LC Nur Liya EDIT

Long Case Report
Acute Post Streptococcal Glomerulonephritis

and Grade 2 Hypertension
Nur Liya Abd. Kadir
Local Board Examination

Makassar, 11th November 2021
INDONESIAN COLLEGE OF PEDIATRICS

2021
TIMELIME DIAGRAM
Observation by
candidate
October 12th October October November

2021 13th 2021 22th 2021 11st 2021
Patient was Patient was Final

admitted to admitted to Observation by
Emergency Pediatric Ward candidate Report
Room of “W” of “W” Hospital
Hospital and began to
observation by
candidate
PATIENT’S IDENTITY
Name :M
Gender : Male
Age : 9 years old 6 months
Date of birth : March 26th 2012
Medical record : 949lxxx
Address : Tombolo, Malino
Admission date : October 12th 2021
Hospital length of stay : 11 days
PARENT’S IDENTITIES : Father Mother

Name : Mr. H Mrs. N
Age : 37 years old 35 years old
Last education : Bachelor Diploma
Occupation : Entrepreneur Housewife
Address : Tombolo Tombolo
Initial observation by candidate began on November 12 th 2019
PATIENT’S HISTORY (Alloanamnesis from the mother)

Chief Complaint:
History of seizures
History of present illness
A 9-year 6-months-old male referred from M Hospital with diagnose
Acute Nephritic Syndrome. There was seizures 1 day before admitted to
the hospital, frequency 2 times, duration 5 minutes, generalized, after
seizure the child was sleepy. There was headache from 3 days ago. No
fever, but there was history of fever 2 weeks before admitted to the
hospital, intermittent and released with antipyretic medication. There were
cough and sore throat since 1 week before, no phlegm. There was no
vomit.
Local Board Examination, Makassar, November 11th 2021 Page 1

His defecation was within normal limit. Urine output was considered
normal, dark colored urine.
History of previous illness
History of edema in face and eyelid 3 days before admitted to the
hospital. There was history of dark colored urine 3 days before, no foam.
There were no history of seizure and hypertension. There was history of
recurrent respiratory tract infection and hypertension in his family,
grandfather and grandmother.
There was history of skin lesions 3 weeks ago. There were no
history of hair fall, joint pain, mouth ulcer, consuming prednisone, kidney
disease, autoimmune disease, metabolic disease and malignancy in
family.
There was history of being treated in M hospital for 5 days and get
therapy paracetamol, ondansentron, furosemide, ceftriaxone, gentamycin,
captopril, nifedipine. At emergency room of W hospital, the patient got
nifedipine sublingual.
History of illness in the family

There was no history of kidney disease in his family before.
Patient’s personal and social history

a) Prenatal history
During pregnancy, the mother had routine control at the midwives,
and was given vitamin and iron supplementation, she never had any
herbal nor drugs other than prescript from medical professional. She felt
healthy enough with full-term pregnancy, and never experienced any
trauma or other problems during the pregnancy.
Conclusion: A mother had a normal prenatal history.
b) History of delivery
Patient was born at a hospital. It was full-term, spontaneous
delivery, assisted by doctor. The baby cried immediately, no cyanosis.

Birth weight was 2600 grams, birth length and head circumference were
forgotten.
Conclusion: Patient was born full-term, normal birth weight, with
normal history of delivery.
c) Post-natal history
Hepatitis B vaccination was given on the first day, and oral polio at
discharge time. No history of cyanosis, pale, jaundice, seizure nor
bleeding. The mother stayed at the hospital for two more days after
delivery.
Conclusion: post-natal history was unremarkable.
d) Feeding history
Patient was breastfed since born up to 6 months old.
Complementary food was first introduced at 6 months of age in form of
milk porridge, followed by steam rice by the age of 9 months old and
had family meal since 1-year-old. At the moment patient consumed rice,
fish, chicken/meat, eggs, tofu/tempeh, vegetables and fruits.
Conclusion: Patient had an adequate quality and quantity of
intake.
e) Growth and developmental history

Growth
Up until the patient was 1 years old, the mother routinely took him
to posyandu, and based on Kartu Menuju Sehat (KMS), patient’s growth
was always above the green line, hence normal growth.
Developmental
Patient was able to show responsively smile at the age of 2 months
old, roll over at 4 months old, sat without support at 7 months old, stand
alone at 12 months old, was able to walk well by the age of 14 months
old and was able to speak at 12 months old.

