Case report

Nephrotic Syndrome
Preseptor : dr Ihsanil Husna, Sp.PD
Arranged by : Agung Dwi Saputro
(2011730118)

Patients identity
Name

: Ms. A

Age

: 27nd years old

Education

: Junior High school

Marital

status : Not Married

Occupation
Religion
Date
MR

: Shopkeeper
: Moslem

of admission

: 08 April 2016

number : 00930613

Anamnesis

Chief complaint :

Patient complained of swelling in the legs since 3 weeks ago.

Another complaint :

Body weakness, dizziness, decreased appetite, and there are

abrasions on both of her ankles.

History of present illness

Patients
come
to
the
hospital with complaints of
swelling in both legs since
three weeks ago. Swelling
felt arise gradually, initially
swelling occurs in the legs
and face when she wakes
up, then at noon swelling in
the face disappeared, but
the swelling in both legs still
have not disappeared, on
waking the patient feel a
little breathless, then after
that breathless disappeared.
The more swelling in her
legs getting bigger. Patients
admitted when pressed with
a finger in the second leg
swelling will form a concave.

Patients also complained of

decreased appetite, body
felt weak and a little
nauseous.
normal
defecated, urination 3 times
a day, a little frothy, no
pain, sand during urinary
and blood during urination.
There is no fever and no
vomiting.
There
were
abrasions on both her ankles
that arise 3 days ago..

History of past illness

Have

history of same problem 3

months ago.

No

history of Hypertension

No

history of DM

No

history of urinary or kidney disease

No

history of asthma

No

history of allergic

No

history of hematologic disease

History of family
None

of his family has same

problem

No

history of hypertension

No

history of DM

No

history of allergic

No

history of hematologic disease

History of allergy

Patient has no allergy to food, drugs

and weather.

History of treatment
When complaints swelling, which first
appeared in December 2016, the patient
went to the hospital and given
medication by a doctor, the patient drink
it regularly and diligently control to the
hospital every two weeks, then the
complaint is not there anymore.
When the control back in the patient not
to buy one of the drugs prescribed by the
doctor is ramipril. After 2 weeks,
complaints swelling reappeared in March
2016 until now.

Habits
Smoking

habits

: Denied

Drinking

alcohol

: Denied

Taking

any medication : patient was

consumed a herbal medicine to reduce
the swelling, but the swelling was not
reduced

Physical examination

Generalis
status
Vital
signs

General condition: Moderate ill

Conciusness: composmentis

blood pressure: 110/90 mmHg

Heart rate: 86x/minute
Respiratory rate: 20x/minute
Temperature : 36.6 C
Body weight : 65 kg
Body height : 160 cm
Index mass body : 25,6 (Obess I)

General
physical
examination

Thorax

Heart

Head : normocephal, deformity (-)

Faces : symmetric
Eyes : anemic conjungtiva (-/-), icteric sclera (-/-)
Mouth : the oral mucosa moist
Neck : not palpable mass, lymphadenopathy (-)

Inspection : the movement of the chest symmetrical

Palpation : same vocal fremitus in dextra and sinistra
Percussion : Sonor
Auscultation : vesicular breath sounds + / +, ronkhi - /
-, wheezing - / -

Inspection : ictus cordis not seen

Palpation : ictus cordis palpable in ICS 5
Percussion: margin left heart midclavicula ICS 5,
margin the right heart linea right parasternalis ICS 4
Auscultation : Regular 1st & 2nd heart sounds, murmur
(-), gallop (-)

Abdomen

Extremitie
s

Inspection: enlargement
Auscultation: bowel (+) sounds, 7x/minutes
Palpation: pressure pain (-), Ascites (-)
Percussion: timpani, shifting dullness (-)

Superior: Edema (- / -), warm akral(+ / +), RCT

<2 seconds (+ / +)
Inferior: Edema (+/ +), warm akral (+ / +), RCT
<2 seconds (+ / +)

Laboratory examination
(12th December 2015)
Examination

Value

Units

Normal

Kimia Klinik

Cholesterol

H 696

g/dL

13,2-17,3

Protein total

L 3.9

g/dL

6.0 8.0

Albumin
Ureum blood

L 1.3

g/dL

4.0 5.2

39

mg/dL

10-50

Kreatinin blood

1.1

mg/dL

< 1.4

Urinalisis

Color

Yellow

Purity

Sligty turbid

BJ

1.047

1.015 1.025

pH

7.0

Protein

Positive

4.8 7.4

Negative

(150mg/dl)
Glukosa

Negative

Negative

Keton

Positive 1 (5mg/dl)

