmotic pressure. Capillary
hydrostatic fluid pressure becomes greater than capillary osmotic pressure, which results in generalized
edema. As fluid is lost into the tissues, the plasma volume decreases, stimulating secretion of
aldosterone to retain sodium and water, which decreases the glomerular filtration rate to retain water.
This additional water also passes out of the capillaries into the tissue, leading to even greater edema. •

SOAPIE

S:
O:
A: Knowledge deficit related to chronic illness
P: After 4 hours of nurse-patient and significant others interaction,
the patient and the significant others will be able to:
 Identify interferences to learning and specific actions to deal with it.
 Perform necessary procedures correctly and explain reasons for the actions.
 Initiate necessary lifestyle changes and participate in treatment regimen.
 Provided an environment that is conducive to learning.

I:Assessed readiness to learn.

Provided written information/guidelines and self-learning modules for client to refer to as
necessary.
Allowed practice and demonstrations.

E:Goal was met. After 4 hours of nurse-patient and significant others interaction, the patient and the
significant others will be able to identified the interferences to learning and made specific actions to
deal with it. And they were to performed necessary procedures correctly and they explained the
reasons for the actions they made.And they were able to initiated necessary lifestyle changes and
participated in treatment regimen by allowing them to practice and
demonstrate the treatment regimen.

SOAPIE
S-“Wala koy gana mukaon.”, as verbalized by the patient.
O- : protein-creatinine ratio of 1.55 Serum albumin of 0.9g/dl
A- Imbalanced Nutrition, less than body requirements related to poor appetite, restricted diet, and
protein loss.

P- After 8 hours of nurse-patient interaction, the patient will be able to:

 Identify the appropriate diet for her condition. (Low-sodium diet)

 Follow the diet prescribed.
 Verbalize realization of the importance of proper diet.
I- Assessed and monitored food/fluid ingested and calculate caloric intake.
 Monitored weight daily at same time, same clothing and same scale.
 Recommended small, frequent meals.
 Restricted sodium as indicated, and limited fluid intake to 100ml
 Administered multivitamins, as indicated.
 Administered medications as appropriate.
 Monitored laboratory studies.

E- Goals met. After 8 hours of nurse-patient interaction, the patient was able to identify the
appropriate diet for her condition. (Low-sodium diet). Follow the diet prescribed. Verbalize
realization of the importance of proper diet

SOAPIE
S- “Murag nanghupong akong anak sa iya bitiis.”, as verbalized by the mother.

O- Edema, weight gain, changes in vital signs

A-Excess fluid volume related to compromised regulatory mechanism with changes in hydrostatic
vascular pressure and increased activation of rennin angiotensin aldosterone system.
P-After 5 hrs of nursing interventions, the patient will be able to: display stable weight
vital signs within patient’s normal range
nearly absence of edema.

I-Record accurate intake and output of the patient Monitor urine specific gravity
 Weight daily at same time of the day, on same scale, with
 same equipment and clothing
 Assess skin, face, dependent areas of edema
 Monitor heart rate and blood pressure
 Assess level of consciousness: investigate changes in mentation, presence of restlessness.

E-Goals were fully met. After 5 hrs of nursing interventions, the patient was able to display stable
weight, vital signs within patient’s normal range, and nearly absence of edema.