We use Pediatric Symptom Checklist (PSC) to detect risk of mental
and behavioral disturbance that might happen due to the disease
(appendix), total score was 2.
Conclusion: Growth and developmental history were within normal
limit.
f) History of immunization
The immunizations that has been obtained were hepatitis B only
once after delivery, and he did not got immunization. His parent refused
immunization for their child.
Conclusion: incomplete basic immunization
g) Basic needs
Physical-bio medic needs
Patient’s main caregiver was his mother. Patient did adequately
breastfed. Complementary food was introduced after 6 months old, and
since the age of 1 year, he had family meal. Clothing needs was also
fulfilled.
Conclusion: Patient’s parent is able to fulfill all of the patient’s
physical-bio medic needs adequately.
Emotional needs
Parents-child relationship seems close and lovingly. Both the
mother and father love the patient very much. The mother is patient
enough. She also tried to be more concerned about her child illness.
Conclusion: Adequate emotional needs from both parents.
Mental stimulation needs

Early stimulations were given by both parents since early age that
includes touch and hug, playing together, and talking. He also likes to
play with his brothers.
Conclusion: Mental stimulation needs are fulfilled.
h) Family socio-economy history/environment/ housing

The father is 37 years old, a Muslim, graduated with bachelor
degree, and works as entrepreneur with monthly income around
Rp.4.000.000. The mother is 35 years old, a Muslim, graduated with
diploma degree as housewife. Patient lives with his parents in a
permanent house, around 8 x 13 m 2, consisted of 2 bedrooms, 1 living
room, 1 kitchen, 1 bathroom, and 1 working room.
Source of the family Drinking water is from tap water. Water for
daily activities such as for washing and bath are from water supply
company (PDAM). Electricity source is coming from national electricity
company (PLN). Ventilation and light at the house is sufficient. The
nearest health facility from the patient’s house is primary health center
(Puskesmas) about ± 500 m away. Hospital bill is covered by national
health insurance.
Conclusion: Patient comes from a middle economic class. Health
facility is easily accessible and health care fees are covered by
government.
PATIENT’S HOSPITAL ADMISSION SUMMARY

A 9-years 6-months-old male presented with a 1-day history of
seizure, frequency 2 times, duration 5 minutes, generalized, after seizure
the child was sleepy. There was headache from 3 day ago. No fever, but
there was history of fever 2 weeks before admitted to the hospital,
intermittent and released with antipyretic medication. There were cough
and sore throat since 1 week before, no phlegm. There was no vomit. His
defecation was within normal limit. Urine output was considered normal,
dark colored urine.
Growth and development of the patient was always in normal
range. Basic immunization was incomplete.
The patient was diagnosed with Acute Post Streptococcal
Glomerulonephritis with Grade II Hypertension. Then treated with
antibiotic, diuretic, antihypertension, antiseizures, diet and bed rest.

PHYSICAL EXAMINATION
General condition : Moderately ill
Consciousness : Glasgow coma scale 15 (E4M6V5)
Vital signs
Blood pressure : 140/100 mmHg (> P95+12mmHg)
Blood pressure percentile based on age, height and sex
50th percentile : 97/58 mmHg
95th+12mmHg percentile : 124/86 mmHg
Heart rate : 95 beats per minute, regular, adequate volume
Respiratory rate : 22 breaths per minute, regular, no chest indrawing
Temperature : 36,8oC
Pain scale : 3 NRS (Numeric Rating Scale)
Anthropometric status
Actual BW : 24.5 kg
Ideal BW : 26 kg
Body Height :129 cm (< P3 CDC-NCHS 2000 Chart,
appendix)
Head circumference (HC) : 51 cm (-2 SD<HC<0 SD, Nellhaus
curve, Appendix)
Weight-for-Height : 94% (normal, CDC NCHS 2000 chart,
Appendix)
Height-for-age (H/A) : 94.8% (Normal, CDC-NCHS 2000
chart, Appendix)

