NEPHROTIC SYNDROME

I. INTRODUCTION
Nephrotic syndrome is primarily a pediatric disorder and is 15 times more
common in children than adults. The characteristic features of nephrotic syndrome
are heavy proteinuria ( >3.5 gr/24hours in adults or 40mg/m2/hour in children),
hypoalbuminemia (<2.5gr/dL), edema, and hyperlipidemia1
The incidence is 23/100,000 children per year, and the vast majority of
affected children will have steroid-sensitive minimal change disease. Most
children (90%) with nephrotic syndrome have a form of the idiopathic nephrotic
syndrome. Causes of idiopathic nephrotic syndrome include minimal change
disease (85%), mesangial proliferation (5%), and focal segmental
glomerulosclerosis (10%). The remaining 10% of children with nephrotic
syndrome have secondary nephrotic syndrome related to glomerular diseases such
as membranous nephropathy or membranoproliferative glomerulonephritis. 1 There
is epidemiological evidence of a higher incidence of nephrotic syndrome in
children from south Asia.2

Picture 1. The normal structure of glomerulus

Picture 2. Average ages of types of nephrotic syndrome

The cause of the condition is unknown, but a few cases are secondary to
systemic diseases such as Henoch-Schonlein purpura, and other vasculitides, e.g.
systemic lupus erithematosus (SLE), infections (e.g. malaria) or allergens (e.g.
bee sting).3
The etiology of nephrotic syndrome is divided into congenital, primary
nephrotic syndrome (idiopathic), and secondary nephrotic syndrome.4
The underlying abnormality in nephrotic syndrome is an increase in
permeability of the glomerular capillary wall, which leads to massive proteinuria
and hypoalbuminemia. The cause of the increased permeability is not well
understood. In minimal change disease, it is possible that T-cell dysfunction leads
to alteration of cytokines, which causes a loss of negatively charged glycoproteins
within the glomerular capillary wall.
In focal segmental glomerulosclerosis, a plasma factor, perhaps produced
by lymphocytes, may be responsible for the increase in capillary wall
permeability.
Although the mechanism of edema formation in nephrotic syndrome is
incompletely understood, it seems likely that, in most instances, urinary protein
loss leads to hypoalbuminemia, which causes a decrease in the plasma oncotic
pressure and transudation of fluid from the intravascular compartment to the
interstitial space. The reduction in intravascular volume decreases renal perfusion
pressure, activating the renin-angiotensin-aldosterone system, which stimulates
tubular reabsorption of sodium. The reduced intravascular volume also stimulates
the release of antidiuretic hormone, which enhances the reabsorption of water in
the collecting duct. Because of the decreased plasma oncotic pressure, fluid shifts
into the interstitial space, exacerbating the edema.
This theory does not apply to all patients with nephrotic syndrome,
however, because some patients actually have increased intravascular volume
with diminished plasma levels of renin and aldosterone. Therefore, other factors,

including a primary renal avidity for sodium and water, may be involved in the
formation of edema in some patients with nephrotic syndrome.
In the nephrotic state, serum lipid levels (cholesterol, triglycerides) are
elevated for two reasons. Hypoalbuminemia stimulates generalized hepatic
protein synthesis, including synthesis of lipoproteins. In addition, lipid catabolism
is diminished, as a result of reduced plasma levels of lipoprotein lipase, related to
increased urinary losses of this enzyme.1

Picture 3. The pathogenesis of nephrotic syndrome

Overview of pathophysiology of edema formation in nephrotic syndrome.

Massive proteinuria induces tubulointerstitial inflammatory infiltrate with
stimulation of vasoconstrictive mediators (angiotensin II) and inhibition of
vasodilatory substances (e.g., nitric oxide). In the glomeruli, proteinuria causes a
reduction in glomerular ultrafiltration coefficient (Kf) and single nephron
glomerular filtration rate (SNGFR). As a consequence, there is a net increase in
tubular reabsorption and a reduction in filtered sodium load that result in primary
sodium retention and a tendency to "overfilled" intravascular volume and
increased capillary hydrostatic pressure (PC). The decrease in plasma oncotic
pressure (PCOP) favors fluid movement outwards from the vascular compartment
and thereby buffers the changes in blood volume induced by primary sodium
retention. If hypoalbuminemia is severe and renal inflammatory infiltrate is
minimal or absent, as in most children with minimal-change nephrotic syndrome
(MCNS), the reduction in PCOP may cause "underfilled" intravascular volume and
secondary (compensatory) sodium retention. Nephrotic edema results when
edema-removal mechanisms are overwhelmed by increased P C and decreased
PCOP.5
Classification of nephrotic syndrome is divided to:
1) Steroid-sensitive nephrotic syndrome
In 85-90% children with nephrotic syndrome, the proteinuria resolves with
corticosteroid therapy ( steroid sensitive nephrotic syndrome ). These children
do not progress to renal failure. It is commoner in boys than in girls. In Asian

children than in Caucasians and there is a weak association with atopy. It is

often precipitated by respiratory infections. Features suggesting steroidsensitive nephrotic syndrome are:
-

Age between 1 and 10 years

No macroscopic hematuria
Normal blood pressure
Normal complement levels
Normal renal function

2) Steroid-resistant nephrotic syndrome

These children should be referred to a pediatric nephrologist. Management of
the oedema is by diuretic therapy, salt restriction, ACE inhibitors, and
sometimes NSAIDs, which may reduce proteinuria.
3) Congenital nephrotic syndrome
Congenital nephrotic syndrome presents in the first 3 months of life. It is rare.
The commonest kind is recssively inherited and the gene frequency is
particularly high in Finns. It is associated with a high mortality, usually due to
complications of hypalbuminemia rather than renal failure. The albuminuria is
so severe that bilateral nephroctomy may be necessary for its control,
inevitably precipitating the need for dialysis, which is then continued until the
child is large and fit enough for renal transplantation.3
Clinical manifestations:
-

Periorbital oedema (particularly on waking). It is the earliest sign.

