Timeline: October 7 2017 October 8 2017 October 12 2017 October 13 2017

TIMELINE
October 7th2017 October 8th 2017 October 12nd 2017 October 13rd 2017
Patient was
admitted to K Initial Final
Hospital observation Report
Diagnosis : by candidate observation
Steroid
Resistant Observation
Nephrotic started
Syndrome
1
PATIENT’S RECORD
Candidate : Ansye Runtukahu
I. IDENTITY
1.1. IDENTITY OF PATIENT
Registration Number : 50.XX.XX

Patient Name : SY
Date of birth : November 9th 2007
Age : 9 years 11 months
Place of birth : Hospital
Gender : Male
Nationality : Indonesian
Number of children : second from two childrens
Health insurance : Patient use government insurance
class III
Date of admission : October 7 th 2017, at 11.50
1.2. IDENTITY OF PARENTS
FATHER MOTHER
Name : FS YT
Age : 60 years old 48 years old
Occupation : Farmer Teacher
Education : Primary school Bachelor
2
II. HISTORY
(Auto-anamnesis and allo-anamnesis from patient’s parents and medical

records)
 Chief complaint
Swelling on the face
 Additional complaints
Patient come to hospital to receive the second cycle of pulse
cyclophosphamid (CPA) therapy
2.1 HISTORY OF PRESENT ILLNESS

Patient admitted to hospital on October 7th 2017 at 11.50 with chief
complaint swelling on the face. Swelling experienced by patient since ±
4 weeks before admitted to the hospital. At first, swelling was started
on eyelid, appeared more clearly in the morning, over time the swelling
spreading to the whole face.
Patient has good appetite, the patient's parents said that during this
time the patient eat home meal 3 times a day. Patient denied the
presence of dark coloured urine such as meat washing or pain during
urination. Patient also denied fever and common cold. No complaint on
defecation in patient.
At this time, the patient has been treated for 1 day with diagnosis of
steroid-resistant nephrotic syndrome. Patient has been on pulse CPA
cycle I on September 11st 2017 and currently come to undergo the
second (II) cycle of pulse CPA therapy.
2.2 HISTORY OF PREVIOUS ILLNESS

The patient being find out to have swollen body by his parents in early
August 2017. At first, swelling occurs on the face and then spread to the
entire body. Full body swelling in patient also accompanied by cloudy
urine. Patient was admitted to B hospital in mid-August 2017 and
3
diagnosed with nephrotic syndrome. Patients received a prednisone drug
of 11 tablets taken daily for 4 weeks and captopril. Patient was then
outpatient and routine control in polyclinic. Because there was no changes
on urinalysis results, the patient was referred to K general hospital on
September 2017 for further evaluation and treatment. Patient was
diagnosed with steroid-resistant nephrotic syndrome on September 2017
and received prednisone therapy 7 ¼ tablets alternating dose and starting
pulse CPA cycle I. He denied history of red coloured urine, swallowing
pain or infection of the skin previously.
2.3 HISTORY OF ILLNESS IN THE FAMILY
History of the same illness in the family was denied
FAMILY TREE
4
STRUCTURE OF FAMILY MEMBERS
No Name Relationship Sex Age Information
1. FS Father M 60 years Healthy

2. YT Mother F 48 years Healthy
3. SS Child M 15 years Healthy
4. SY Child M 9 years 11 Patient
months
2.4. PERSONAL/SOCIAL HISTORY

A. HISTORY OF ANTENATAL CARE
Patient’s mother had regular antenatal examinations (6 times) at T
hospital. The mother had Tetanus Toxoid immunization (TT) twice
and took iron tablets. The mother was healthy during the
pregnancy.
B. HISTORY OF LABOR
Patient was born at full term with birth weight 3,500 grams at T
Hospital, directly cry, helped by obstetrician, by caesarian section.
C. HISTORY OF POSTNATAL
Patient had never experienced any cyanotic or yellowish skin
color. He could drink milk well and was routinely taken to health
care facility for vaccination
D. HISTORY OF FEEDING
The patient was never given breastmilk since born instead
formula milk until two years old. Milk porridge was given at 6
months old, then changed to strained porridge at 9 months old.
He started to eat porridge at 10 months and continued soft rice at
12 months old. He ate home meals at 1 years old until now with a
5
frequency of three times a day of 1 plate main portion. One plate
consist of rice with fish, or eggs and vegetables.
E. GROWTH AND DEVELOPMENTAL HISTORY

Flip over :3 months
Turning in prone position : 5 months
Sitting :7 months
Crawling :9 months
Standing : 10 months
Walking : 12 months
Social smile :3 months
Chattering :4 months
Call papa/mama :9 months
F. HISTORY OF VACCINATION
The patient received BCG vaccination with scar (+) on upper right
arm, polio 5 (five) times, DPT 4 (four) times, hepatitis B 3 (three)
times, measles 2 (two) times.
G. HISTORY OF BASIC NEEDS

Physic-biomedic:
Patients recieved adequate primary needs (food, clothes and
shelter)
Emotional needs:
Affection obtained from both parents and other family members.
Mental stimulation:
Patient is currently sitting in the 4th grade and can follow the
lessons well.
6
H. SOCIO-ECONOMIC AND ENVIRONMENT CONDITIONS
The patient's family comes from the lower middle-level socio-
economic level with an income about 3,000,000 rupiah per month.
The patient lives with both parents in permanent house with tin
roofed house, concrete-walled, tiles floor. There are 2 rooms in
the house, occupied by 4 peoples, 2 adults and 2
children.Bathroom and restroom are located inside the house.
Source of electricity comes from goverment electricity company.
Source of drinking water comes from refilled drinking water.
Waste is handled by dumping outside the house.
PATIENT CONDITIONS BEFORE BECOME LONG CASE

The patient is hospitalized on October 7th 2017 at 11.50 with chief
complaint swelling on the face. Swelling experienced by patient since ±
4 weeks before admitted to the hospital. Initially swelling is only visible
on the eyelid, appear more clearly in the morning,over time the swelling
Patient has good appetite. The patient's parents said that during
this time the patient eat home meal 3 times a day. Patient denied the
presence of dark coloured urine as meat washing or pain during
urination. Patient also denied fever and common cold. No complaint on
defecation in patient.
The patient has been treated for 1 day with a diagnosis of steroid-
resistant nephrotic syndrome. Patient has been on pulse CPA cycle I
on September 11st 2017 and currently come to undergo the second (II)
cycle of pulse CPA therapy.
On physical examination when admitted to hospital, the weight is 24

