TIMELINE

October 7th2018 October 8th 2017 October 12nd 2017

Patient was
admitted to K
Hospital
Diagnosis :
Steroid
Initial
Resistant Final
observation by Report
Nephrotic
candidate observation
Syndrome
Observation
started
 PATIENT’S RECORD
Candidate : Ronald Rompies

I. IDENTITY
I.1. IDENTITY OF PATIENT
Patient Name : HDA
Date of birth : April 20th 2007
Age : 10 years 10 months old
Gender : Female
Nationality : Indonesian
Date of admission : May 30th 2018, at 21.00
Registration Number : 52.76.XX

I.2. PARENTS IDENTITY

FATHER MOTHER
Name : NH JG
Age : 46 years old 41 years old
Occupation : Farmer Housewife
Education : Senior High School senior high school

II. HISTORY
(Auto-anamnesis and allo-anamnesis from patient’s parents and medical
records on May 30th, 2018)

Chief complaint
Swelling on the face and lower limbs

2.1 HISTORY OF PRESENT ILLNESS

Patient was admitted to hospital on May30th, 2018 at 21.00 with chief complaint
of swollen on the face and lower limbs since 3 months. She was reffered from
primary health care. Her mother noticed she had swelling on the face,
occurred 3 month before admission and followed by lower limbs swelling. The
chief complaint didn’t accompanied by shortness of breath during sleep time or
on daily activity. Patient didn’t complaint any pain, redness nor itchiness.
 Patient denied any history of insect bite. Patient also didn’t complaint about
abdominal pain.
Patient has good appetite. He usually eats home meal food 3 times a
day. Patient denied history of dark colored urine and pain during urination.
Patient also denied history of fever before. There was no complaint about
patient defecation pattern too.
At this time, , the patient was diagnosed with nephrotic syndrome steroid
resistant, treated with corticosteroid since March 17 th, 2018 and treated with
cyclophosphamide puls since 1 month ago.

2.2 HISTORY OF PAST ILLNESS

Patient was admitted to L hospital in February 2018 and diagnosed with
nephrotic syndrome. She was treated with corticosteroid 13 tablets each day for
6 weeks. 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 March 2018 for further evaluation and treatment. Patient
was diagnosed with steroid-resistant nephrotic syndrome and treated since
April 2018. She denied history of red coloured urine, swallowing pain or
infection of the skin previously. Patient has no allergy to drugs.

2.3 FAMILY HISTORY OF ILLNESS

History of the same illness in the family was denied. There was no family
history about kidney disease.

FAMILY PEDIGREE
STRUCTURE OF FAMILY MEMBERS

No Name Relationship Sex Age Information

1. NH Father M 46 years Healthy

2. JG Mother F 41 years Healthy
3. JH Child M 17 years Healthy
4. YH Child M 14 years Healthy
5. CH Child F 10 years Patient
10 months

2.4. PERSONAL/SOCIAL HISTORY

A. HISTORY OF ANTENATAL CARE
Patient’s mother had nine times antenatal examinations at primary health
care and got Tetanus Toxoid immunization (TT) twice, and took iron tablets
routinely during pregnancy. She was healthy during the pregnancy.

B. HISTORY OF LABOR
Patient was born spontaneously, fullterm at primary health care, 4000 gram,
birth length was unknown, directly crying, helped by midwife.

C. HISTORY OF POSTNATAL
 Patient had never experienced any cyanotic or yellowish skin color. Patient
is brought for routine control and immunization at primary health care.

D. HISTORY OF FEEDING
Patient got exclusive breastfeeding since she was born until six months old
and continued until 2 years old. Milk porridge was given at 6 months old,
then changed to strained porridge that was given at 8 months old. Soft rice
was given at 10 months old. She started to eat home meals at 12 months
old until now. She eats three times a day of 1 plate main portion. One plate
consist of rice with fish, or chicken, eggs and vegetables and fruits.
Conclusion: No history of abnormal feeding

E. DEVELOPMENTAL MILESTONES
Patient was routinely examined for growth and development at primary
health care until 9 months old and said that she had normal growth and
development was normal. According to the mother, the growth of the patient
was equal with her peers.
Right now, patient was on fifth grade elementary school. At elementary
school age, patient actively socialized with her peers, had curiousity and
learn well. She never failed her educational degree. According to patient’s
parents, the patient’s development was the same as her peers.
Conclusion: patient’s growth and developmental milestones was normal
according to her age.