Negative

Bilirubin

Negative

Urobilinogen

Normal

Negative
<1

Nitrit

Negative

Negative

Darah

Positive 1 (50/uL)

Negative

Leukosit

Negative

Negative

Sedimen

Eritosit

3-5

/lp

0-2

Leukosit

5-7

/lp

0-5

Epitel

15-20

/lp

5-15

Silinder

Negative

Kristal

Negative

Others

Bakteri (+)

Fungsi hati

SGOT

27

0-31

SGPT

26

0-35

Laboratory examination
(11th Maret 2016)
Examination

Value

Units

Normal

Profil Lemak

Cholesterol

734

mg/dL

< 200

Trigliserida

381

mg/dL

< 150

HDL

61

mg/dL

40 60

LDL

549

mg/dL

< 100

Ratio LDL/HDL

9.0

Cardio risk index (CRI)

<3 : low risk

3-5 : moderat
>5 : high risk

Urinalisis

Color

Yellow

Purity

Limpid

BJ

1,013

1,015 1,025

pH

5,0

4,8 7,4

Glukosa

Negative

Negative

Protein

Negative

Negative

Keton

Negative

Negative

Bilirubin

Negative

Negative

Urobilinogen

Normal

<1

Nitrit

Negative

Negative

Blood

Negative

Negative

Lekosit

Negative

Negative

Sedimen

Eritrosit

0-1

/lp

0-2

Lekosit

1-2

/lp

0-5

Epitel

1-2

/lp

5-15

Silinder

Smooth granule /lp

1-2
Kristal

Negative

Others

Negative

Resume
Ms. A, 27nd years old, came to the hospital with complaints of
swelling in both legs since three weeks ago. Swelling felt arise
gradually, initially swelling occurs in the legs and face when she
wakes up, then at noon swelling in the face disappeared, but the
swelling in both legs still have not disappeared, on waking the
patient feel a little breathless, then after that breathless
disappeared. The more swelling in her legs getting bigger.
Patients admitted when pressed with a finger in the second leg
swelling will form a concave. Patients also complained of
decreased appetite, body felt weak and a little nauseous.
urination 3 times a day, a little frothy. History of past illness :
have history of same problem 3 months ago.
Physical examination : Blood pressure: 110/90 mmHg, Heart
rate: 86x/minute, Respiratory rate: 20x/minute, Temperature :
36.6 C, Extremities Inferior : Edema (+/ +).
Laboratory
examination:

Lab examination :
11th Maret 2016

12th Desember 2015

Total Cholesterol : 696 mg/dL
(H), Total Protein : 3.9 g/dL (L),
Albumin

Urinalisis

1.3
;

d/dL

BJ

(L).

1,047,

Cholesterol : 734 mg/dL,

Triglisrida : 381 mg/dL,

Protein : Positive 2 (150mg/dl),

LDL : 549 mg/dL.

Keton : Positive 1 (5mg/dl),

Urinalisis ; protein :

blood

Positive

(50/uL).

Sediment ; Eritrosit : 3-5,

Lekosit : 5-7, Bakteri Positive

Positive 3 (500mg/dl),

Problem list

Edema

Proteinuria

Hipoalbuminema

Hiperkolesterolemia

Assesment
1. Nephrotic Syndrome
-

Edema
Proteinuria
Hipoalbuminema
Hiperkolesterolemia

2. Differential Diagnosis :
Glomerulonefritis akut

S : Patient complaints of swelling in both legs since three weeks ago,

Patients also complained of decreased appetite, body felt weak and
a little nauseous. urination 3 times a day, a little frothy.

O: Blood pressure: 110/90 mmHg, Heart rate: 86x/minute,

Respiratory rate: 20x/minute, Temperature : 36.6 C, Extremities
Inferior : Edema (+/ +).

Lab examination :
11th Maret 2016

12th Desember 2015

Total Cholesterol : 696 mg/dL
(H), Total Protein : 3.9 g/dL (L),
Albumin

Urinalisis

1.3
;

d/dL

BJ

(L).

1,047,

Cholesterol : 734 mg/dL,

Triglisrida : 381 mg/dL,

Protein : Positive 2 (150mg/dl),

LDL : 549 mg/dL.