kg, height 121 cm, good nutrition status. Patient is compos mentis,
blood pressure 100/70 mmHg, pulse 90 beats /min (strong, enough fill),
respiratory rate 20 cycles/min, temperature 36,5˚C axilla. On head
7
examination, there was edema of the palpebra and face. On chest
examination, there was no retraction, normal breathing sound. On
abdominal examination, there was no ascites, liver and spleen were
not palpable. There was no abnormality in the examination of genitalia,
whereas in the lower limb there was no pretibial pitting edema on both
limbs.
On laboratory examination when admitted to the hospital, the
hemoglobin was 12.8 g/dL, hematocrit 38.5%, leucocytes 17.220/ mm3,
platelets 499.000/mm3, SGOT 7 U/L, SGPT 12 U/L, ureum 12 mg /dL,
creatinine 0.6 mg/dL (GFR: 90.75 ml/min/1.73m2), uric acid 4.34
mg/dL, albumin 3.02 g/dL, total cholesterol 336 mg/dL, HDL 48 mg/dL,
LDL 147 mg/dL, trigyceride 186 mg/dL, sodium serum electrolytes 134
mEq / L, potassium 3.5 mEq / L, chloride 100 mEq / L, CRP <6 mg / L.
Peripheral blood smear: normochromic normocytic erythrocytes,
negative polychromasia erythrocytes, negative follicular cells, negative
target cells, negative achantocytes, negative tear drop cells, negative
agglutination, negative nucleated erythrocytes. Sufficient leukocyte
amount, no visible vacuolization and toxic granulation, giant, negative
blue plasma lymphocytes, negative atypical lymphocytes, Differential
count: 0/0/7/57/31/5. Platelet count was normal, negative platelet giant,
negative clumping platelets, negative megakaryoblasts. The
impression of blood smear was within normal limits. Urinalysis revealed
light yellow, clear, SG 1.080, pH 6, leukocyte 2-3 / hpf, erythrocyte 3-5 /
hpf, protein +3, negative nitrite, negative glucose, negative ketone,
negative urobilinogen and bilirubin. Stool examination revealed brown
color, soft consistency, negative mucus, negative leucocytes, negative
erythrocytes, negative worm eggs / larvae.
Patient was initially diagnosed with steroid-resistant nephrotic
syndrome. The treatment that given when the patient was admitted to
hospital were prednison 7 ¼ tab once a day, alternating dose and
8
captopril 7,5 mg three times a day, The patient was planned for cycle
II of pulse cyclophosphamide.
III. PHYSICAL EXAMINATION

The examination was performed in the pediatric nephrology room, on
October 7th, 2017 (1st day care).
General condition : looked ill, Consciousness: composmentis
Antropometri status:
Bodyweight : 24 kg normal weight (CDC 2000)
Body weight/ age: 24/31x 100% = 77%
Height : 121cmnormal height (CDC 2000)
Height/ age: 121/138 x 100% = 87%
Weight/Height :24/23x 100% = 104%
 Normal nutritional status (CDC 2000)
Vital signs : Blood pressure 110/70 mmHg, pulse 96 bpm

(regular, enough content), respiratory rate 24
cycles/min, thoracal, body temperature 36,5°C (axilla)
Information:
Blood pressure percentile
Percentile 50 : 96/58 mmHg
Percentile 90 :110/72 mmHg
Percentile 99 : 114/76 mmHg
Percentile95 : 121/83 mmHg
Hypertension Crisis :≥180/120 mmHg
Skin : light brown colored, no efflorescent, no

hypopigmentation or hyperpigmentation, BCG
scar on right upper arm.
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Head and Neck
Head : normocephaly, head circumference 52 cm
(between - 2 SD and +2 SD)  normal, black
hair, not easily pluckable, large fontanele are
already closed.
Eyes : palpebral edema +/+, no anemic conjunctiva,
anicteric sclera, isochoric pupils diameter 3 mm -
3 mm, reactive to light, centered eyeballs, good
eye movements to all direction, clear lenses,
cornea reflex +/+
Nose : no deformities, no secretion, nasal breathing (-)
Ears : no deformity, no fluid secretion
Mouth : no cyanosis, moist buccal mucosa and lips, no
tongue papiles atrophy, symmetric nasolabial
sulcus, no teeth caries, no stomatitis, white
tongue (-)
Throat : tonsil T1/T1 not hyperemic, pharynx not
hyperemic
Neck : centered trachea, lymph node enlargement not
palpable, no stiff neck, JVP not increase
Chest : symmetrical chest expansion, the intercostal
space is not widened, no retraction
Heart
Inspection : ictus cordis unseen, no precordial bulging
Palpation : ictus cordis palpable in left midclavicular line,
5th intercostal space, no thrill
Percussion : right border at right parasternal line, left border
at left midclavicular line, upper border at 3rd left
intercostal space.
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Auscultation : heart rate frequency 96 bpm, regular, pure S1
and S2, no murmur
Lungs
Inspection : symmetrical movement of breathing, no
retraction,the intercostal space is not widened.
Palpation : symmetrical vocal fremitus
Percussion : symmetrical resonant sounds, no dullness
Periksa Dengar : vesicular breath sounds, no rales, no wheezing
Abdomen
Inspection : flat, following the movement of the breath,no
venectation
Palpation : soft, spleen and liver are not palpable, no
suprapubic pain, abdominal circumference 59 cm
Percussion : negatif shifting dullness, no costovertebral pain
Auscultation : normo-active bowel sounds
Genitalia : male, penis length 6 cm, palpable bilateral
testicle inside the scrotum
Puberty Scale : Tanner scale 2
Extremities : warm, no cyanosis, no deformity, normal muscle
tone, CRT ≤2 seconds, edema (-)
Reflexes : normal physiological reflexes, no pathological
reflexes
Sensory : normal
Motoric : Normal muscles strength
5/5
5/5
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Cranial nerves examination:
NI = no interference in smell
N II = no visual disturbance
N III, IV, VI = isocor, round pupil, direct light reflex and indirect
+/+, no strabismus and ptosis, normal eyeball
movement
NV = no abnormality
N VII = symmetrical nasolabial sulcus, lagophthalmus (-)
N VIII = no hearing loss and balance impairment
N IX = clear articulation, can swallow well
NX = no abnormality
N XI = can shrug the left and right shoulders upward
N XII = no deviation of the tongue
Laboratory (07/10/2017)
Urinalysis :
 Color : yellow - Nitrite : (-)
 Clarity : clear - Protein : +3
 Sediment : epitel cell 0-1 - Ketones : (-)
 Leucosytes : 2-3/hpf - Glucose : (-)
 Erythrocytes : 3-5/hpf - Urobilinogen: (-)
 Cylinder : (-) - Bilirubin : (-)
 Cyrstal : (-) - pH :6
 Density : 1.080
SUMMARY
Patient admitted to hospital on October 7th 2017 at 11.50 with chief
complaint swelling on the face. Swelling experienced by patient since ± 4
weeks before admitted to the hospital. At first, swelling was started at the
eyelid, appear more clearly in the morning, over time the swelling
12
The patient was diagnosed with nephrotic syndrome in the mid-
August 2017. Patients received a prednisone drug of 11 tablets taken daily
for 4 weeks and captopril. Because there is no changes on urinalysis
results, the patient was referred to K general hospital on September 2017
for further evaluation and treatment. Patient was diagnosed with steroid-
resistant nephrotic syndrome in September 2017 and received prednisone
therapy 7 ¼ tablets alternating dose and starting pulse CPA cycle I.
On physical examination at hospital admission, body weight was 24
kg, body height was 121 cm, and good nutritional status. Patients was
compos mentis, blood pressure was 100/70 mmHg, pulse 90 beats per
minute (strong lift, enough content), respiration rates 20 cycles per minute,
body temperature 36,5˚C (axilla). On head examination there was edema
of the palpebra and face. On chest examination there was no retraction,
normal breath sound. On abdominal examination was not found ascites,
liver and spleen were not palpable enlarged. On genital examination there
were no abnormality, In the lower extremity was not obtained pretibial
pitting edema on both limbs.
On laboratory examination when admitted to thehospital, the
hemoglobin was 12.8 g/dL, hematocrit 38.5%, leucocytes 17.220/mm3,
platelets 499.000/mm3, SGOT 7 U/L, SGPT 12 U/L, ureum 12 mg/dL,
creatinine 0.6 mg / dL (GFR: 90.75 ml / min / 1.73m 2hpf), uric acid 4.34
mg/dL, albumin 3.02 g/dL , total cholesterol 336 mg/dL, HDL 48 mg/dL,
LDL 127 mg/dL, trigyceride 186 mg/dL, sodium serum electrolytes 134
mEq/L, potassium 3.5 mEq/L, chloride 100 mEq/L, CRP <6 mg/L.
Peripheral blood smear: normochromic normocytic erythrocytes, negative
polychromasia erythrocytes, negative follicular cells, negative target cells,
negative achantocytes, negative tear drop cells, negative agglutination,
negative nucleated erythrocytes. Sufficient leukocyte amount, no visible
vacuolization and toxic granulation, giant, negative blue plasma
lymphocytes, negative atypical lymphocytes, differential count:
0/0/7/57/31/5. Platelet count was normal, negative platelet giant, negative
13
clumping platelets, negative megakaryoblasts. The impression of blood
smear was within normal limits Urinalysis revealed light yellow, clear, SG
1,080, pH 6, leukocyte 2-3/hpf, erythrocyte 3-5/hpf, protein +3, negative
nitrite, negative glucose, negative ketone, negative urobilinogen and
bilirubin. Stool examination revealed brown color, soft consistency,
negative mucus, negative leucocytes, negative erythrocytes, negative
worm eggs/larvae.
Patient was diagnosed with steroid-resistant nephrotic syndrome.
The treatment that given when the patient was admitted to hospital were
prednison 7 ¼ tab once a day, alternating dose and captopril 7,5 mg three
times a day. The patient was planned for cycle II of pulse
cyclophosphamide.
IV. DIAGNOSIS
Steroid Resistant Nephrotic Syndrome (N00-N08)
V. LIST OF PROBLEM
1. Diagnosis Problem
Determination the histopathological abnormalities of nephrotic
syndrome were still not possible, must be done by kidney biopsy.
2. Treatment Problem
Side effects can due to prolonged used of cytostatic and
corticosteroids.
3. Follow up Problem
Clinical improvement has not been achieved in this case.
Monitoring in steroid-resistant nephrotic syndrome is not only in
the possible complications but also of corticosteroid and cytostatic
side effects.
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VI. MANAGEMENT PLANS
1. Diagnosis plan
Examination of renal biopsy.
2. Treatment plans
Medication therapy:
 Cyclophosphamide 650 mg intravenously
 Prednisone 40 mg/m2BSA/day (alternating dose) = 36 mg
orally
 Captopril 7.5 mg orally three times a day.
 Simvastatin 10 mg once a day orally
3.Pediatric Nutritional Care