Scrotal or vulval, leg, and ankle oedema
Ascites
Breathlessness due to pleural effusions and abdominal distension.3

Diagnosis:
1) Urine protein on test strips (dipstick) or quantitative urine protein/24 hours or
protein/creatinine ratio on morning urine
2) Full blood count and ESR
3) Urea, electrolytes, creatinine, albumin
4) Complement levels (C3, C4)
5) ASTO ( antistreptolysin O titre) and throat swab
6) Urin microscopy and culture
7) Urinary sodium concentration
8) Hepatitis B antigen3,4
INITIAL LABORATORY EVALUATION
Urine
Urine deposits
Transient microscopic hematuria is found in 23% patients with steroid sensitive
MCD.1 Persistence of microscopic hematuria is more indicative of FSGS but this
should not be used to discriminate between the two. The presence of macroscopic
hematuria is suggestive of more aggressive forms of glomerulonephritis.
Urine protein
The ISKDC definition of NS in children is proteinuria greater than 40
mg/m2/hour in an overnight specimen of urine, which is equivalent to 1.7 g/24
hours in adults. Some experts suggest that nephrotic range proteinuria be defined
as greater than 100 mg/m2/hour.18 Timed urine collections in children can be
cumbersome and urine protein : creatinine or albumin : creatinine (UAlb : UCr )
ratios provide a convenient approximation. UAlb : UCr of 400 mg/mmol (3.5
mg/mg) or urine protein : creatinine ratio of 200 mg/mmol (1.8 mg/mg) indicate
nephritic range proteinuria.
Urine sodium
Measurement of the urinary sodium concentration is avaluable tool for the
diagnosis of suspected hypovolemia, which leads to renal sodium retention. A
urinary sodium value less than 10 mEq/l is diagnostic of intravascular volume
contraction, while a value above 20 mEq/l makes it unlikely. However, this is not
applicable if the child has received potent diuretics such as frusemide.
Blood Investigations
Proteins
Hypoalbuminemia (< 25 g/dL) is essential for the diagnosis of nephrotic
syndrome. IgG levels were also reduced, but to a lesser degree than the albumin,
and IgM is usually elevated. Plasma complement proteins, namely the C3 and C4
fractions are usually not altered, which help to differentiate SSNS from other
forms of NS.
Lipids

Total plasma cholesterol, low-density and very lowdensity lipoproteins are grossly
elevated, while highdensity lipoproteins remain within the normal range.
Creatinine, urea and electrolytes
Plasma creatinine and urea concentrations are usually normal at presentation in
SSNS, but mild to moderate increases may result from hypovolemia and renal
underperfusion. Plasma electrolytes too are usually normal at presentation but
hyponatremia is occasionally seen as a complication of hypovolemia. If the
plasma volume is contracted, then anti-diuretic hormone is secreted in response to
the baroreceptor stimulation leading to water retention and dilutional
hyponatremia.
Calcium
The total plasma calcium concentration is low in parallel to the reduction of
albumin level as it is partly albumin bound. However, the ionized calcium
concentration is normal and it is not necessary to treat the low total calcium
concentration that eventually returns to normal with normalization of albumin
concentration.6

Treatment:
Pharmacology
Oral corticosteroids form the cornerstone for management of most
children with nephrotic syndrome.2

Children with the first episode of nephrotic syndrome and mild to

moderate edema may be managed as outpatients. Affected children may attend
school and participate in physical activities as tolerated. The pathophysiology and
treatment of nephrotic syndrome should be carefully reviewed with the family to
enhance their understanding of their child's disease. Sodium intake should be
reduced by the initiation of a low sodium diet and may be normalized when the
child enters remission. Although there are no data to support their safety or

efficacy, oral diuretics are used by many clinicians for children with nephrotic
syndrome. Because of the possibility of increasing the risk of thromboembolic
complications, diuretic use should be judicious and should be carefully supervised
by a pediatric nephrologist.
Children with severe symptomatic edema, including large pleural
effusions, ascites, or severe genital edema, should be hospitalized. In addition to
sodium restriction, fluid restriction may be necessary if the child is hyponatremic.
A swollen scrotum may be elevated with pillows to enhance the removal of fluid
by gravity. Diuresis may be augmented by intravenous administration of
chlorothiazide (10 mg/kg/dose every 12 hr) or metolazone (0.1 mg/kg/dose bid)
followed by furosemide 30 min later (12 mg/kg/dose q 12 hr). Intravenous
administration of 25% human albumin (0.5 g/ kg/12 hr) is often necessary when
this potent combination is used. Such therapy mandates close monitoring of
volume status, serum electrolyte balance, and renal function. Symptomatic
volume overload, with hypertension and heart failure, is a potential complication
of parenteral albumin therapy.
Children with onset of nephrotic syndrome between 1 and 8 yr of age are
likely to have steroid-responsive minimal change disease; therefore, steroid
therapy may be initiated without renal biopsy. Children with features that make
minimal change disease less likely (hematuria, hypertension, renal insufficiency,
hypocomplementemia, age < 1 yr or > 8 yr) should be considered for renal biopsy
before treatment.
In children with presumed minimal change disease, prednisone should be
administered (after confirming a negative PPD test) at a dose of 60 mg/m 2/day
(maximum daily dose, 80 mg), divided into two to three doses for at least 4
consecutive weeks. There is some evidence that an initial 6 wk course of daily
steroid treatment may lead to a lower relapse rate, although the frequency of
steroid-induced side effects is significantly higher. Eighty to 90% of children will
respond to steroid therapy (urine trace or negative for protein for 3 consecutive
days), with the median time to remission of 10 days. The vast majority of children
who will respond to prednisone therapy will do so within the first 4 wk of
treatment.
After the initial 46 wk course, the prednisone dose should be tapered to 40
mg/m2/day given every other day as a single morning dose. The alternate-day dose
is then slowly tapered and discontinued over the next 23 months. Children who
continue to have proteinuria (2+ or greater) after 8 wk of steroid therapy are
considered steroid resistant, and a diagnostic renal biopsy should be performed.
Many children with nephrotic syndrome will experience at least one
relapse (34+ proteinuria plus edema). Although relapse rates of 6080% have
been noted in the past, the relapse rate in children treated with longer initial
steroid courses may be as low as 3040%.
Relapses should be treated with daily divided-dose prednisone at the doses noted
earlier until the child enters remission (urine trace or negative for protein for 3
consecutive days). The prednisone dose is then changed to alternate-day dosing
and tapered over 12 mo.