Keton : Positive 1 (5mg/dl),

Urinalisis ; protein :

blood

Positive

(50/uL).

Sediment ; Eritrosit : 3-5,

Lekosit : 5-7, Bakteri Positive

Positive 3 (500mg/dl),

A: Nephrotik Syndrome
P: Laboratory :

Full peripheral blood

Total Protein

Ureum and creatinine blood

Urinalisis

USG Abdomen

Renal Biopsy

Therapy :

Bedrest until until the swelling disappears

Protein intake is restricted from 0.8 to 1 g / kg / day

Diet low in salt 2 grams / day and low-fat

Prednisone 5 mg full dose 3 x 8 tab

Furosemid 40 mg/day

Prognosis

Quo ad vitam

: bonam

Quo ad functionam

: dubia ad bonam

Quo ad sanationam

: dubia ad bonam

LITERATURE
REVIEW

Definition of Nephrotic Syndrome

Nephrotic syndrome is a set of clinical manifestations
characterized by

massive proteinuria (greater than 3.5 g / 1.73 m2

body surface area per day),

hypoalbuminemia (less than 3.5 g / dl),

edema,

hyperlipidemia ( >200) and lipiduria.

Anatomy of Renal
Renal parenchyma
composed of two
special areas: the
renal cortex which is
located on the outside
and looks granular, as
well as the inner
regions that form a
triangle striped (renal
pyramids), which are
collectively referred to
Each
Renalkidney
is bean-shaped
is composed
organ
of about
locatedone
on million
both sides
functional
of the units
vertebral
(the
as the renal medulla.
smallest
column. In
unit
general,
that islower
capable
thanofthe
forming
right kidney
urine) left
microscopic
kidney because
called
nephrons.
of the liver Each
and isnephron
closer to consists
the midline
of of
the
theBowman's
body. It is as
capsule
high asand
XII
capillary
thoracic vertebra,
glomerolus,
while
proximal
the upper
convoluted
pole of the
tubule,
left kidney
loop is
of located
Henle,
distal
as high
convoluted
as thoracictubules
vertebra
which
XI. empties into the collecting tubules.
Each kidney obtain blood supply from the renal artery.

The glomerulus is a dominant

part in the vascular
component of the nephron.
Under
normalfunction
The most
important
circumstances,
about
20%
of glomerolus is
formed
of plasmawhich
that went
into
ultrafiltrate
can fit
into
glomerolus
filtrated
with
a
the tubules due to capillary
net filtration
pressure
10
hydrostatic
pressure
greater
mmHg,
produces filtration
than
the hydrostatic
pressure
rate
glomerolus
average
intrakapiler and colloid
(GFR)
of 125pressure.
mL / min. As
osmotic
the
filtrate
flows
The
layers
of through
the membrane to function as molecular sieves
the tubules,holding
added or
glomerolus
red blood cells and plasma proteins, but skip
taken
substances
H2Ovarious
and other
solute molecular size is quite small. Although
from
the proteins
filtrate, so
that
plasma
can
not be filtered because it can not pass through
eventually
about
1.5 the pore itself is large enough to pass the
the poresonly
from
above,
L / day is
excreted
as which is the smallest.
plasma
protein
albumin
urine.

Physiology of
Glomerulus

Epidemiology

Incidence may affect all ages but most (74%) was found at
the age of 2-7 years. The ratio of male: female = 2: 1,
whereas in adolescence and adulthood this ratio ranges
from 1: 1. Usually 1 of 4 patients with nephrotic syndrome
are patients with age> 60 years. But in exact incidence
and prevalence of nephrotic syndrome in geriatrics is not
known because often misdiagnosed.

Etiology
Primary
glomerulonephritis
with an unknown cause
(idiopathic) with a wide
variety of
histopathological
abnormalities, include:
minimal lesion
glomerulonephritis
focal
glomerulosclerosis
membranous
glomerulonephritis
glomerulonephritis
membranoproliferative
the other proliferative
glomerulonephritis

Glomerulonephritis secondary to:

infections, such as HIV infection,
hapatitis virus B and C, syphilis,
malaria, Schistosomal,
tuberculosis, and leprosy.
Malignancy, such as
adenocarcinoma of the lung,
breast, colon, Hodgkin's
lymphoma, multiple myeloma, and
renal carcinoma.
connective tissue diseases, such as
systemic lupus erythematosus,
rheumatoid arthritis, MCTD (mixed
connective tissue disease)
The effects of drugs and toxins,
such as non-steroidal antiinflammatory drugs, gold
preparations, penicillamine,
probenecid, mercury, captopril, and
heroin.
Other, including diabetes mellitus,
amyloidosis, pre-eclampsia, chronic
allograft rejection, vesicoureteric
reflux, or a bee sting.