a. Nutritional status assessment
Body Weight : 24 kg
Body height : 121 cm
Nutritional status : weight/height = 24 / 23 x 100% = 104%
 good nutrition (CDC, 2000)
Body surface area (BSA) : 0.89/m2
b. Determination of needs based on Recommended Daily
Allowances (RDA)
Ideal body weight = 23 kg
Calories needed = 70 kcal/kg/day = 1.610 kcal/day
Protein needed = 1 g/kg/day = 23 g/day
≈ 92 kcal/day
Fluidneeded =70-85 ml/ kg/ day= 1610-1955 ml/day
c. Nutritional route
Nutritions were given orally
d.Determination type of food, given informs:
- Nefrisol® milk(@ 200ml, 260 kcal, 5 g protein) 1 cup
twice a day
15
- Solid food (@300 kcal, 5 g protein) 1 portion three times
a day
- Snack (@100 kcal) 1 portion twice a day
- Salt 1g/hari
- Mineral water 1.600 mL
Menu variations:
BREAKFAST LUNCH DINNER
¾ cup of rice ¾ cup of rice ¾ cup of rice
1 medium size of 1 piece medium size 1 piece medium
chicken(no skin) of beef size of grilled fish
Broccoli 1 piece medium size 1 piece medium
Banana of tempe size of tofu
Pumpkin Long beans
Papaya
10.00 AM 09.00 PM
1 cup of milk 1 cup of milk
e. Monitoring and evaluation

Periodically assessment of food tolerance, body weight, nausea or
vomit, and diarrhea
f. Follow up and monitoring

 Monitoring of vital signs, body weight, abdominal
circumference, fluid balance and diuresis.
 Complete blood count, serum electrolytes, urea, creatinine,
SGOT, SGPT, lipid profile, total protein, albumin, and
urinalysis.
 Urine culture
16
 Monitoring drugs’ adverse effect (steroid, cytostatica, and
other drugs)
 Nutrition monitoring
 Education to maintain hygiene for patient’s parents,
caregiver, and medical personnel.
 Educate the family members
5. Counseling plans
Diseases, therapy, prognosis, and follow-up at home
Nursing care :
1. Monitoring of vital signs
2. General cleanliness of the patient
3. Hygiene monitoring for parents / caregivers, nurses, medical
personnel
4. Weight everyday
5. Measurement of abdominal circumference everyday
6. Input and output monitoring
7. Mental and emotional support
17
VII. FOLLOW UP
October 8th 2017(1stobservation day, 2nd day of hospitalization)

S fever (-), swelling (+) on face, oral intake (+)
O General condition : looked ill, compos mentis
Blood pressure : 100/70 mmHg Respiratory rate : 24 cpm
Pulse : 84 bpM Temperature : 36.6oC (axilla)
Body weight : 24kg BSA : 0,89/m2
Fluid balance : -67 mL Diuresis : 2.5 mL/kg/hr
Eyes : palpebral edema (+), facial edema (+)
pink conjunctiva, anicteric sclera,
Nose : normal form, secretions -/-, nasal lobe breathing(-)
Ear : normal form, secretions - /-
Mouth : wet mouth mucosa, T1 / T1 tonsils are not
hyperemic, pharynx is not hyperemic
Neck : lymph node enlargement (-), JVP not increase
Chest : no retraction
Lungs-heart : within normal limit
Abdomen : flat, soft, normal bowel sound, liver and spleen were
not palpable, Abdominal circumference:
60 cm, ascites (-)
Genitalia : male, normal, edema (-)
Extremities : Warm, lower limb edema (-), capillary refill time
< 2 seconds
Laboratory :
Urinalysis : Glucose :-
Color : Clear, yellow Ketone :-
Specific gravity : 1.015 Urobilinogen : -
pH :6 Bilirubin :-
Leukocyte : 2-3/hpf Blood : +1
Nitrite :- Erythrocyte : 10-15/hpf
Protein :+3
A Steroid Resistant Nephrotic Syndrome (N00-08)