F. HISTORY OF VACCINATION
Patients received BCG vaccination with scar (+) on upper right arm, polio 5
(five) times, DPT 4 (four) times, DT once, Td once hepatitis B 5 (five) times,
measles twice.
Conclusion: patients received basic immunization and booster according
to age.

G. HISTORY OF BASIC NEEDS

Physic-biomedic:
 Patients recieved adequate primary needs (food, clothes and shelter). She
received a home meal three times a day. When she gets sick, her parents
took him to the nearest health facility in the area.

Emotional needs:
The patient received sufficient affection from both parents and other family
members. Parents accepted patient’s medical condition, care and give
adequate affection for patient’s recovery.

Mental stimulation:
Patient learn and play like her peers. Patient has many friends and easily
socialize with new friend. Currently, patient in fifth grade of elementary
school and can follow the lessons taught in school very well.
Conclusion: Patient received adequate affection, care and attention from
her family

H. SOCIO-ECONOMIC AND ENVIROMENT CONDITIONS

The patient’s father worked as farmer and mother as a housewife. Medical
treatment cost is covered by class III national health insurance.
Patient live with both parents in semi-permanent house with tin roofed
house, concrete-walled, tiles floor. There are 3 rooms in the house,
occupied by 5 peoples, 2 adults and 3 children. Bathroom and restroom are
located outside the house. Source of electricity comes from goverment
electricity company. Source of drinking water comes from public water
company. Garbage is handled by dumping outside the house.
Conclusion: Social economic condition middle to lower family class

I. Patient’s Hospital Admission Summary (May 30h 2018)

(Patient’s history during hospitalization was provided by patient’s parents
and hospital medical record).

Patient was admitted to hospital on May 30th, 2018 at 21.00 with chief
complaint of swollen on the face and lower limbs. She was referred from
primary health care. Her mother noticed she had swelling on the face,
 occurred 3 month before admission and followed by lower limbs swelling.
The chief complaint didn’t accompanied by shortness of breath during sleep
time or on daily activity. Patient didn’t complaint any pain, redness nor
itchiness. Patient denied any history of insect bite. Patient also didn’t
complaint about abdominal pain. Patient denied history of dark colored
urine. Patient also denied history of fever before. There was no complaint
about patient defecation pattern too. Patient had good appetite. He usually
eats home meal food 3 times a day.The patient has been treated with
diagnosis of nephrotic syndrome with corticosteroid since March 2018. At
this time, the patient diagnosed with resistance steroid nephrotic syndrome
and had been treated with cyclophosphamide (CPA) puls.
On physical examination when admitted to hospital, the weight is 31.8
kg, height 139 cm, good nutrition status. Patient was compos mentis, blood
pressure 120/80 mmHg, pulse 96 beats / min (strong, enough content),
respiratory rate 26 cycles/min, temperature 36,5˚C axilla. On head
examination, there was no swollen on the 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 genital examination. There was no lower limbs
pitting edema.
On laboratory result when admitted to the hospital we found the
hemoglobin was 12,5 g/dL, hematocryte 42.9%, leucocytes 13.700 /mm3,
platelets 467.000 /mm3, AST 23 U/L, ALT 30 U/L, ureum 42 mg/dL,
creatinine 0.6 mg/dL (GFR: 129 ml/min/1.73m2), albumin 3,64 g/dL, total
cholesterol 373 mg/dL, HDL 93 mg/dL, LDL 231 mg/dL, trigyceride 245
mg/dL, sodium serum electrolytes 139 mEq/L, potassium 4.5 mEq/L,
chloride 92.9 mEq/L. Urinalysis found that urine was yellow and cloudy,
with microscopically erythrocytes 1-2 cells/hpf, leucocytes 1-2 cells/hpf,
protein (+3), nitrite (-), keton (-), glucose (-), bilirubin (-), and urobilin (-).
Patient diagnosed as having nephrotic syndrome steroid resistant. Patient
was treated with prednisone 1 x 46,8 mg alternating dose, furosemide 2 x
10 mg orally (dose 0,5 mg/kgBW/day), low salt diet 1 g/day. Monitoring vital
signs, urinalysis, fluid balance regularly.
III. PHYSICAL EXAMINATION
The examination was performed in pediatric nephrology ward, on May 30th,
2018 (1st day of hospitalization).