A subset of patients will relapse while on alternate-day steroid therapy or

within 28 days of stopping prednisone therapy. Such patients are termed steroid
dependent. Patients who respond well to prednisone therapy but relapse four or
more times in a 12-mo period are termed frequent relapsers. Children who fail to
respond to prednisone therapy within 8 wk are termed steroid resistant.
Steroid-dependent patients, frequent relapsers, and steroid- resistant
patients may be candidates for alternative agents, particularly if the child suffers
severe corticosteroid toxicity (cushingoid appearance, hypertension, cataracts,
and/or growth failure). Cyclophosphamide has been shown to prolong the
duration of remission and to reduce the number relapses in children with
frequently relapsing and steroid-dependent nephrotic syndrome. The potential side
effects of the drug (neutropenia, disseminated varicella, hemorrhagic cystitis,
alopecia, sterility, and increased risk of future malignancy) should be carefully
reviewed with the family before initiating treatment. The dose of
cyclophosphamide is 23 mg/kgBW/24hr given as a single dose, for a total
duration of 812 weeks. Alternate-day prednisone therapy is often continued
during the course of cyclophosphamide administration. During cyclophosphamide
therapy, the white blood cell count must be monitored weekly and the drug
withheld if the count falls below 5,000/mm3.
An additional option for the child with complicated nephrotic syndrome is
high-dose pulse methylprednisolone. Methylprednisolone is usually given as a 30mg/kg bolus (maximum 1,000 mg), with the first 6 doses given every other day,
followed by a tapering regimen for periods up to 18 mo. Cyclophosphamide may
be added to this regimen in selected patients.
Prolonged administration of cyclosporine (36 mg/kgBW/24 hr) has also
been effective in maintaining a prolonged remission in children with nephrotic
syndrome and is useful as a steroid- sparing agent. Children must be monitored
for side effects, including hypertension, nephrotoxicity, hirsutism, and gingival
hyperplasia. Unfortunately, most children who respond to cyclosporine therapy
tend to relapse when the medication is discontinued.
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-II
blockers may be helpful as an adjunct therapy to reduce proteinuria in steroidresistant patients.2
Diet
In the past, both low and high protein diets have been recommended for SSNS. A
low protein diet reduces albuminuria but increases the risk of malnutrition.Animal
studies show that high protein diets increase the synthesis of albumin, but do not
increase the albumin concentration or growth significantly. Based on current
evidence, no specific dietary advice is necessary for uncomplicated cases of
SSNS. Modest salt restriction is beneficial during severe relapses, especially in
patients with edema.6
Activity
All efforts should be taken to actively mobilize the child; bed rest should be
avoided if possible to minimize the risk of thrombosis.6

Immunizations
All killed vaccines are generally regarded as safe for administration when a child
is in remission. However, relapses are noted to cluster following meningococcal C
conjugate vaccination program in the United Kingdom. Caution should be
exercised and parents counseled regarding the risk of relapse before administering
this vaccine. All live vaccinations should be avoided until children are off daily
steroids for at least 6 weeks. Additionally, they should be avoided where
cyclophosphamide or cyclosporine A therapy has been initiated. 6
Complications:
The chief complication of nephrotic syndrome is infection, followed by
thromboembolic events. Hypertension, hyperlipidaemia, features of corticosteroid
toxicity and behavioural disorders are less frequent.2
Infections:
Increased predisposition to infections occurs due to loss of
immunoglobulins, complement and properdin, altered T cell functions,
immunosuppressive therapy and presence of oedema. Of the severe infections,
peritonitis has an incidence of 2-6%. Other common infections are cellulitis,
pneumonias and upper respiratory tract viral infections. Varicella and
pneumococcal vaccination is recommended for all children with nephrotic
syndrome once they are in remission and off steroid therapy.2
Thromboembolism:
Patients with nephrotic syndrome are at an increased risk (2-8%) for
venous and arterial thrombosis, though the overall risk is lower compared to
adults. Additional predisposing factors including volume depletion, infections,
diuretic use, venepuncture and immobilization aggravate the risk.2
A hypercoagulable state, due to urinary losses of antithrombin,
thrombocytosis which may be exacerbated by steroid therapy, increased synthesisi
of clotting factors and increased blood viscosity from the raised haematocrit,
predisposes to thrombosis. This is usually arterial and may effect the brain, limbs
and sphlancnic circulation with potentially catastrophic results.3
Hyperlipidaemia:
Hyperlipidaemia in most patients with steroid-sensitive nephrotic
syndrome is transient and does not have long-term implications. However, raised
blood levels of lipids may persist in patients with SRNS and potentially contribute
to cardiovascular morbidity and progression of glomerulosclerosis Patients are
encouraged to achieve a normal weight for height; diet should be restricted in
saturated fats.2

Osteoporosis:

The risk of steroid-induced osteoporosis has significant long-term

implications. Based on the available evidence, it seems reasonable to provide
calcium supplements to patients with frequent relapses, steroid dependence or
resistance who are likely to receive long term therapy with corticosteroids.2
Hypovolemia:
During the initial phase of oedema formation, the intravascular
compartment may become volume depleted. The child who becomes
hypovolaemic characteristically complains of abdominal pain and may feel paint.
There is peripheral vasocontriction and urinary sodium retention. A low urinary
sodium (<20 mmol/L) and a high packed red cell volume are indications of
hypovolaemia, which requires urgent treatment with intravenous albumin as the
child is at risk of vascular thrombosis and shock. Increasing peripheral oedema,
assessed clinically and by daily weight, may cause discomfort and respiratory
compromise. If severe, this may need tereatment with intravenous albumin. Care
must be taken with colloid, as it may precipitate pulmonary oedema and
hypertension from fluid overload, and also with diuretics, which may cause or
worsen hypovolaemia.3
Prognosis:
The most important factor that determines prognosis in children with
nephritic syndrome is steroid responsiveness. While more than 70% of children
with steroid-sensitive nephrotic syndrome relapse and almost 50% have frequent
relapses or steroid dependence, their risk of progression to chronic renal failure is
minimal. The majority of children with steroid-responsive nephrotic syndrome
have repeated relapses, which generally decrease in frequency as the child grows
older.
Although there is no proven way to predict an individual child's course,
those children who respond to steroids rapidly and those who have no relapses
during the first 6 months after diagnosis tend to follow an infrequently relapsing
course. It is important to indicate to the family that the child with steroidresponsive nephrotic syndrome will not develop chronic renal failure, that the
disease is generally not hereditary, and that the child (in the absence of prolonged
cyclophosphamide therapy) will remain fertile. To minimize the psychological
effects of the condition, the physician should emphasize that the child should be
considered normal when in remission and may have unrestricted diet and activity,
without the need for urine testing for protein.
Children with steroid-resistant nephrotic syndrome, most often caused by
focal segmental glomerulosclerosis, generally have a much poorer prognosis.
These children develop progressive renal insufficiency, ultimately leading to endstage renal failure requiring dialysis or renal transplantation. Recurrent nephrotic
syndrome develops in 3050% of transplant recipients with focal segmental
glomerulosclerosis. Plasmapheresis, plasma protein absorption onto protein A
based columns, high-dose cyclosporine or tacrolimus, and angiotensin-converting
enzyme (ACE) inhibitors may reduce proteinuria in these patients.1
II. OBJECTIVE

The aim of doing this paper is to report a case of nephrotic syndrome in a 13year-old boy.
III.CASE
AP, male, 13 years old, weight is 72 kg, height is124 cm. was admitted to
the non-infection unit of H.Adam Malik General Hospital on 14th Mei 2010 at
17.30 WIB. Chief complaint was full body oedema. This condition had occurred
for 2 month. Oedema begin at both of lower extrimities, then to abdomen and
face. Increased of body weight since 3 months, from 58 kg up to 72 kg.
History of meat-washed color urine was positive since 2 weeks
ago.Urinary pain was negative, sandy urine was negative. Last defecation was 3
hours before arrive to RSUP HAM. History of recurrent fever was negative. Easy
fatigue when doing activities was negatve, cyanosis was negative. Cough was
positive since 2 months ago, sputum was negative. History of contact with chronic
cough patient was not confirmed. History of dysphagia was positive since 1 day,
no vomiting, no nausea, and no diarhea. History of previous disease was
negative. History of drug use was negative.

Physical Examination
Generalized Status
Sens : Compos mentis. Temperature : 36,5 C.
anemia (-), dyspnea (-), edema (+), cyanosis (-), icteric (-).
Localized Status
Head
: Eye: light reflex +/+, pupil isocor right = left, pale inferior
conjungtiva palpebra -/-, oedem papebra (+)
Ear / nose= within normal limits.
Mouth: tonsil T2-T2 hyperemis.
Neck
: Lymph node enlargement (-),
Thorax
: Fusiformed symmetrical, retraction (-)
HR = 110 bpm, regular, murmur (-)
RR = 20 tpm, regular, rales (-).
Abdomen : Shifting dullness (+), ascites (+), peristaltic (+) N, sleeping abdomen
circumference = 98cm, sitting abdomen circumference = 102 cm
Liver / spleen = difficult to be measured
Extremity : Pulse 110 bpm, regular, Pressure/ Volume = adequate, blood
pressure = 120/90 mmHg, pitting oedema (+).
Genital
: Male, oedem in scrotum (+)

Differential Diagnosis

Nephrotic Syndrome
Acute Glomerulonephritis
Working Diagnosis.
Nephrotic syndrome
Management
Inj. Ceftriaxone 1 gr/12 hr/IV
Inj. Furosemide 20 mg/8 hr/IV
Aldactone 3x 25 mg tab
Captopril 2x12,5 mg tab
Diet low salt
Investigation plan.
C3
ASTO/CRP
Serum Protein Elektrophoresis
Daily Urinalysis
Culture Urine and Sensitivity Test
Daily Feces
Lipid Profile
Urine Esbach
Blood Sedimentation rate
Diftel
Laboratory results on 14th Mei 2010
Full Blood Count
WBC : 9,4 K/uL
RBC : 5,43 M/uL
Hb
: 13,2 g/dl
Ht
: 41,0 %
PLT : 367 K/uL
Carbbohydrate Metabolism
Ad random glucose level : 100 mg/dL
Blood Electrolite
Na: 134 mEq/L
K : 3,2 mEq/L
Cl : 113 mEq/L
Renal Function Test
Ureum : 47 mg/dL
Creatinin : 1,2 mg/dL
Cardiac Enzyme

SGOT : 20 U/L
SGPT : 6 U/L
Liver
Albumin: 12 g/dl
Dipstick urine
Leu : Nit
:Uro : Pro
: ++++
pH
:6

Blo
SG
Keton
Bil
Glu

: +++
: 1,020
:::-

Consult Thorax X-ray to Radiology on May 14th 2010

Results can be interpretated as:
Ascites + lung oedem + bilateral pleural effusion especially right lung
Follow Up May 15th 2010
S : Full body oedema (+)
O : Sens : compos mentis. Temperature : 36,8 C. BW: 72 kg, BSA: 1,84 m2
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (+)
ear / nose=within normal limits
M= tonsil T2-T2 hyperemis
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 108 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+) N
sleeping abdomen circumference: 98 cm, sitting abdomen
circumference: 102 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 108 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
120/80 mmHg,
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
P: - Inj. Ceftriaxone 1gr/12hr/IV
- Inj Furosemide 20 mg/8hr/IV
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Diet low salt
- Fluid balance/6 hr