Clinical Manifestations
Proteinuria
Proteinuria due to increased capillary permeability to proteins
from damage glomerolus. In nomal circumstances basement
membrane barrier glomerolus have a mechanism to prevent
the leakage of protein. The first barrier mechanism based on
molecular size (size barrier) and the second by an electric
charge (charge barrier). In nephrotic syndrome, both
mechanisms involved subject. In addition, the configuration of
the protein molecules also determine whether or not the
protein passes through the basement membrane glomerolus.

Hypoalbuminemia
Plasma albumin concentration is determined by the intake of
protein, albumin synthesis of the liver, and loss of albumin in
the urine. In nephrotic syndrome, hypoalbuminemia caused
by the loss of albumin in urine and increased catabolism of
albumin in the kidney

Clinical Manifestations
Hyperlipidemia

EDEMA
Edema inlevels
nephrotic
syndrome
can bewhile
explained
Cholesterol
generally
increased,
triglycerides
theorytoof slightly
underfillelevated.
and overfill.
Underfill due to
varies with
from the
normal
Increased
theory
thatlevels.
hypoalbuminemia
causeslevels
a
increased
LDL explains
cholesterol
High triglyceride
are
decrease
plasma oncotic
pressure
so increase
that the in IDL
associated
with in
increased
VLDL. Also
found
fluid shiftdensity
from thelipoprotein)
intravascular
to the
interstitial(Lp) a,
(intermediate
and
lipoprotein
and to
edema.
As a result
whereastissue
HDL tend
be normal
or low of
. a decrease in
plasma oncotic pressure and plasma fluid shifts
occur hypovolemia.
compensate
by
This situation
is due to Kidneys
increased
lipid synthesis
in the
sodium
and water
The(decrease
liver andincreasing
decreased
catabolism
in retention.
peripheral
mechanism
will improve
lipoprotein, compensation
VLDL, intermediate
density
lipoproteins and
intravascular
volume,
but also
exacerbates
the
chylomicrons
from the
blood).
Increased
lipoprotein
lipid
of hypoalbuminemia
so edema
synthesis occurrence
is stimulated
by a decrease in serum
albumin and
increasingly continue.
decrease in oncotic pressure.

DIAGNOSIS
Anamnesis
Supporting
investigation

It should ofbe
noted
the problem
of drug
use, the
Examination
urine,
including
urine protein,
urinalysis,
possibility
various
infections,
and and
the sediment
history of
hamaturia,
dipstickof
urine
specific
gravity of urine
other systemic
examination.
Volume is diseases.
usually less than 400 ml / 24 hours.
Blood tests, including serum albumin, serum cholesterol,
Physical
triglycerides,
hemoglobin,
hematocrit, erythrocyte sedimentation
examination
rate (ESR), and serum electrolytes.

There anasarca edema. Not infrequently eyes closed

due toand
edema
the eyelids.
Serology
renalof
biopsy
is often needed to confirm the

diagnosis and rule out possible causes of nephrotic syndrome

secondary. Serology is often not a lot of information and it is
expensive because it should only be done by a strong indication.

Treatment
Some definitions / limitations used in SN :

Remission: negative or trace proteinuria (proteinuria <4 mg / m2 LPB /

h) 3 consecutive days in one week

Relapse: 2+ proteinuria (proteinuria 40 mg / m2 LPB / h) 3

consecutive days in the first week 3

Relapse rare: relapses occurred less than two times in the first 6 months
after the initial response to or less than 4 times per year of observation

Relapses often (frequent relapses): relapses occurred 2 times in the

first 6 months after the initial response or 4 times in a period of 1
year

Dependent steroids relapses occurred during steroid doses lowered or

within 14 days after treatment was stopped, and this occurs two times
in a row

Steroid Resistant: no remission in the treatment of full-dose prednisone

(full dose) 2 mg / kg / day for 4 weeks.