General condition : looked ill, Consciousness: compos mentis

Antropometri status:
Antropometric status based on CDC 2000:
Actual Body Weight (BW) : 31.8 kg
Body Height (BH) : 139 cm
Ideal Body Weight : 32.5 kg
Body surface area : 1.11 m2
Based on CDC 2000:
Body weight/Age : 31.8/ 35 x 100% = 90.9%
Body height/Age : 139/142 x 100% = 97.9%
Body Weight/Height : 31.8/32.5 x 100% = 97.8 %
 Nutritional status: good nutritional status(CDC 2000)

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

(regular,enough content), respiratory rate 26 cycles/min,
thoracal, body temperature 36,5°C (axilla).

Skin :light brown colored, no efflorescent,

No hypopigmentation or hyperpigmentation,
BCG scar on right upper arm.

Head and Neck

Head : normocephaly, head circumference 53 cm
(betweeen -2 SD and +2 SD)  normal, black hair,
not easily pluck, large fontanelle is not palpable
(already closed).
Eyes : eyelid swelling -/-, no anemic conjunctiva,
anicteric sclera, isochoric pupils  3 mm-3 mm,
reactive to light, centered eyeballs, good eye
movements to all direction, clear lenses, corneal
reflex +/+
Nose :no deformities, no secret found, nasal breathing (-)
Ears : no deformities, no secret found
Mouth : no cyanosis, moist buccal mucosa and lips, no
tongue papiles atrophy, symmetrical nasolabial
sulcus, no teeth caries, no stomatitis, no beslag.
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 inter costalspace
is not widened, no retraction

Heart
Inspection : ictus cordis was unseen, no precordial bulging
Palpation : ictus cordis palpable in left midclavicular line, 5 th
intercostal space, there was no thrill
Percussion : right border at right parasternal line, left border at left
midclavicular line, upper border at 3 rd left intercostal
space.
Auscultation :heart rate frequency 96 bpm, regular, pure S1 and
S2, no murmur was found

Lungs
Inspection : symmetrical movement of breathing, no retraction,
the intercostal space is not widened.
Palpation : symmetrical vocal fremitus
Percussion : symmetrical resonant sounds, no dullness
Auscultation :vesicular breath sounds, no rales, no wheezing.

Abdomen
Inspection : flat, following movement of the chest wall, no
venectation
Palpation : soft, spleen and liver not palpable, no suprapubic
pain, abdominal circumference was 52cm
Percussion : no shifting dullness, no costovertebral pain
 Auscultation : normo-active bowel sounds

Genitalia : female, normal

Puberty Scale: Tanner scale II (M2A1P1)
Extremities : warm, no cyanosis, no deformities, normal muscle
tone, CRT ≤2 seconds,lower limbs pitting edema (-)
Reflexes : normal physiological reflexes, no pathological
Reflexes,
Sensory : normal
Motoric : normal muscles strength
5/5
5/5