P Therapeutic :
- Captopril 7.5 mg three times a day orally
- Simvastatin 10 mg one a day orally
Pro : CPA 2nd cycle
Hyperhidration IVFD Sodium Chloride 0,45% in D5% + 20mEq Sodium
Bicarbonate: 100ml/ hour ( for 12 hours)
Monitoring and evaluation :
Water balance, diuresis
Body weight, abdominal circumference
Pediatric nutritional care
Same as before
Mineral water 1000 ml
Nursing care :
Same as before
18
October 9th 2017(2ndobservation day, 3rd day of hospitalization)
S fever (-), swelling (+) on face, oral intake (+)
Pulse : 88 bpM Temperature :36,7oC (axilla)
Body weight : 24kg BSA : 0.89/m2
Fluid balance : +20 mL Diuresis : 1.9 mL/kg/hr
60 cm, ascites (-)
< 2 seconds
P Therapeutic :
- Prednison 5 mg orally, 7 1/4 tablet once a day alternating dose
- Captopril 7.5 mg three times a day orally
- Simvastatin 10 mg once a day orally
- Pulse Cyclophosphamide
 Hyperhidration IVFD Sodium chloride 0,45% in D5% + 20mEq Sodium
Bicarbonate: 100 ml/ hour ( for 12 hours)
 IVFD Mesna 130 mg in 100 ml Sodium chloride 0,9% = 100ml/ 30
minutes
 IVFD cyclophosphamide 650 mg + Mesna 260 mg in 500ml Sodium
chloride 0,9% = 250 ml/hour ( for 1 hour)
 Hyperhidration IVFD Sodium Chloride 0,45% in D5% + 20 mEq Sodium
Bicarbonate: 100 ml/ hour ( for 12 hours)
Premedication : Ondansentron 4mg IV
Dexamethasone 2 mg IV
Water balance, diuresis.
Same as before
Nursing care :
Same as before
19
October 10th 2017(3rdobservation day, 4th day of hospitalization)
S fever (-), swelling (+) on face, good oral intake (+)
Blood pressure : 100/60 mmHg Respiratory rate : 24cpm
Pulse : 80 bpm Temperature : 36,2oC (axilla)
Body weight : 24 kg BSA : 0,89/m2
Fluid balance : +28 mL Diuresis : 1,93 mL/kg/hr
60 cm, ascites (-)
< 2 seconds
P Therapeutic :
- Captopril 7,5 mg orally three times a day.


Same as before
Nursing care :
Same as before
20
October 11st 2017(4thobservation day, 5th day of hospitalization
S fever (-), swelling (+) on face decrease, good oral intake (+)
Pulse : 84 bpm Temperature : 36,8oC (axilla)
Fluid balance : +46mL Diuresis : 1.2 mL/kg/hr
59 cm, ascites (-)
< 2 seconds
Laboratory :
Urinalysis :
Color :Clear, yellow Glucose :-
Specific gravity: 1,010 Ketone :-
pH :6 Urobilinogen :-
Leukocyte : 3-4/hpf Bilirubin :-
Nitrite :- Blood : +1
Protein :+1 Erythrocyte : 5-10/hpf
P Therapeutic :
- Prednison 5 mg orally, 7 1/4 tablet once a day alternating dose
- Captopril 7.5 mg orally three times a day.
Same as before
Nursing care :
Same as before
21
October 12nd 2017(5thobservation day, 6th day of hospitalization)
S fever (-), swelling (+) on face decrease, good oral intake (+)
Pulse : 88 bpM Temperature : 36.8oC (axilla)
Fluid balance : +22 mL Urine output : 1.05 mL/kg/hr
decrease
: pink conjunctiva, anicteric sclera,
Mouth wet mouth mucosa, T1 / T1 tonsils are not
: hyperemic, pharynx is not hyperemic
Abdomen flat, soft, normal bowel sound, liver and spleen were
: 60 cm, ascites (-)
Extremities Warm, lower limb edema (-), capillary refill time
< 2 seconds
Laboratory :
Hematology Urea : 54 mg/dL
Hemoglobin : 11,2 g/dL Creatinin : 0,4 mg/dL
Hematocrit : 32,7% GFR :166,3
Leukocyte : 11.6x 103/µL Uric acid : 5,8 mg/dL
Thrombocyte : 345x 103/µL Albumin : 2,78 g/dL
Sodium : 135 mEq/L Chloride : 102 mEq/L
Potassium : 3,52 mEq/L Calsium : 8,14 mg/dL
P Therapeutic :
- Captopril 7,5 mg orally three times a day.


Same as before
Nursing care :
Same as before
22
VIII. PROGNOSIS
Ad vitam : bonam
Ad functionam : dubia ad bonam
Ad sanationam : dubia ad malam
23
DISEASE COURSE TIMELINE
When used as a case
August 2017 October 7th 2017 October 8th 2017 October 9th 2017 October 10-11th 2017 October 12th 2017
Swelling on the Swelling on the face(+), Swelling on the face(+), Swelling on the face(+) Swelling on the
Admitted to B intake (+) intake (+) ↓, intake (+) face(+) ↓, intake (+)
hospital face(+), intake (+)
Diagnosis PE : Head : edema of PE : Head : edema of

PE : Head : edema of PE : Head : edema of PE : Head : edema of
Nephrotic Syndrome the face and palpebra the face andpalpebra
the face and palpebra the face andpalpebra (+) the face andpalpebra
(+) (+) ↓
(+) Abdomen : abdominal
Abdomen : abdominal (+) ↓
Abdomen : abdominal circumference 60 cm, Abdomen : abdominal
Abdomen : abdominal circumference 59 cm,
circumference 60 cm, shifting dullness(-) circumference 60 cm,
circumference 59 cm, shifting dullness(-)
shifting dullness(-) Extremities :edema (-) shifting dullness(-)
No improvement shifting dullness(-) Extremities :edema (-)
Extremities :edema (-) Extremity :edema (-)
Extremities :edema (-)
K General Hospital Urinalysis: +3protein Urinalysis: +1 protein Leucocytes: 11.600 /

Laboratory: mm3
Leucocytes: 17.220 /mm3 Diagnosis : Ur / Cr: 54mg / dl / 0.4
Ur / Cr: 12mg / dl / 0.6 mg / Steroid Resistant mg / dl
dl Nephrotic Syndrome LFG: 166.3 ml / min /
GFR: 90.75 ml / min / Diagnosis : 1.73m2lpLPB
Diagnosis : 1.73m2 Diagnosis :
Steroid Resistant Albumin: 2.78 g / dL
Steroid Resistant Albumin: 3.02g / dL Steroid Resistant
Nephrotic Syndrome Nephrotic Syndrome
Nephrotic Syndrome Cholesterol total : 336 mg/dl
Urinalysis: +3 protein
Diagnosis :
Diagnosis : Therapy : Therapy : Steroid Resistant
Cyclosfamide puls I Steroid Resistant Therapy : -Prednison 5 mg 7 ¼ tab - Prednisone 5 mg 7 ¼ Nephrotic Syndrome
(September 2017) Nephrotic Syndrome - Captopril 3 x 7.5 mg (AD) p.o tab (AD)
- Simvastatin 1x 10 mg - Captopril 3 x 7.5 mg - Captopril 3 x 7.5 mg
- Hyderhydration IVFD - Simvastatin 1x 10 mg - Simvastatin 1x 10 mg
NaCl 0.45% in D5% + - Cyclophosphamide puls Therapy :
Therapy : 20 mEq Sodium - Captopril 3 x 7.5 mg
- Prednisone 5 mg 7 ¼ bicarbonate = 100 ml / - Simvastatin 1x 10 mg
tab (AD) p.o h (for 12 hours)
Captopril 3 x 7.5 mg Plan:
- Simvastatin 1x 10 mg - Cyclophosphamide iv
26 7 ¼
Prednisone 5 mg
Plan:
- Cyclophosphamide tab ( AD )
pulse iv
CASE ANALYSIS DIAGRAM
A boy, 9 years 11 months old - Response therapy