Non Pharmacology
Diet for patients with nephrotic syndrome is 35 cal / kg /
day, consisting mostly of carbohydrates. Proteinuria may
improve hypoalbuminemia control and reduce the risk of
complications caused. Normal protein diet recommended 0.81.0 g / kg / day. In patients with dietary protein 0.6 g / kg / day
plus the number of grams of protein according to the number
Proteinuri result Proteinuri reduced, increased blood levels of
albumin and fibrinogen levels decreased. To reduce edema
given a low salt diet (1-2 grams of sodium / day) along with
diuretics and bedrest.

Pharmacology
CORTICOSTEROIDS
Minimal lesion nephropathy and membranous
nephropathy are two disorders that respond well to
steroid therapy. Other researchers have found that
focal segmental glomerulosclerosis up to 40% of
patients respond well to steroids with a complete
remission. In most patients with idiopathic
membranous nephropathy, symptomatic therapy
with better kidney function for a longer period and
can heal spontaneously.

Figure 1. The initial treatment with

corticosteroids

Information:
The full dose prednisone (full dose)
60 mg / mLPB / day (2mg / kg /
day) divided into 3 doses given
daily for 4 weeks, followed by
prednisone 40 mg / mLPB / day
(2/3
full
dose),
can
given
intermittently (3 consecutive days
in the first week) or alternating
(every other day) for 4 weeks.

When remission occurs within

the first 4 weeks, then
intermittent
prednisone
/
alternating 40 mg / mLPB /
day administered for 4 weeks.
When remission does not occur
in the first 4 weeks, then the
patient is diagnosed as a
steroid-resistant
nephrotic
syndrome.

Figure 2. Treatment of nephrotic syndrome relapse

Information:
Prednisone full dose every day until remission (maximum
of 4 weeks) followed by intermittent prednisone /
alternating 40 mg / mLPB / day for 4 weeks.
When you get a full dose treatment for 4 weeks did not
also occur revision, the patient was diagnosed as a steroidresistant SN and should be given other immunosuppressive
therapy

Figure 3.
Treatment of
nephrotic syndrome
relapsed frequently

Information:
Full dose prednisone daily until remission (maximum of 4 weeks)
followed by intermittent prednisone / alternating 40 mg / mLPB / day
and immunosuppressive / oral cytostatic (cyclophosphamide 2-3 mg /
kg / day) dose for 8 weeks


Information:

Prednisone full Monitoring

dose everyofday
until remission
(maximum 4 weeks),
Hb,day
leukocytes,
platelets
Or, Prednisone full dose every
until remission
(maximum of 4
followed by cyclophosphamide
puls
with
a
dose
of 500-750 mg /
every
weeks) , followed
by week
oral cyclophosphamide 2-3 mg / kg / day dose for
mLPB given byLeukocytes
infusion once
a month
6 consecutive months and
<3000
/ ml 40
for
CPA
12 weeks and alternating prednisone
mg / mLPB.hari for 12 weeks.
intermittent prednisone
/ alternating 40 mg / mLPB for 12 Sunday.
first
Then tapering stopped
off prednisone
at a dose of 1 mg / kg / day for 1 month,
Then tapering off
prednisone
at
a dose
of 1 mg / kg / day for 1 month,
5000
followed by 0.5Leukocytes>
mg / kg / day
for 1/ ml
monthCPA
(long tapering off: 2 months)
followed by 0.5
mg / kg
/ day for 1 month (long tapering off: 2
awarded
again
months)
Figure 4. The treatment of steroid dependent nephrotic
syndrome

Figure 5.
Treatment
of steroidresistant
nephrotic
syndrome.

Information:
Or,
oral Cyclophosphamide
cytostatic: cyclophosphamide
mg /of
kg500-750
/ day dose
puls with 2-3
a dose
mgfor/ 3-6
mLPB
months
dibertikan
via intravenous infusion once a month for six months,
may
Prednisone
dose ofdepending
40 mg / mLPB
/ alternating
days during
be continued
on the
patient's condition.
Prednisone
administration
of oral cyclophosphamide.
alternating
doses of 40 mg / mLPB / day during
administration
Then prednisonofincyclophosphamide
tapering-off with apuls
dose(5ofmonths).
1 mg / kg
/ day
for 1
Then
tapering
month,
followed
0.5 mg
1 month
(long tapering
off
prednisone
atby
a dose
of /1kg
mg/ day
/ kg for
/ day
for 1 month,
followedoff
by
2 months).
0.5
mg / kg / day for 1 month (long tapering off 2 months).