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 left and right shoulders upward
N XII = no deviation of the tongue
SUMMARY
Patient was admitted to hospital on May 30th, 2018 at 21.00 with chief complaint
of swollen on the face and lower limbs. She was reffered from primary health care.
Her mother noticed she had swelling on the face, occurred 3 month before
admission and followed by lower limbs swelling. The chief complaint didn’t
accompanied by shortness of breath during sleep time or on daily activity. Patient
didn’t complaint any pain, redness nor itchiness. Patient denied any history of insect
bite. Patient also didn’t complaint about abdominal pain. Patient denied history of
darked colored urine and pain during urination. Patient also denied history of fever
before. There was no complaint about patient defecation pattern too. Patient has
good appetite. He usually eats home meal food 3 times a day. At this time, the
patient has been treated with diagnosis of nephrotic syndrome steroid resistant with
corticosteroid since March 2018, and cyclophosphamide puls since 1 month ago.
Patient was admitted to L hospital in February 2018 and diagnosed with
nephrotic syndrome. She was treated with corticosteroid 13 tablets each day for 6
weeks.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 March 2018 for further evaluation and treatment. Patient was diagnosed with
nephrotic syndrome steroid resistant on March 2017. She denied history of red
coloured urine, swallowing pain or infection of the skin previously. Patient has no
allergy to drugs.
On physical examination when admitted to hospital, the weight is 31.8 kg,
height 139 cm, good nutrition status. Patient was compos mentis, blood pressure
110/70 mmHg, pulse 96 beats / min (strong, enough content), respiratory rate 26
cycles/min, temperature 36,5˚C axilla. On head examination, there was no swollen
on the 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 genital examination. There was no lower limbs pitting
edema.
On laboratory result when admitted to the hospital,we found the hemoglobin
was 12,5 g/dL, hematocryte 42.9%, leucocytes 13.700 /mm3, platelets 467.000 /mm3,
AST 23 U/L, ALT 30 U/L, ureum 42 mg/dL, creatinine 0.6 mg/dL (GFR: 129
ml/min/1.73m2), albumin 3,64 g/dL, total cholesterol 373 mg/dL, HDL 93 mg/dL, LDL
231 mg/dL, trigyceride 245 mg/dL, sodium serum electrolytes 139 mEq/L, potassium
4.5 mEq/L, chloride 92.9 mEq/L. Urinalysis found that urine was yellow and cloudy,
with microscopically erythrocytes 1-2 cells/hpf, leucocytes 1-2 cells/hpf, protein (+3),
nitrite (-), keton (-), glucose (-), bilirubin (-), and urobilin (-). Patient diagnosed as
having nephrotic syndrome steroid resistant. Patient was treated with prednisone 45
mg (9 tablets) daily alternating dose, simvastatin 10 mg daily, captopril 10 mg three
times a day, low salt diet 1 g/day. Monitoring vital signs, urinalysis, fluid balance
regularly.
IV. DIAGNOSIS

Nephrotic Syndrome Steroid Resistant (N00-08)

V. LIST OF PROBLEM
Prognostic of a girl 10 years 10 months old with nephrotic syndrome steroid
resistant.

VI. MANAGEMENT PLANS

1. Treatment plans
Medication therapy:
 Prednisone 45 mg daily (9 tablets) alternating dose
 Captopril 10 mg three times a day
 Simvastatin 10 mg daily

2.Pediatric Nutritional Care

A. Assessment:
10 years 10 months old girl: body weight 31.8 kg, height 139 cm
Nutritional status: good nutrition status (based on CDC 2000 growth
chart stature for age and weight for age percentiles, girls age 2-20 years)
B. Nutritional requirements according to the Recommended Daily
Allowance:
Energy : 70 kcal/kg/day = 2275 kcal/day
Protein : 1 g/kg/day= 32.5 g/day
Fat : 30% x 2275 kcal = 682 kcal/day = 76 g/day
Fluid : 70-85 mL/kgBW = 2300-2700 mL/day
Salt : 1 g/day
C. Nutritional route: per oral
D. Determination the mode of administration
Given in the polymeric form
In the form of:
- Solid food 3 x 1 portion(@ 570 kcal, 10 g protein, 25 g fat)
- Rice 3/4 glass, 1 medium slice chicken with skin, 1 medium fermented
soybean cake slice, vegetables (spinach100 g)
- 2 x 1 snacks (@ 150 kcal)
- 1 glass of milk 200 ml (@ 260 kcal, 5 g protein)
 E. Monitoring and evaluation:
Monitoring of acceptability, food tolerance, adverse reactions and body
weight changes

3. Follow up and monitoring

 Monitoring of vital signs, body weight, abdominal circumference, fluid
balance and diuresis.
 Monitoring kidney function
 Monitoring urinalysis
 Monitoring nutrition
 Monitoring therapies, response, and drugs adverse effect (steroid)

4. Educations plans
a. Describes the illnesses: causes, complications, treatment plans, side
effects, follow up, and prognosis.
b. Educate proper feeding to meet nutritional needs and disease
c. Educate to maintain oral hygiene and environment
d. Educate about further evaluation after patient’s discharged (routine
follow-up)

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. Input and output monitoring
6. Mental and emotional support
VII. FOLLOW UP

May 31th 2018(1stobservation day, 2nd day of hospitalization)