Complaint: swelling on the face - Evaluation of laboratory results
- Complications
-
Nephrology
Probelms
Symptoms Swelling on the face
Diagnosis Steroid Resistant Nephrotic Syndrome
Workup Complete blood, total protein, albumin, Na, K, Cl, Ca, Ur, Cr, Lipid
profile, Urinalysis
Treatment Cyclophosphamide puls, prednisone alternating dose, captopril, simvastasin,

Salt diet 1 gram / day, protein diet 1 g/kgBW/day
Prognosis Therapy response Ad vitam bonam Parent education

Evaluation of laboratory Ad functionam dubia ad bonam Prevention of
results Ad sanationam dubia ad malam infection
LoE
Complications Regular treatment
 Zagury, et al. J Bras Nefrol.2013. Level of evidence 2b, recommendation B

 Inaba, et al. Pediatr Nephrol Jour. 2016. Level 2 of Evidence 2b, recommendation B
 Roy, et al. IOSR J Pharm. 2014. Level of evidence 2b, recommendation B
 Chang, et al. J Epidemiol. 2012. Level of evidence 2b, recommendation B
27
CASE ANALYSIS
Nephrotic syndrome (NS) is the most common kidney disease found in
children with high risk of morbidity and mortality. The incidence of NS in
children in the United States and the United Kingdom is 2-7 cases/100,000
children/year, with prevalence range from 12-16 cases/100,000 children.
The incidence of NS in Indonesia is 6 cases/100,000/year for children
aged <14 years old in Jakarta. Comparison of boys and girls is 3:2. More
than 90% of cases of nephrotic syndrome are idiopathic.1 Most children
are responsive to therapy with steroids, but about 20% of children will
develop resistance to steroid therapy, where the child fails to achieve
complete remission after initial treatment with corticosteroids. 2 In the study
by Bahn et al in 2001-2011, on epidemiological data of children with
nephrotic syndrome in Europe and Asia, it was found that the incidence of
nephrotic syndrome increased from 1.99/100,000 children to 4.71/100,000
children aged 1-18 years.3 At Cipto Mangunkusumo Hospital Jakarta, as
many as 15.4% of cases of nephrotic syndrome developed into steroid
resistant.4
Etiology of NS is divided into 3 : congenital, primary/idiopathic, and
secondary following systemic disease. Most children (90%) is idiopathic
NS, which has an anatomic pathology description of minimal change
nephrotic syndrome (MCNS). The case of MCNS is common in Asian,
Hispanic, Arab and Caucasian races. In a study conducted in Egypt by
Seif et al, the most common histopathologic abnormality in children aged
1.5-16 years is focal segmental glomerulosclerosis (FSGS) of 30.2%,
minimal change glomerulopathy (MCG) of 24.5%, and IgA nephropathy
was 13.2%.5
The massive proteinuria in NS is a result of increased permeability
of the glomerular membrane wall. This pathology cause a decrease in
serum protein levels in the blood, resulting in an inverse ratio between
serum albumin and serum globulin (1:2). In addition, hypoalbuminemia
occurs due to increased protein catabolism in the body and leakage from
28
the kidneys. Hypoalbuminemia will cause the liver trying to increase the
synthesis of albumin, but this process does not optimal. Hypoalbuminemia
caused edema and hyperlipidemia as a compensation to maintain plasma
oncotic pressure. Other blood chemicals that are wasted due to increased
membrane permeability are immunoglobulins (Ig), hormones, minerals,
serum electrolytes (Na, K, Cl, Mg) and clotting factors in the blood. This
will facilitate the occurrence of thrombus in blood vessels, other than that
hyperlipidemia can also trigger the platelet aggregation which resulted in
the ease of formation of thrombus in blood vessels.1,6
There are two pathophysiological mechanisms on NS (classical
theory) namely, underfill and overfill theory. The underfill theory says that
due to the release of albumin through the urine, the plasma volume in the
vascular will decrease, so the kidneys will respond and compensate by
retention of water and sodium. As a result the volume of plasma will
increase, but the oncotic pressure decreases, because the plasma
albumin maintains intravascular oncotic pressure. This causes edema.
Overfill theory says that there is a disruption in the arrangement of ANP
(Atrial Natriuretic Peptide), thus stimulate water and sodium retention in
the kidneys that will cause an increase in plasma volume. Increased
plasma volume directly increases blood volume and indirectly increases
blood pressure and this is also due to sodium retention.1,5
Based on the pathophysiology, anasarca edema is often the main
complaint of patients with nephrotic syndrome. This patient got swelling on
the whole body since August 2017. The swelling was initially visible on the
face, followed by swelling in the whole body.
Currently there are several new theories about the pathophysiology
of nephrotic syndrome, including immune dysregulation, which mostly
involves cell mediated immunity. T cell abnormalities are also reported in
nephrotic syndrome with minimal changes. Antigen presentation to T cells
induces an immune response, which can be type 1 (dominated by
interferon alfa, interleukin (IL) -2) or type 2 (IL4, IL 10, and IL13). There is
29
evidence to suggest that activation of innate immunity due to activation of
TLR (toll like receptors) by microbial products, can directly affect podosit. 7
Diagnosis of nephrotic syndrome based on the presence of
massive proteinuria (> 40mg/m2/h or 50mg/kg/day or protein/creatinine
ratio in urine >2mg or dipstick ≥+2), hypoalbuminemia (albumin <2.5 g/dl),
edema and may be accompanied by hypercholesterolemia (total
cholesterol >200 mg/dL). The recommended investigations are complete
peripheral blood count, serum albumin, serum protein, serum urea, serum
creatinine. Steroid-resistant nephrotic syndrome occurs when there is no
remission after 4 weeks of initial therapy using full doses of prednisone (2
mg/kg/day).1,5,8,9 In an study in Egypt conducted by Seif et al, in children
aged 1,5-16 years old with steroid-resistant nephrotic syndrome, found
that 100% of children had swelling in lower extremities and 17% of
children had hematuria.5
The diagnosis of nephrotic syndrome in this patient are based on
history of illness, physical findings, and laboratory examination. This
patient had a history of swelling on whole body on August 2017. The
patient also came with swelling on the face. Laboratory findings revealed
massive proteinuria, with +3 protein in urinalysis, hypoalbuminemia
(albumin 3.02 g/dL), and hyperlipidemia (total cholesterol 336 mg/dL, HDL
48 mg/dL, LDL 147 mg/dL, trigyceride 186 mg/dL).
Children with clinical manifestations of NS for the first time should
be admitted to the hospital for examination and evaluation of diet,
management of edema, initiation of steroid treatment, and parental
education. Before steroid treatment begins, the following examination are
performed: general physical examination, signs of edema, infection focus
and mantoux test. If the mantoux test is positive then give INH (isoniazid)
prophylaxis for 6 months with steroids, and give the anti-tuberculosis drug
if the tuberculosis is positive.1,6,10
The patient was diagnosed with nephrotic syndrome in August
2017. The patient was treated with full-dose prednisone for 4 weeks, but
30
did not under go remission and then diagnosed with steroid-resistant
nephrotic syndrome. In the initial examination on October 7 th 2017 when
the patient came to the hospital, there is still have proteinuria (+3 protein)
from urinalysis.
According to the ISKDC (International Study of Kidney Diseases in
Children), when the child does not provide a clinical response after 4
weeks of treatment with a full dose of prednisone, the child had a steroid
resistant.6 Theories about the pathophysiology of steroid resistance have
been developed over the past few years. The gene mutation is one that
underlies the occurrence of steroid resistance. The most common
mutations found are those genes encoding nephrin, podocin and WT1, so
screening of these genes is suggested to guide clinical management and
to provide genetic advice.11 Some recent studies also suggest a genetic
examination to avoid possible long-term steroid therapy that may not
produce satisfactory results in the child carrying the gene.12
In the steroid resistance, cyclophosphamide (CPA) may be
considered.1,5,10,13-17 Cucer et al (2010), reported that patients with steroid-
resistant nephrotic syndrome given CPA treatment obtained a complete
remission rate of 11.8% - 17.6%. The incidence of complete remission
rates increased to 25% when administered simultaneously with alternating
dose of oral prednisone.14 In a study conducted by Roy et al in
Bangladesh, a response rate of 65.63% was obtained in patients treated
with intravenous cyclophosphamide along with corticosteroids.15 Side
effects that need to be monitored at the time of cytostatic administration
are nausea, vomiting, bone marrow depression, alopecia, haemorrhagic
cystitis, azospermia, and in the long term can cause malignancy.
Therefore, it is necessary to monitor blood tests: haemoglobin, leukocyte,
platelet count, every 1-2 times a week. When the leukocytes is <3000/ul,
Hb<8 g/dl, platelets <100.000/mm3, the drug is suspended and continue
when the leukocyte >5,000 / ul.1,5,7-11 This patient is given intravenous
pulse of cyclophosphamide and oral prednisone alternating dose as a
31
theraphy for steroid-resistant nephrotic syndrome. The patient came to the
hospital to get the cycle II intravenous pulse CPA.
Diuretics in nephrotic syndrome is recommended especially if there
is anasarca edema. The first option is furosemide (loop diuretic) which can
be administered 1-3 mg/kg/day. If there is no improvement with the
administration of diuretics, although a combination of diuretics to treat
severe edema, albumin may be considered. Indication to give intravenous
albumin 20-25% is when serum albumin ≤ 1 gram/dl and given at a dose
of 1 gram/kgBW for 2-4 hours to draw fluid from the interstitial tissue and
continue with intravenous furosemide 1-2 mg/kgBW.6,8 Angiotensin
converting enzyme (ACE) inhibitor is an antihypertensive drug that
prevents the formation of angiotensin 2 which acts as a vasoconstriction,
thus increasing vascular resistance. A systematic review of the Cochrane
Database and The Kidney Disease: Improving Global Outcomes (KDIGO)
recommends the administration of ACE inhibitors in patients with steroid-
resistant nephrotic syndrome because it exhibits a 56% improvement in
proteinuria, maintaining blood pressure control better than other anti-
hypertensive drug.9,11 Another effect of the ACE inhibitors is that it has
anti-remodeling effects of blood vessels, as is known in children with
nephrotic syndrome with hyperlipidemia, this can lead to atherosclerosis if
it continues. ACE inhibitors also have a renoprotector effect through the
decline of transforming growth factor (TGF) -β1 and plasminogen activator
inhibitor (PAI) -1 synthesis, both of which are important cytokines that play
a role in the process of glomerulosclerosis.11 Based on two prior
randomized controlled trials, KDIGO recommends the administration of
ACE inhibitors in patients with SNRS.2 In this case, the patient is given
ACE inhibitors, captopril with the dose of 0.3 mg/kgBW/dose.
Administration of high-protein diet is considered to be
contraindicated because it will increase the glomerular load to excrete