Dipstick urine on May 15th 2010

Leu : Blo
: +++
Nit
:SG
: 1,03
Uro : 0,2
Keton : Pro
: +++
Bil
:pH
:5
Glu
:-

Laboratory results on May 15th 2010

Complete Blood Count
Hb : 12,60 g%
RBC : 5,30. 106/mm3
WBC : 10,18 103 mg/dl
Ht : 39,40 %
PLT : 335 103/mm3
MCV : 74,30 fL
MCH : 23,80 pg
MCHC : 32,00 g%
RDW : 17,90 %
MPV : 9,30 fL
PCT : 0,31 %
PDW : 10,1 fL
ESR : 18 mm/hr
Lipid Profile
Total cholesterol
Trigliserida
HDL cholesterol
LDL cholesterol

: 637 mg/dL
: 562 mg/dL
: 25 mg/dL
: 470 mg/dL

Imunoserologi
ASTO : < 200
AUTOIMMUNE
CRP Kualitatif : negative
Answer Consult from Nephrology division on May 15th 2010
- Diagnose: Nephrotic Syndrome
- Treatment : - IVFD D 5% NaCl 0,45% 15 gtt/i
- Inj. Ceftriaxone 1 gr/12 hr/IV
- Inj. Furosemide 20 mg/8 hr/IV
- Aldactone 3 x 25 mg
- Captopril 3x 12,5 mg
- Diet usual food low salt
- Fluid balance per 6 hr

- evaluation signs of shock

Follow Up May 16th 17th 2010
S : Full body oedema (+)
O : Sens : compos mentis. Temperature : 37,50C. BW: 72 kg, BSA: 1,84 m2
Head
: light reflex +/+, pupil isocor right = left, pale inferior conjungtiva
palpebra -/-, oedem palpebra (+)
ear / nose= within normal limits
M: T2-T2 hyperemis
Neck
: lymph node enlargement (-)
Thorax : fusiformed symmetrical, retraction (-)
HR = 140 bpm, regular, murmur (-)
RR = 37 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+) N
sleeping abdomen circumference: 98 cm, sitting abdomen
circumference: 102 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 140 bpm, regular,
Pressure/ Volume = adequate,
Blood pressure=140/100 mmHg, pitting oedema (-)
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
P: - IVFD D5% + 0,45% 15 gtt/i mikro
- Inj. Ceftriaxone 1g/12hr/IV
- Inj. Furosemide 20mg / 8h / iv
- Spironolactone 3 x 25 mg
- Captopril 3x12,5 mg
- Diet low salt
- Fluid balance/6 hr
Report from Pediatric Social Modul on May 17th 2010
There is no abnormal of emotional and mental status
Dipstick urine on May 16th 2010
Leu : 15
Blo
: +++
Nit
:SG
: 1,03
Uro : 0,2 (3,5)
Keton : 5 (0,5)
Pro
: 300 (3,0)
Bil
: 1 (17)
pH
:6
Glu
:Dipstick urine on May 17th 2010

Leu
Nit
Uro
Pro
pH

:::: ++
:6

Blo
SG
Keton
Bil
Glu

: +++
: 1,010
:::-

Follow Up May 18th 2010

S : Full body oedema (+)
O : Sens : compos mentis. Temperature : 36,8 C. BW: 70 kg, UHC = 28 cm
Head
: light reflex +/+, pupil isocor right = left, pale inferior conjungtiva
palpebra -/-, oedem palpebra (+)
ear / nose=within normal limits
M= tonsil T2-T2 hyperemis
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 98 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+) N
sleeping abdomen circumference: 93,5
cm, sitting abdomen
circumference: 98 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 98 bpm, regular, pressure/ volume = adequate, pitting oedem
(+), blood pressure = 140/100 mmHg,
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
P: - IVFD D5% + 0,45% 15 gtt/i mikro
- Inj. Ceftriaxone 1gr/12hr/IV D5%, finish for 20 minutes
- Inj Furosemide 20 mg/8hr/IV diluted with aquabidest 10 cc
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Diet low salt
- Fluid balance/6 hr
Dipstick urine on May 18th 2010
Leu : Blo
: ++
Nit
:SG
: 1,020
Uro : 0,2
Keton : Pro
: 2000
Bil
:+
pH
: 6,5
Glu
:-

Follow Up May 19th 2010

S : Full body oedema (+)
O : Sens : compos mentis. Temperature : 37,10C. BW: 69 kg,
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (+)
ear / nose = within normal limits
M= tonsil T2-T2 hyperemis
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 108 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+) N,
sleeping abdomen circumference: 93,5
cm, sitting abdomen
circumference: 96,5 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 108 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
130/80 mmHg, papule on right and left femoralis regio (+).
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
P: - IVFD D5% + 0,45% 15 gtt/i mikro
- Inj. Ceftriaxone 1gr/12hr/IV D5%, finish for 20 minutes
- Inj Furosemide 60 mg/8hr/IV diluted with aquabidest 10 cc
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Ambroxol 3x1 tab
- Gentamicin cream 2x applic I
- Diet usual food low salt 2000 kkal with 98 gr protein
- Fluid balance/6 hr
Dipstick urine on May 19th 2010
Leu : +
Blo
:Nit
:+
SG
: 1,03
Uro : 0,2
Keton : Pro
: ++++
Bil
:pH
:6
Glu
:Culture and Sensivisity Test Result on May 19th 2010
Growth was not found

Follow Up May May 20th 2010

S : Full body oedema (+)
O : Sens : compos mentis. Temperature : 36,7 C. BW: 68 kg
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (+)
ear / nose=within normal limits
M= tonsil T2-T2 hyperemis
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 98 bpm, regular, murmur (-)
RR = 24 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic +
sleeping abdomen circumference: 94
cm, sitting abdomen
circumference: 94,5 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 98 bpm, regular,

Genitalia

Pressure/ Volume = adequate, pitting oedem (+), blood pressure =

140/100 mmHg, papule on right and left femoralis regio (+).
: male, oedem scrotum (+)

P: - IVFD D5% +
0,45% 15 gtt/i mikro A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
DD/: - Impetigo krustosa
- Furunkel
-