S fever (-), swelling (-) on face, oral intake (+)
O General condition : looked ill, compos mentis
Blood pressure : 110/70 mmHg Respiratory rate : 24 cpm
Pulse : 86 bpM Temperature : 36.8oC (axilla)
Body weight : 34,2 kg BSA : 1,14/m2
Fluid balance : -442 mL Diuresis : 1,75 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:
62 cm, ascites (-)
Genitalia : female, 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 :7 Bilirubin :-
Leukocyte : 2-4/hpf Blood : +1
Nitrite :- Erythrocyte : 10-20/hpf
Protein :+3

A Steroid Resistant Nephrotic Syndrome (N00-08)

P Therapeutic :
- Prednison 5 mg orally, 9 tablet once a day alternating dose
- Captopril 10 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

June 1st 2018(2ndobservation day, 3rd day of hospitalization)

S fever (-), swelling (-) on face, oral intake (-)
O General condition : looked ill, compos mentis
Blood pressure : 110/60 mmHg Respiratory rate : 24 cpm
Pulse : 88 bpM Temperature :36,7oC (axilla)
Body weight : 34,2kg BSA : 1,14/m2
Fluid balance : +120 mL Diuresis : 1.9 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
A Steroid Resistant Nephrotic Syndrome (N00-08)
P Therapeutic :
- Prednison 5 mg orally, 9 tablet once a day alternating dose
- Captopril 10 mg three times a day orally
- Simvastatin 10 mg one a day orally
- Puls Cyclophosphamide
 Hyperhidration IVFD Sodium chloride 0,45% in D5% + 20mEq Sodium
Bicarbonate: 100 ml/ hour ( for 12 hours)
 IVFD Mesna 120 mg in 100 ml Sodium chloride 0,9% = 100ml/ 30
minutes
 IVFD cyclophosphamide 600 mg + Mesna 240 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 5 mg IV
Dexamethasone 5,5 mg IV
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

June 2nd 2018 (3rdobservation day, 4th day of hospitalization)

S fever (-), swelling (-) on face, good oral intake (+)
O General condition : looked ill, compos mentis
Blood pressure : 100/60 mmHg Respiratory rate : 24cpm
Pulse : 80 bpm Temperature : 36,2oC (axilla)
Body weight : 31.8 kg BSA : 1.11/m2
Fluid balance : +28 mL Diuresis : 1,93 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
A Steroid Resistant Nephrotic Syndrome (N00-08)

P Therapeutic :
- - Prednison 5 mg orally, 9 tablet once a day alternating dose
- Captopril 10 mg three times a day orally
- Simvastatin 10 mg one a day orally
Monitoring and evaluation :
Water balance, diuresis
Body weight, abdominal circumference
Pediatric nutritional care
Same as before
Mineral water 1600 ml
Nursing care :
Same as before

June 3rd 2018 (4thobservation day, 5th day of hospitalization

S fever (-), swelling (+) on face decrease, good oral intake (+)
O General condition : looked ill, compos mentis
Blood pressure : 100/70 mmHg Respiratory rate : 24 cpm
Pulse : 84 bpm Temperature : 36,8oC (axilla)
Body weight : 31.8kg BSA : 1.11/m2
Fluid balance : +46mL Diuresis : 1.2 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 hypere
lymph node enlargement (-), JVP not increase
Neck : no retraction
Chest : within normal limit
Lungs-heart : flat, soft, normal bowel sound, liver and spleen were not palpable, Abdomin
Abdomen : 59 cm, ascites (-)
male, normal, edema (-)
Warm, lower limb edema (-), capillary refill time
Genitalia : < 2 seconds
Extremities :

Laboratory :
Urinalysis :
Color : Clear, yellow
Specific gravity : 1.020
pH :7
Leukocyte : 1-3/hpf
Nitrite :-
Protein : +1
Glucose :-
Ketone :-
Urobilinogen :-
Bilirubin :-
Blood : +1
Erythrocyte : 5-8/hpf

A Steroid Resistant Nephrotic Syndrome (N00-08)

P Therapeutic :
- - Prednison 5 mg orally, 9 tablet once a day alternating dose
- Captopril 10 mg three times a day orally
- Simvastatin 10 mg one a day orally
Monitoring and evaluation :
Water balance, diuresis
Body weight, abdominal circumference
Pediatric nutritional care
Same as before
Mineral water 1400 ml
Nursing care :
Same as before