Pharmacology
ACE inhibitors and
angiotensin receptor blockers
In patients who are not responsive to corticosteroids, to reduce
Proteinuri used symptomatic therapy with angiotensin converting
enzyme inhibitors (ACEI), for example, captopril or enalapril low doses,
and the dose is increased after 2 weeks, or anti-inflammatory drugs
non-steroidal (NSAIDs), such as indomethacin.
Antiproteinurik effect of this drug lasts longer (approximately two
months after the drug is stopped). Angiotensin receptor blockers
(ARBs) were also able to improve Proteinuri because it inhibits
inflammation and interstitial fibrosis, inhibiting the release of cytokines,
growth factors, adhesion molecules occupational local angiotensin II in
the kidneys.

Pharmacology
Non-steroidal anti-inflammatory
drugs (NSAIDs)

may be used in patients with membranous nephropathy and

focal segmental glomerulosclerosis to decrease the
synthesis of prostaglandins. It causes renal vasoconstriction,
decreased glomerular capillary pressure, filtration surface
area and reduces proteinuria to 75%. Besides NSAIDs can
reduce the levels of fibrinogen, fibrin-related antigenic and
prevent platelet aggregation. However, please note that
NSAIDs cause a progressive decline in kidney function in
some patients. This drug should not be given if creatinine
clearance <50 ml / min.

Pharmacology
Cyclophosphamide and Chlorambucil

In patients with frequent relapses with corticosteroids or

corticosteroid resistant to other therapies may be used with
cyclophosphamide or chlorambucil. Cyclophosphamide give
remission longer than corticosteroids (75% over 2 years) at
a dose of 2-3 mg / kg / day for 8 weeks. The side effects of
cyclophosphamide is bone marrow depression, infections,
alopecia, hemorrhagic cystitis and infertility when given
over 6 months. Chlorambucil given at a dose of 0.1-0.2 mg /
kg / day for 8 weeks.

Pharmacology
Cyclosporine

Cyclosporine A may be tried in patients who

relapsed after being given cyclophosphamide or
to extend the period of remission after
corticosteroid administration. A dose of 3-5 mg /
kg / day for 6 months to 1 year (after 6 months
the dose reduced by 25% every 2 months).
Cyclosporine A may also be used in
combination with prednisolone at the failed
cases of nephrotic syndrome in combination
with other therapies.

Pharmacology
DIURETICS

To reduce edema diuretics (furosemide 40 mg / day or class

thiazides) with or without combination with potassiumsparing diuretics (spironolactone).

In patients with nephrotic syndrome can occur resistance to

diuretics (furosemide 500 mg and 200 mg spironolactone).
Resistance to this diuretic is multifactorial. Suspected
hipoalbuminemi cause a reduction in drug transport to the
workplace, while binding by urinary protein is not the main
mechanism of this resistance.
This therapy may increase plasma volume, increases in
glomerular filtration rate, urine flow, and sodium excretion.
However, albumin infusion is still doubt its effectiveness because
albumin rapidly excreted through urine, but it can increase blood
pressure and even pulmonary edema in patients hypervolemi.

Pharmacology
Anticoagulants

Risk of thromboembolism is increased in nephrotic syndrome

and the need to get treatment. Although the long-term
administration is still controversial, but in one study proved
beneficial. To prevent complications hypercoagulable namely
thromboembolism occurring in approximately 20% of cases of
nephrotic syndrome (most often in membranous nephropathy),
used dipyridamole (3 x 75 mg) or aspirin (100 mg / day) as an
anti-platelet aggregation and deposition of fibrin / thrombus.

Complication

Infection

Hipogamaglobulinemi, particularly immunoglobulin G (IgG), together

with factors B causes nephrotic syndrome sufferers are highly
susceptible to infection. Much more use of corticosteroids which we
know as immunosuppression, susceptibility to infection is greater.

Thrombosis

Thrombosis can occur in veins and arteries, especially the large vein
in the liver, pelvis, renal, mesenteric and pulmonary.

Acute Renal Failure

The cause of ARF is not known for sure, but there is evidence
involving hypovolemia and renal ischemia resulting in acute tubular
necrosis, interstitial edema and elevation of pressure occurs in
proximal tubules with consequent reduction in filtration rate
glomelurus.

Prognosis

Mortality and the prognosis of patients with nephrotic

syndrome varies by etiology, severe, extensive
damage to the kidneys, the child's age, the underlying
condition, and response to treatment

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