- Inj. Ceftriaxone 1gr/12hr/IV D5%, finish for 20 minutes

- Inj Furosemide 60 mg/8hr/IV diluted with aquabidest 10 cc
- Aldactone 3x25 mg
- Captopril 3x12,5 mg

Ambroxol 3x1 tab

- Gentamicin cream 2 x applic I
- Diet low salt
- Fluid balance/6 hr
Dipstick urine was not done because patients urine was not store
Report from Respirology division on May 20th 2010

Diagnose: pleural effusion

Treatment: correction of albumin and treatment suitable in room

Report from Cardiology division on May 20th 2010

From EKG result that was done on May 25th 2010
- No ASD, VSD, and PDA
- Normal Left ventrikel systolic function
- Moderate pericardial effusion with diameter 15 mm
Follow Up May 21st 2010
S : Full body oedema (+)
O : Sens : compos mentis. Temperature : 360C. BW: 68 kg,
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (+)
ear / nose/mouth = within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 98 bpm, regular, murmur (-)
RR = 27 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic +
sleeping abdomen circumference: 88
cm, sitting abdomen
circumference: 95 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 98 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
130/90 mmHg, papule on right and left femoralis regio (+).
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
P: - IVFD D5% + 0,45% 15 gtt/i mikro
- IVFD albumin 20% 100 cc/day
- Inj. Ceftriaxone 1gr/12hr/IV D5%, finish for 20 minutes
- Inj Furosemide 60 mg/8hr/IV diluted with aquabidest 10 cc
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- prednison 6-5-5
- Ambroxol 3x1 tab
- Gentamicin cream 2 x applic I
- Diet usual food low salt 2000 kkal with 98 gr protein
- Fluid balance/6 hr
Dipstick urine on May 21st 2010
Leu : (15)
Blo
: ++
Nit
:SG
: 1,03

Uro
Pro
pH

: 0,2
: ++++
: 7,5

Keton : Bil
:Glu
:-

Follow Up May 22nd-23rd 2010

S : Full body oedema (+)
O : Sens : compos mentis. Temperature : 370 C. BW: 65 kg
Head
: light reflex +/+, pupil isocor right = left, pale inferior conjungtiva
palpebra -/-, oedem palpebra (+)
ear / nose/mouth = within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 110 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+) N
sleeping abdomen circumference: 89
cm, sitting abdomen
circumference: 94 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 110 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
130/80 mmHg, papule on right and left femoralis regio (+).
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
P: - IVFD D5% + 0,45% 15 gtt/i mikro
- IVFD albumin 20% 100 cc/day
- Inj. Ceftriaxone 1gr/12hr/IV D5%, finish for 20 minutes
- Inj Furosemide 60 mg/8hr/IV diluted with aquabidest 10 cc and bolus slowly
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Prednison 6-5-5
- Ambroxol 3x1 tab
- Gentamicin cream 2 x applic I
- Diet low salt
- Fluid balance/6 hr
Dipstick urine on May 22nd 2010
Leu : Blo
:+
Nit
:SG
: 1,015
Uro : 0,2
Keton : Pro
: +++
Bil
:pH
:7
Glu
:-

Dipstick urine on May 23rd 2010

Leu : Blo
: ++
Nit
:SG
: 1,020
Uro : 0,2
Keton : Pro
: +++
Bil
:pH
:6
Glu
:Follow Up May 24th 2010
S : Pretibial oedem (+)
O : Sens : compos mentis. Temperature : 36,50 C. BW: 63,5 kg
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra (-/-), oedem palpebra (-/-)
ear / nose/mouth =within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 88 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+) N
sleeping abdomen circumference: 89
cm, sitting abdomen
circumference: 94 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 88 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
120/90 mmHg, papule on right and left femoralis regio (+).
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
DD/- Impetigo krustosa
- Furunkel

P: - IVFD D5% + 0,45% 15 gtt/i mikro

- IVFD albumin 20% 480 cc/day
- Inj. Ceftriaxone 1gr/12hr/IV in 50 cc D5%, finish for 30 minutes
- Inj Furosemide 60 mg/6hr/IV diluted with D5% 20 cc
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Prednison 6-5-5
- Ambroxol 3x1 tab
- Gentamicin cream 2 x applic I
- Diet low salt
- Fluid balance/6 hours

Dipstick urine on May 24th 2010

Leu : Blo
:+
Nit
:SG
: 1,02
Uro : Keton : Pro
: +++
Bil
:pH
:7
Glu
:USG result on May 24th 2010
Glomerulopathy
Follow Up May 25th 2010
S : Pretibial oedem (+)
O : Sens : Compos mentis. Temperature : 36,70 C. BW: 62 kg
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (-/-)
ear / nose/mouth =within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 98 bpm, regular, murmur (-)
RR = 24 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+)
sleeping abdomen circumference: 93
cm, sitting abdomen
circumference: 96 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 98 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
130/80 mmHg
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis
P: - IVFD D5% + 0,45% 15 gtt/i micro
- IVFD albumin 20% 100 cc/day
- Inj. Ceftriaxone 1gr/12hr/IV in 50cc D5%, finish for 30 minutes
- Inj Furosemide 60 mg/6hr/IV diluted with 20cc D5% 40 gtt/i
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Prednison 6-5-5
- Ambroxol 3x1 tab
- Diet low salt 2000 kcal with 98 gr protein
- Fluid balance/6 hr
Laboratory result on May 25th 2010

Imunoserologi
C3 complemen: 46 mg/dL
Dipstick urine on May 25th 2010
Leu : Blo
: 5,1
Nit
:SG
: 1,010
Uro : 0,2
Keton : Pro
: 2000
Bil
:1
pH
: 7,5
Glu
:Follow Up May 26th-27th 2010
S : Pretibial oedem (+)
O : Sens : compos mentis. Temperature : 36,50 C. BW: 63 kg , BSA = 1,66m2
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (-/-)
ear / nose/mouth =within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 88 bpm, regular, murmur (-)
RR = 20 rpm, regular, rales (-).
Abdomen : ascites (+) , peristaltic +
sleeping abdomen circumference: 87
cm, sitting abdomen
circumference: 92,5 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 88 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
120/90 mmHg
Genitalia : male, oedem scrotum (+)
A: DD/- Nephrotic Syndrome
-Acute Glomerulonephritis