protein metabolism (hyperfiltration) and cause glomerular sclerosis. A low-
protein diet also will cause protein energy malnutrition (PEM) and cause
32
child growth restriction. Therefore it is recommended a normal protein diet
in accordance with the Recommended Dietary Allowances (RDA) (1.5-2
grams/kg/day, low salt diet 1-2 grams/day). Fats can be administered in
maximum 30% of the total diet, preferably providing a complex
carbohydrate rather than a simple sugar.1,5 Fluid restriction is only
necessary in severe edema. In such circumstances, the fluid intake is
limited according to the insensible water loss added to the amount of urine
of the day before. Patients with mild edema does not require diuretics. It
starts with furosemide 1-3 mg/kgBW/day 2 times a day. If unresponsive, it
can be raised up to 4-6 mg/kgBW/day along with spironolactone
(aldosterone antagonist) 2-3 mg/kgBW/day, as potassium-sparing agent
(potassium-sparing diuretics). If the therapy failed, it can be added with
thiazide (hydrochlorothiazide). However, it is necessary to monitor the
occurrence of hypovolemia and monitoring of serum electrolyte. 5,10
Hyperlipidemia in nephrotic syndrome can be caused by several
factors such as increased synthesis of cholesterol, triglycerides and
lipoproteins by the liver, decreased lipoprotein lipase activity which in
normal circumstances will convert VLDL to LDL, decrease LDL receptor
activity and increase HDL loss through urine. Total cholesterol and LDL
usually increase while HDL is unchanged or slightly decreased resulting in
an increase in the LDL/HDL ratio. Patients with severe hypoalbuminemia
also experienced elevated levels of triglycerides and VLDL. Increased
levels of lipoproteins that occur in nephrotic syndrome also play a role in
increased cardiovascular risk, thrombosis complications and progressivity
of renal failure.18,19 Clinical experience of using statins in children with
nephrotic syndrome is limited but existing studies show that statins are
effective in reducing hyperlipidemia and can be considered in patients with
persistent hyperlipidemia.20,21 Hyperlipidemia is thought to exacerbate
glomerulosclerosis and progression of glomerular disease and may
increase the risk of cardiovascular disease. A study by Prescott et al21
showed that the use of HMG-CoA reductase inhibitors in nephrotic
33
syndrome reduced total cholesterol by 42%, 46% LDL, and 44%
triglyceride but no other outbreak reports such as cardiovascular events
and glomerolus effects. Research conducted by Kong et al22 concluded
that the use of statins may increase HDL (5.4 mg/dl with 95% CI 2.31-
8.49) as well as decreased of total cholesterol, LDL, and triglycerides.
Based on consensus management of idiopathic nephrotic syndrome in
children by Nephrology Unit of Indonesian Pediatric Society, statins can be
considered for steroid-resistant nephrotic syndrome. Cholesterol levels
may return to normal if the patient has had a remission. 6 There was also
hyperlipidemia in this patient and has been given simvastatin 10 mg once
daily.
The prognosis of steroid-resistant NS is determined by age, onset,
cause and type of renal impairment. There was an increase in remission to
25% in the steroid-resistant NS given cyclophosphamide along with
prednisone. In this case, prognosis ad vitam is bonam, due to the patient
condition is well and have good response on pulse cyclophosphamide
therapy dan prednisone alternating dose. In this patient, there was no
renal failure or other complications so the prognosis ad functionam is
dubia ad bonam. Prognosis ad sanationam is dubia ad malam. This is
because of resistance to steroids. On the literature, children with steroid
resistant nephrotic syndrome can developed to end stage renal disease
because of progressive damage on glomerulus filtration barrier. Besides,
the patient can have side effects of long term steroid administration such
as growth disorders, hypertension, osteoporosis, moon face, and obesity
can cause concerns from the family. Children with steroid resistant NS
tend to progress to end stage renal disease (ESRD) due to progressive
damage to glomerular filtration barrier.12
Zagury et al in a study of 136 children aged 3 to 18 years with
idiopathic steroid-resistant nephrotic syndrome in January 1974 to
September 2010, found that 57 of 136 patients (41.9%) developed into
ESRD. Risk factors for ESRD include older age onset, FSGS (focal
34
segmental glomerulosclerosis), early steroid resistance, resistance to
immunosuppressant agents, hematuria, and hypertension at presentation.
Clinical manifestations of hematuria were found in 79.5% of patients with
ESRD and 44.4% of patients without ESRD (p = 0.0006). (Level of
evidence 2B, recommendation B)24
Inaba et al, in a study of 69 children with steroid-resistant nephrotic
syndrome, 9 patients developed into ESRD. Risk factors contributing to
the occurrence of ESRD included age >11 years of diagnosis of steroid-
resistant nephrotic syndrome (HR = 36.3, 95% CI 2.2-604.6, p = 0.012)
and FSGS type biopsy (HR 10.7 ; 95% CI 1.3-89.7; p = 0.029). (Level of
evidence 2B, recommendation B)25
Roy et al., in a study of 32 patients aged 1-18 years with steroid-
resistant nephrotic syndrome treated with intravenous cyclophosphamide
and corticosteroids from January 2011 to June 2014, 65.63% of patients
with steroid-resistant nephrotic syndrome responded to therapy, 12.5%
developed decreased renal function to ESRD stage, and 15.63% died.
(Level of evidence 2B, recommendation B)26
Chang et al., in a study of 4,083 children aged 6 months to 18 years
with idiopathic nephrotic syndrome, 145 children (3.6%) developed into
ESRD. Predictors of ESRD included older age at onset (p <0.001, hazard
ratio = 1.16), acute kidney failure (p = 0.038, hazard ratio = 2.64),
encephalopathy hypertensive (p <0.001, hazard ratio = 146, 23), and
histologic type of FSGS (p <0.001, hazard ratio = 4.87). (Level of evidence
2B, recommendation B)27
35
REFERENCES
1. Noer MS. Sindroma nefrotik idiopatik. In: Noer MS, Soemyarso NA,
Subandiyah K, Prasetyo RV, Alatas H, Tambunan T, et al, editor.
Kompendium nefrologi anak. Jakarta: BP IDAI, 2011; p. 72-88.
2. Lombel RM, Hodson EM, Gipson DS. Treatment of steroid-resistant
nephrotic syndrome in children: new guidelines from KDIGO.
PediatrNephrol. 2012. 1-6
3. Bahn THM, Hussain-Shamsy N, Patel V, Vasilevska-Ristovska J,
Borges K, Sibbald C. Ethnic differences in incidence and outcomes
of childhood nephrotic syndrome. Clin J Am SocNephrol.
2016;11:1760-8.
4. Trihono PP, Putri ND, Pulungan AB. Prognostic factors and
survivals of children with steroid-resistant nephrotic syndrome.
PediatricaIndonesiana. 2013;53:42-9.
5. Seif EI, Ibrahim EAS, Elhefnawy NG, Salman MI. Histopathological
patterns od idiopathic steroid resistant nephrotic syndrome in
Egyptian children: a single center study. J Nephropathology.
2013;2:53-60.
6. Alatas H, Tambunan T, Trihono PP, Pardede SO. Konsensus
tatalaksana sindroma nefrotik idiopatik pada anak. Jakarta:
Nephrology Unit Indonesian Pediatric Society, 2005; p. 1-20.
7. Rahman MH, JEsmin T, Muinuddin G. An update of Management of
idiopathic nephrotic syndrome: a review article. Bangladesh J Child
Health. 2013;37:102-21
8. Trihono PP, Pardede SO, Alatas H, Sekarwana A, Rusdidjas, Noer
SM, dkk. Sindroma nefrotik. In: Pudjiadi AH, Hegar B, Handryastuti
S, Idris NS, Gandaputra EP, Harmoniati ED, editor. Pedoman
pelayanan medis IDAI. Jakarta: BP IDAI, 2010; p. 274-6.
36
9. Dantas S, Vera HK, Maria DF,Yassuhiko O. Influence of nephrotic
state on the Infectious profile in childhood idiopathic Nephrotic
syndrome. Rev. Hosp. Clín. Fac. Med. S. Paulo.2004;59(5):273-8.
10. BeataBanaszak&PawełBanaszak. The increasing incidence of
initial steroid resistance in childhood nephrotic syndrome.
PediatrNephrol. 2012; 27:927–932.
11. Saleem MA. New development insteroid-resistant nephrotic
syndrome. PediatrNephrol. 2012;1-9
12. Renda R, Aydog O, Bulbul M, Cakici EK. Children with steroid-
resistant nephrotic syndrome: 1 single center study. Int J Pediatr.
2016;4:1233-42.
13. Hidayati EL, Pardede SO, Trihono PP. Comparison of oral and
intravenous siklofosfamid in children with steroid resistant nephrotic
syndrome. Paediatrica Indonesiana.2011;vol 51(5):266-271.
14. Florentina C, Ingrith M, Robert M, Codruta IH. Treatment with
cyclophospamide for steroid resistant nephrotic syndrome in
children. Journal of Clinical Medicine. 2010;5(3):167-71.
15. Roy RR, HAque SMS, Mamun AA, Muinuddin G, Rahman MH.
Steroid resistant nephrotic syndrome in children: clinical
presentation, renal histology, complications, treatment and outcome
at Bangabandhu Sheikh Mujib Medical University, Dhaka,
Bangladesh. IOSR J Pharm. 2014;4:1-7.
16. Rebecca M. Lombel& Elisabeth M. Hodson & Debbie S. Gipson.
Treatment of steroid-resistant nephrotic syndrome in children: new
guidelines from KDIGO. 2012. PediatrNephrol. DOI
10.1007/s00467-012-2304-8
17. Van Husen M, Kemper MJ. New therapies in steroid-sensitive and
steroid resistant idiopathic nephrotic syndrome. PediatrNephrol.
2011;26:881-92
37
18. Apais P, Avner ED.Nephrotic syndrome. Dalam: Nelson WE,
Behrman RE, Kliegman RM, Arvin AM, eds. Nelson textbook pf
Pediatrics. 20th ed. Philadelphia: WB Saunders; 2016. h.2521-7.
19. Downie ML, Gallibois C, Parekh RS, Noone DG. Nephrotic
syndrome in infants and children: patophysiology and management.
Paediatr Int Child Health. 2017;15:1-11.
20. Mbarek IB, Abroug S, Omezzine A, Pawtowski A, Gubler MC,
Bouslama A. Novel mutations in steroid-resistant neprotic
syndrome diagnosed in Tunisian children. PediatrNeprol.
2011;26:241-9.
21. Gulati S, Sengupta D, Sharma RK, Gupta RK, Sigh U, Gupta A.
Steroid resistant nephrotic syndrome: role of histopathology. Indian
Pediatr. 2006;43:55-60.
22. Prescott WA, Streetman PA, Streetman DS. The potential role of
HMG-CoA reductase inhibitors in pediatric nephrotic syndrome.
Ann Pharmacother. 2004;38:205-14.
23. Kong XY, Yuan H, Fan JM, Li I, Liu TX, Jiang LH. Lipid-lowering
agents for nephrotic syndrome. Cochrane Database Syst Rev.
2013;10:CD005425.
24. Zagury A, Oliveira AL, Montalvao JA, Novaes RH, Sa VM, Moraes
CA, et al. Steroid-resistant idiopathic nephrotic syndrome in
children: long-term follow up and risk factors for end-stage renal
disease. J Bras Nefrol. 2013;35:191-9.
25. Inaba A, Hamasaki Y, Ishikura K, Hamada R, Sakai T, Hataya H, et
al. Long-term outcome of idiopathic steroid-resistant nephrotic
syndrome in children. PediatrNephrol. 2016;31:425-32
38
27. Chang JW, Tsai HL, Yang LY, Cheb TJ. Steroid-resistant idiopathic
nephrotic syndrome in children: long-term follow up and risk factors
for end-stage renal disease. J Epidemiol. 2012;22:517-22.
39
REFERENCES OF LEVEL OF EVIDENCE
23. Zagury A, Oliveira AL, Montalvao JA, Novaes RH, Sa VM, Moraes
CA, et al. Steroid-resistant idiopathic nephrotic syndrome in
children: long-term follow up and risk factors for end-stage renal
disease. J Bras Nefrol. 2013;35:191-9.
24. Inaba A, Hamasaki Y, Ishikura K, Hamada R, Sakai T, Hataya H, et
al. Long-term outcome of idiopathic steroid-resistant nephrotic
syndrome in children. PediatrNephrol. 2016;31:425-32
26. Chang JW, Tsai HL, Yang LY, Cheb TJ. Steroid-resistant idiopathic
nephrotic syndrome in children: long-term follow up and risk factors
for end-stage renal disease. J Epidemiol. 2012;22:517-22.
40
ABBREVIATIONS
ACE Angiotensin Converting Enzyme