June 4th 2018 (5thobservation day, 6th day of hospitalization

S fever (-), swelling (+) on face decrease, good oral intake (+)
O General condition : looked ill, compos mentis
Blood pressure : 90/60 mmHg Respiratory rate : 22 cpm
Pulse : 84 bpm Temperature : 36,6oC (axilla)
Body weight : 31 kg BSA : 1.11/m2
Fluid balance : +32mL Diuresis : 1.1 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:
58 cm, ascites (-)
Genitalia : male, normal, edema (-)
Extremities : Warm, lower limb edema (-), capillary refill time
< 2 seconds

A Steroid Resistant Nephrotic Syndrome (N00-08)

P Therapeutic :
- Prednison 5 mg orally, 9 tablets once a day alternating dose
- Captopril 10 mg three times a day orally
- Simvastatin 10 mg one a day orally
Monitoring and evaluation :
Water balance, diuresis
Body weight, abdominal circumference
Pediatric nutritional care
Same as before
Mineral water 1500 ml
Nursing care :
Same as before

June 5th 2018 (6thobservation day, 7th day of hospitalization

S fever (-), swelling (-) on face, good oral intake (+)
O General condition : looked ill, compos mentis
Blood pressure : 100/60 mmHg Respiratory rate : 22 cpm
Pulse : 80 bpm Temperature : 36,7oC (axilla)
Body weight : 31 kg BSA : 1.11/m2
Fluid balance : +40mL Diuresis : 1.2 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:
57,5 cm, ascites (-)
Genitalia : male, normal, edema (-)
Extremities : Warm, lower limb edema (-), capillary refill time
< 2 seconds

A Steroid Resistant Nephrotic Syndrome (N00-08)

P Therapeutic :
- Prednison 5 mg orally, 9 tablets once a day alternating dose
- Captopril 10 mg three times a day orally
- Simvastatin 10 mg one a day orally
Monitoring and evaluation :
Water balance, diuresis
Body weight, abdominal circumference
Pediatric nutritional care
Same as before
Mineral water 1400 ml
Nursing care :
Same as before

June 6th 2018 (7thobservation day, 8th day of hospitalization

S fever (-), swelling (-), good oral intake (+)
O General condition : looked ill, compos mentis
Blood pressure : 90/60 mmHg Respiratory rate : 24 cpm
Pulse : 86 bpm Temperature : 36,6oC (axilla)
Body weight : 31 kg BSA : 1.11/m2
Fluid balance : +46mL Diuresis : 1.2 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:
57,5 cm, ascites (-)
Genitalia : male, normal, edema (-)
Extremities : Warm, lower limb edema (-), capillary refill time
< 2 seconds
Laboratory :
Urinalysis :
Color : Clear, yellow
Specific gravity : 1.010
pH :7
Leukocyte : 1-3/hpf (-)
Nitrite :-
Protein :-
Glucose :-
Ketone :-
Urobilinogen : -
Bilirubin :-
Blood :-
Erythrocyte : 2-3/hpf (-)
A Steroid Resistant Nephrotic Syndrome (N00-08)

P Therapeutic :
- Prednison 5 mg orally, 9 tablet once a day alternating dose
- Captopril 10 mg three times a day orally
- Simvastatin 10 mg one a day orally
- Outpatient today with the arrangement of cyclophospamide pulse cycle 3 next
month.
Monitoring and evaluation :
Water balance, diuresis
Body weight, abdominal circumference
Pediatric nutritional care
Same as before
Mineral water 1400 ml
Nursing care :
Same as before

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 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 3 months before admitted to hospital. 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 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 since 3 months . 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
Patient was diagnosed with nephrotic syndrome from 3 months ago. Patient
was treated with full-dose prednisone for 6 weeks, but did not under go remission
and then diagnosed with steroid-resistant nephrotic syndrome. In the initial
examination in April 2018 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 4-6 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, 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/mm 3, 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 theraphy for steroid-
resistant nephrotic syndrome. The patient came to the hospital to get the cycle II
intravenous pulse CPA.
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 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 al 21
showed that the use of HMG-CoA reductase inhibitors in nephrotic 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 al 22 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 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

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.

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
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
26. 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.
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.
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
25. 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.
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.