P: - IVFD D5% + 0,45% 15 gtt/i micro

- IVFD albumin 20% 100 cc/day
- Inj. Ceftriaxone 1gr/12hr/IV in 50 cc D5%, finish for 30 minutes
- Inj Furosemide 60 mg/hr/IV diluted with D5% 20cc 40gtt/i
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Prednison 6-5-5
- Ambroxol 3x1 tab
- Diet low salt 2000 kcal with 98 gr protein
- Fluid balance/6 hr

Dipstick urine on May 26th 2010 was not done because patients urine was not
store
Dipstick urine on May 27th 2010
Leu : Blo
:
Nit
:SG
: 1,010
Uro : 0,2
Keton : Pro
: 300
Bil
:pH
:6
Glu
:-

Laboratory results on May 26th 2010

Complete Blood Count
Hb : 13,20 g%
RBC : 5,45 106/mm3
WBC : 15,68 103 mg/dl
Ht : 40,90 %
PLT : 359 03/mm3
MCV : 75,00 fL
MCH : 24,20 pg
MCHC : 32,30 g%
RDW : 18,30 %
MPV : 9,80 fL
PCT : 0,35 %
PDW : 10,9 fL
ESR : 23 mm/hr
Liver
Albumin: 1,5 g/dl
Renal Function Test
Ureum : 59 mg/dL
Kreatinin: 0,60 mg/dL
Uric Acid : 4,6 mg/dL
Electrolyte
Na: 136 mEq/L
K : 3,0 mEq/L
Cl: 104 mEq/L
Follow Up May 28th 2010
S : Pretibial oedem (+)
O : Sens : Compos mentis. Temperature : 36,70 C. BW: 61 kg
Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (-)

ear / nose/mouth =within normal limits

: lymph node enlargement (-),
: fusiformed symmetrical, retraction (-)
HR = 92 bpm, regular, murmur (-)
RR = 24 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+)
sleeping abdomen circumference: 87
cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 92 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+).
Neck
Thorax

A: Nephrotic Syndrome
P: - IVFD D5% + 0,45% 15 gtt/i mikro
- IVFD albumin 20% 490 cc/day
- Inj. Ceftriaxone 1gr/12hr/IV in 50cc D5%, finish for 30 minutes
- Inj Furosemide 60 mg/6hr/IV diluted with 20cc D5% 40 gtt/i
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Ambroxol 3x1 tab
- Diet low salt 2000 kcal with 95 gr protein
- Fluid balance/6 hr
Dipstick urine on May 27th 2010
Leu : Blo
:
Nit
:SG
: 1,015
Uro : 0,2
Keton : Pro
: +++
Bil
:pH
:6
Glu
:Follow Up May 29th 2010
S : Pretibial oedem (+)

O : Sens : compos mentis. Temperature : 36,70 C. BW: 58 kg , BSA = 1,56m2

Head
: light reflex +/+, pupil isocor right = left,pale inferior conjungtiva
palpebra -/-, oedem palpebra (-)
ear / nose/mouth =within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 84 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : ascites (+) , peristaltic +
sleeping abdomen circumference: 96
cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 84 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+), blood pressure =
120/70 mmHg,
A: Nephrotic Syndrome
P: - IVFD D5% + 0,45% 15 gtt/i mikro
- Inj. Ceftriaxone 1gr/12hr/IV in 50 cc D5%, finish for 30 minutes
- Inj Furosemide 60 mg/6hr/IV diluted with D5% 20cc 40gtt/i
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Ambroxol 3x1 tab
- Diet low salt 2000 kcal with 95 gr protein
- Fluid balance/6 hr
Dipstick urine on May 29th 2010 was not done because patients urine was not
store
Follow Up May 30th 2010
S : Pretibial oedem (+)
O : Sens : Compos mentis. Temperature : 36,70 C. BW: 54 kg, BSA: 1,48 m2
Head
: light reflex +/+, pupil isocor right = left, pale inferior conjungtiva
palpebra -/-, oedem palpebra (-)
ear / nose/mouth =within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 90 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : ascites (+), peristaltic (+)
sleeping abdomen circumference: 96
cm
Hepar/ spleen = difficult to be measured

Extremity : pulse 90 bpm, regular,

Pressure/ Volume = adequate, pitting oedem (+) , blood pressure:
110/70 mmHg
A: Nephrotic Syndrome
P: - IVFD D5% + 0,45% 15 gtt/i micro
- IVFD albumin 20% 490 cc/day
- Inj. Ceftriaxone 1gr/12 hr/IV in 50cc D5%, finish for 30 minutes
- Inj Furosemide 60 mg/6 hr/IV diluted with 20cc D5% 40 gtt/i
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Ambroxol 3x1 tab
- Diet low salt 2000 kcal with 95 gr protein
- Fluid balance/6 hr
Dipstick urine on May 30th 2010
Leu : Blo
:Nit
:SG
: 1,010
Uro : 0,2
Keton : Pro
:+
Bil
:pH
:7
Glu
:Follow Up May 31st 2010
S : Pretibial oedem (+)
O : Sens : Compos mentis. Temperature : 36,70 C. BW: 54 kg, BSA: 1,48 m2
Head
: light reflex +/+, pupil isocor right = left, pale inferior conjungtiva
palpebra -/-, oedem palpebra (-)
ear / nose/mouth =within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 92 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : soepel, peristaltic (+)
sleeping abdomen circumference: 87
cm, sitting abdomen
circumference: 90 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 92 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+) , blood pressure:
100/70 mmHg