AD Alternating Dose
ANP Atrial Natriuretic Peptide
Apo B Apoprotein B
BW Body Weight
BCG Bacillus Calmette Guerin
Ca Calsium
CDC Centers for disease Control and Prevention
Cl Chloride
Cm centimeter
CPA Cyclophosphamide
CRP C- Reactive Protein
CRT Capillary Refill Time
DPT DiphteriaPertussis Tetanus
ESRD End Stage Renal Disease
FSGS Focal Segmental Glomeulosclerosis
g Gram
g/dL gram per deciliter
GFR Glomerular Filtration Rate
Hb Hemoglobin
Ht Hematokrit
HDL High Density Lipoprotein
HR Hazard Ratio
Ig Imunoglobulin
IgA Imunoglobulin A
IL Interleukin
INH Isoniazid
ISKDC International Study of Kidney Disease in Children
IVFD Intravenous Fluid Drips
JVP Jugular Venouse Pressure
K Kalium
KDIGO The Kidney Disease: Improving Global Outcomes
Kg Kilo Gram
KgBB Kilo Gram Body Weight
Kcal Kilocalories
LDL Low Density Lipoprotein
MCG Minimal Change Glomerulopathy
mEq/L Milli Equivalen per Litre
Mg MilliGram
MG Magnesium
Mg/dL MilliGram per decilitre
mL milliLitre
Mm Millimeter
mmHg millimeter Hg
41
mm3 cubic millimeter
Na Natrium
NaCL Natrium Chloride
NS Nephrotic Syndrome
NSMC Nephrotic Syndrome Minimal Changes
PAI Plasminogen Activator Inhibitor
RDA Recommended Daily Allowances
RIFLE Risk, Injury, Failure, Loss, End Stage
SD Standard Deviation
SGOT Serum Glutamic Oxaloacetic Transaminase
SGPT Serum Glutamic Pyruvic Transaminase
SRNS Steroid-resistant Nephrotic Syndrome
TGF Transforming Growth Factor
TLR Toll Like Receptors
TT Tetanus Toxoid
USG Ultrasonograph
U/L Unit per Litre
VLDL Very Low Density Lipoprotein
42
APPENDIX
Appendix 1. Nutritional Status based on CDD 2000 Growth Chart
YS
Weight/age: 24/31x 100 % = 77%

