DISCUSSION OF THE DISEASE:

Nephrotic Syndrome is a kidney disorder ( other references ascribe it as a

collective symptom and not as a disease) which is due to the fusion of glomerular membrane
surfaces, causing abnormal loss of protein. The highest incidence is at 3 years of age, and it
occurs more often in boys than girls (Lum, 2008).
It occurred in three forms, a. Congenital( autosomal recessive disorder, b. secondary
(eg. Progressive AGN), c. Primary/ Idiopathic( unknown cause probably due to immunologic
mechanisms).
It can be further classified into the extent of glomerular membrane destruction.
a) MCNS or Minimal Change nephrotic syndrome- often seen in children, about 80%;
there is little scarring only.
b) FGS or Focal Glomerulosclerosis have poor response to
c) MPGN or Membranoproliferative glomerulonephritis therapy (Lu, et al, 2007)

EPIDEMIOLOGY:
It is 15 times more common in children than in adults. The reported annual incidence rate is 2
to 5 per 100,000 children younger than 16 years. The cumulative prevalence rate is
approximately 15.5 per 100,000 individuals. Nephrotic syndrome prevalence is difficult to
establish in adults, because the condition is usually a result of underlying disease.
BRIEF PATHOPHYSIOLOGY:
Etiology: Primary/Secondary/Congenital
Increased glomerular permeability
Unable to filter Albumin/protein, and CHON gets into the urine
(PROTEINURIA)
HYPOALBUMINEMIA
EDEMA
HYPERLIPIDEMIA (to compensate with the protein loss)-not excreted still in the
urine because of its size

Also known as Nephrosis
Not the same with Nephritic syndrome, but it can occur in association with the disease.
DIAGNOSTIC TESTS:
y Creatine - blood test to assess kidney function
y Blood urea nitrogen (BUN)
y Urinalysis- to assess the extent of protein loss


CAUSES:
Its classification of the disorder is based on its etiologic or causative history, either
Primary/Idiopathic or Secondary/Congenital:
PRIMARY CAUSES:
Its idiopathic pathogenecity may be traced to:
Immunologic mechanisms: Antibody-Antigen complexes
T-Lymphocyte abnormalities

SECONDARY CAUSES:
y Diabetes mellitus- causes Renal Neuropathy that affects the glomerular filtration capability of
the renal system
y Lupus erythematosus- autoimmune
y Viral infections (eg, hepatitis B, hepatitis C, human immunodeficiency virus [HIV] )- viruses
dislodged on the Renal system, proliferate then causes the disease.
y Henoch-Schonlein purpura (HSP) causes vasculitis in the renal system

CONGENITAL CAUSES:
y Occurred as an autosomal recessive disorder, most seen in children

SIGNS AND SYMPTOMS:
NOTE: SYMPTOMS USUALLY BEGIN INSIDUOUSLY.
Proteinuria: Abnormal protein leak in the urine; 3 to 3.5 grams per day of CHON is seen
at a single spot urine collection
Hypoalbuminemia: Low levels of proteins in blood (due to protein leakage); 2.5g/dL
(normal=3.5-5g/dL).
Hyperlipidemia: Increased levels of lipid in the blood
Edema : pitting, pleural effusion, ascites, periorbital edema, scrotal edema, anasarca-
due to decreased oncotic pressure intravascularly; fluid shifting occurs thereafter from
intravascular to interstitial.
y Periorbital edema- noticeable when they wake up in the morning from head-
dependent position
SECONDARY SIGNS AND SYMPTOMS:
Skin becomes pale, stretched and taut as edema progresses
Anorexia/vomiting- due to increasing pressure in the stomach secondary to ascites
Difficulty of breathing- due to extensiveness of ascites
Hematuria at the onset of the disease- due to the ongoing inflammatory process
Foamy or frothy urine- one of noticeable signs when patient has proteinuria

NURSING INTERVENTIONS:
Monitor vital signs. It is a baseline for any interventions that will be initiated thereafter. BP
will decrease because of decreased hydrostatic pressure secondary to decreased blood flow. PR
will decrease, likewise. RR will increase in the attempt to compensate.
Collect a 24 hour urine specimen once a week, or as ordered by the physician. To
monitor protein losses.
Monitor weight daily. Weight is the most sensitive index to assess fluid volume in the body.
Assess skin, face, dependent areas of edema. Edema occurs primarily in dependent
tissues of the body. It will serve as a parameter the severity of fluid excess.
Record accurate intake and output of the patient. Accurate intake and output is
necessary for determining the renal function and fluid replacement needs and reducing risk of
fluid overload.
Regulate IV accordingly, esp. IV albumin. IV albumin is given to temporarily correct
hypoalbuminemia. Over/underinfusion would defeat our purpose of giving IV albumin.
indicated to decrease the edema.
Limit water to 800 mL/24 hours. Patients with kidney disorders or diseases are limited to
800 mL/24 hours due to their inability to filter.
Administer corticosteroids such as IV methylprednisolone or oral prednisone as
ordered by the physician. This is given to decrease the inflammatory response occurring in
the renal system. After initial four weeks of Prednisone administration, it is taken every other
day because it has the potential to halt growth and to suppress adrenal gland secretion.
Instruct the client to adhere in high protein and low sodium diet. High protein should
be advised to compensate with the massive loss of protein through urination. Low sodium is
SOURCES:
MATERNAL AND CHILD NURSING, Adele Pilliterri
Scribd.com
Medscape.net
Wikipedia.org
SAINT LOUIS UNIVERSITY
SCHOOL OF NURSING

NEPHROTIC SYNDROME
&
UROLITHIASIS

SUBMITTED BY.
ANTONIO, Auron Adrlunne R.
AOUINO, Renlshe Mlchuel
DEBAN, Juymur Frltz
DEZA, Cllfford John
GALLARDO, Colonel Lunz
GURION, Angelo
PAET, Loulegy
BUENDIA, Jhounnu Murlel
CLAVERIA, Mlkee Muun
COMPELIO, Aprll Joy
COSALAN, Cluudlne Murlunne
KOSALLAVATT, Alvln Ann
BSN III-K1
SUBMITTED TO.
SIR RHOEL ABUBO, RN