A: Nephrotic Syndrome
P: - IVFD D5% + 0,45% 15 gtt/i micro
- Inj. Ceftriaxone 1gr/12 hr/IV in 50cc D5%, finish for 30 minutes
- Furosemide 3 x 20 mg
- Aldactone 2x125 mg
- Captopril 3x12,5 mg
- Prednison 6-5-5
- Ambroxol 3x1 tab
- KSR 4 x 1 tab
- Diet low salt 2000 kcal with 95 gr protein
- Fluid balance/6 hr
Dipstick urine on May 31st 2010
Leu :
Blo
:Nit
:SG
: 1,010
Uro : Keton : Pro
:+
Bil
:pH
:7
Glu
:Laboratory results on May 31st 2010
Complete Blood Count
Hb : 11,90 g%
RBC : 4,84 106/mm3
WBC : 14,11 103 mg/dl
Ht : 37,20 %
PLT : 371 103/mm3
MCV : 76,90 fL
MCH : 24,60 pg
MCHC : 32,00 g%
RDW : 17,70 %
MPV : 9,10 fL
PCT : 0,34 %
PDW : 9,3 fL
ESR : 30 mm/hr
Liver
Total Bilirubin : 0,12 mg/dL
Direct Billirubin : 0,05 mg/dL
ALP
: 86 U/L
SGOT
: 31 U/L
SGPT
: 42 U/L
Renal Function Test

Ureum : 27,10 mg/dL

Kreatinin: 0,57 mg/dL
Uric Acid : 6,1 mg/dL
Electrolyte
Na: 132 mEq/L
K : 2,6 mEq/L
Ca: 6,7 mg/dL
Cl: 89 mEq/L
Mg: 1,24 mEq/L
Follow Up on June 1st 2010
S : Pretibial oedem (+)
O : Sens : Compos mentis. Temperature : 36,80 C. BW: 48 kg, BSA: 1,36 m2
Head
: light reflex +/+, pupil isocor right = left, pale inferior conjungtiva
palpebra -/-, oedem palpebra (-)
ear / nose/mouth = within normal limits
Neck
: lymph node enlargement (-),
Thorax : fusiformed symmetrical, retraction (-)
HR = 98 bpm, regular, murmur (-)
RR = 28 rpm, regular, rales (-).
Abdomen : soepel, peristaltic (+)
sleeping abdomen circumference: 87 cm, sitting abdomen
circumference: 90 cm
Hepar/ spleen = difficult to be measured
Extremity : pulse 90 bpm, regular,
Pressure/ Volume = adequate, pitting oedem (+) , blood pressure:
120/80 mmHg
A: Nephrotic Syndrome
P: - Furosemide 3x20 mg
- Aldactone 3x25 mg
- Captopril 3x12,5 mg
- Prednison 6-5-5
- Ambroxol 3x1 tab
- Calcidol B12 3xCII
- KSR 4 x 1 tab
- Diet low salt
- Fluid balance/6 hr

Dipstick urine on June 1st 2010

Leu :
Blo
:Nit
:SG
: 1,005
Uro : 0,2
Keton : Pro
:+
Bil
:pH
:9
Glu
:V. DISCUSSION
Nephrotic syndrome is a condition which has characteristic features are
heavy proteinuria ( >3.5 gr/24hours in adults or 40mg/m 2/hours in children),
hypoalbuminemia (<2.5gr/dL), edema, and hyperlipidemia. In this patient, from
physical examination, we can find full body edema and from laboratory results
shows urinary dipstick with proteinuria (++++), low albumin level of 1,2 g/dl,
increased amount of cholesterol 637 mg/dl. This condition is defined as nephrotic
syndrome which is a group of clinical manifestations such as massive proteinuria,
hypoalbuminemia, oedema, and hypercholesterolemia.
The clinical manifestations of nephrotic syndrome are periorbital oedema,
scrotal or vulval, leg, and ankle oedema, ascites, breathlessness due to pleural
effusions and abdominal distension. In this case, the patient came to hospital with
complaints of full body edema (periobital oedema, scrotal oedema, and pretibial
oedema). From radiology consult, the result was ascites. But, the patient did not
complaint of breathlessness.
To confirm the amount of heavy proteinuria in this patient, the quantitative
urine protein/ 24 hours must be done, but it was not done in this patient.
The treatment of nephritic syndrome is diet control protein from RDA 1,5-2
g/kgBW/day and low salt 1-2g/day if oedema is exist, diuretic, steroid, levamisol,
and sitostatika. In this case, the patien was treated with furosemide, aldactone,
captopril, prednisone, KSR, and diet low salt.
The criteria of sensitive steroid NS is remission with negative or trace urine
dipstick for 3 days. During prednisone given in several days, protein urine
dipstick was negative or trace for 3 days.

VI. SUMMARY
It has been reported a case of nephrotic syndrome in 13 years-old boy. The
diagnosis was established from clinical manifestation, urinary dypstic and
laboratory findings. He got improvement after 10 days hospitalized.

VII. REFERENCES
1. Richard E., Md. Behrman, Robert M., Md. Kliegman,Hal B., Md. Jenson,
Nephrotic Syndrome. Nelson Textbook of Pediatrics 17th Edition. USA :
W B Saunders Inc.
2. Bangga, A. & Mantan, M. 2005. Nephrotic Syndrome in Children, Indian J
Med. Available from : http://www.icmr.nic.in/ijmr/2005/july/0701.pdf
[ Accesed 26th May 2010]
3. Lissauer T, Clayden G. 2007. Illustrated Textbook of Paediatrics. Spain:
Mosby Elsevier
4. Unit Kerja Koordinasi Nefrologi. 2008. Konsensus Tata Laksana Sindrom
Nefrotik Idiopatik pada Anak. Jakarta: Badan Penerbit Ikatan Dokter
Indonesia
5. Iturbe BR, Acosta JH Johnson JR. 2010. Interstitial inflammation, sodium
retention, and the pathogenesis of nephrotic edema: A unifying hypothesis.
Available from:
http://www.nature.com/ki/journal/v62/n4/fig_tab/4493234f2.html
[Accessed 2nd June 2010]
6. Abeyagunawardena, AS. 2005. Treatment of Steroid Sensitive Nephrotic
Syndrome. Sri Lanka: University of Peradeniya.