Height/age: 121/136x 100 % = 89%
weight/height: 24/ 23 x 100% = 104 %
43
Appendix 2. Head Cirumference Chart
HEAD CIRCUMFERENCE CHART OF THE PATIENT

Head circumference 52 cm = Normocephal
H
d
g
f
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g
g 44
g
g
g
g
Appendix 3. Patient`s Photo
45

Timeline: October 7 2017 October 8 2017 October 12 2017 October 13 2017

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Timeline: October 7 2017 October 8 2017 October 12 2017 October 13 2017

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TIMELINE

Registration Number : 50.XX.XX

1.2. IDENTITY OF PARENTS

(Auto-anamnesis and allo-anamnesis from patient’s parents and medical

2.1 HISTORY OF PRESENT ILLNESS

2.2 HISTORY OF PREVIOUS ILLNESS

2.3 HISTORY OF ILLNESS IN THE FAMILY

History of the same illness in the family was denied

No Name Relationship Sex Age Information

1. FS Father M 60 years Healthy

2.4. PERSONAL/SOCIAL HISTORY

E. GROWTH AND DEVELOPMENTAL HISTORY

G. HISTORY OF BASIC NEEDS

PATIENT CONDITIONS BEFORE BECOME LONG CASE

On physical examination when admitted to hospital, the weight is 24

III. PHYSICAL EXAMINATION

Vital signs : Blood pressure 110/70 mmHg, pulse 96 bpm

Skin : light brown colored, no efflorescent, no

3.Pediatric Nutritional Care

e. Monitoring and evaluation

f. Follow up and monitoring

October 8th 2017(1stobservation day, 2nd day of hospitalization)

A Steroid Resistant Nephrotic Syndrome (N00-08)

Monitoring and evaluation :

Pediatric nutritional care

A Steroid Resistant Nephrotic Syndrome (N00-08)

A Steroid Resistant Nephrotic Syndrome (N00-08)

Monitoring and evaluation :

Pediatric nutritional care

When used as a case

Diagnosis PE : Head : edema of PE : Head : edema of

K General Hospital Urinalysis: +3protein Urinalysis: +1 protein Leucocytes: 11.600 /

A boy, 9 years 11 months old - Response therapy

Symptoms Swelling on the face

Diagnosis Steroid Resistant Nephrotic Syndrome

Treatment Cyclophosphamide puls, prednisone alternating dose, captopril, simvastasin,

Prognosis Therapy response Ad vitam bonam Parent education

 Zagury, et al. J Bras Nefrol.2013. Level of evidence 2b, recommendation B

ACE Angiotensin Converting Enzyme

Weight/age: 24/31x 100 % = 77%

HEAD CIRCUMFERENCE CHART OF THE PATIENT

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