Weight-for-age (W/A) : 82% % (wasted, CDC-NCHS 2000
chart, Appendix)
Height Age : 9 years 6 months
Father’s height : 163 cm
Mother’s height : 155 cm
Genetic potential height : 144 – 161 cm (<P3 – P50,
CDC-NCHS 2000 chart)
Midparental height : 152,5 cm
Conclusion: good nourished, normal stature.
Table 1. General examination
System Description
Skin No erythema, no purpura, good turgor, no striae, no
achantosis nigricans, no jaundice, and no pale. No
BCG Scar on right deltoid.
Head Normocephal, mesocephal, closed fontanels, no
deformities.
Hair Black, evenly distributed, not easily plucked.
Face No swelling, not dysmorphic, no cranial nerves palsy,
no erythema on the cheeks.
Eyes No Swelling on both eyelids, No sunken, no anemic
conjunctiva, no icteric sclera. No scar in cornea, no
cataract. Eye movement is within normal, no
strabismus, pupil round, isochoric, diameter 2,5
mm/2,5mm, normal light reflex.
Nose Septum nasal in the middle, no secret, mucosa not
hyperemic.
Ear No secret, intact tympanic membrane.
Mouth No dry lips, no oral ulcer, no stomatitis.
Teeth No carries dentist.
Throat Pharynx not hyperemic, no tonsillar enlargement.

Neck No thyroid glands enlargement. Normal jugular vein
pressure, no nuchal rigidity.
Chest Shape and movement are symmetric, no deformities,
no piano sign, subcostal chest retraction.
Lung Vocal phremitus symmetrical, percussion sonor,
vesicular breath sound, no additional breath sound
(wheezing and rhales).
Heart Ictus cordis was not visible, heart sound I-II normal,
no murmur or gallop.
Abdominal Supple, normal bowel sound, liver and spleen not
palpable, no costovertebral pain, there was not
ascites.
Genitalia Boy, pubertal status A1G1P1
Lymph nodes No enlargement.
Extremities Warm extremities, capillary refill time less than 2
seconds, and there was not edema. Motoric: muscle
strength and tonus are within normal limit, normal
physiological reflexes, no pathologic reflexes, no
wasting.
LABORATORY EXAMINATION
Blood examination, October 12th 2021:
Hemoglobin 12,5 gr/dl, MCV 76 fL, MCH 26 pg, HCT 36%, LED 33,
leucocytes 21.900/mm3, platelet 371.000/mm3, random blood sugar 132
mg/dL, cholesterol 206 mg/dl, ASTO: 607 IU/ml, albumin 3,6 g/dl, ureum
30 mg/dl, creatinine 0,56 g/dl, SGPT 23, SGOT 31, CRP 0,5 mg/l,
procalcitonin 0,05 ng/ml, sodium 141 mmol/l, potassium 4,3 mmol/l,
chloride 102 mmol/l.
Urinalysis examination, October 12th 2021
Color: Red, Leucocytes: (-), Protein: 300 (+3), Blood: 200 (+3)
Microscopic sediment: Erythrocytes: 1569/lpb, Leucocytes: 5/lpb, Bacteria:
5, Crystal: 0
Blood smear, October 12th 2021

Neutrophilia suspected infection
Nasopharyngeal swab PCR SARS Cov-2: not detected
Head CT-Scan October 12th 2021
- Brain edema
Resume
A 9-year 6-months-old male presented with a 1-day history of
seizures, Frequency 2 times, duration 5 minute, generalized, after seizure
the child was sleepy. There was headache from 3 day ago. No fever, but
there was history of fever 2 weeks before admitted to the hospital,
intermittent and released with antipyretic medication. There were cough
and sore throat since 1 week before, no phlegm. There was no vomit. His
defecation was within normal limit. Urine output was considered normal,
dark colored urine.
History of edema in face and eyelid 3 days before admitted to the
hospital. There was history of dark colored urine since 3 days before, no
foam. There were no history of seizure and hypertension. There was
history of recurrent respiratory tract infection and hypertension in his
family, grandfather and grandmother.
There was history of skin lesions 3 weeks ago.Tthere were no
history of hair fall, joint pain, mouth ulcer, consuming prednisone, kidney
disease, autoimmune disease, metabolic disease and malignancy in
family. There was history of being treated in M hospital for 5 days and get
therapy paracetamol, ondansentron, furosemide, ceftriaxone, gentamycin,
captopril, nifedipine. At emergency room of W hospital, the patient got
nifedipine sublingual.
Physical examination revealed a moderately ill, normal body weight,
conscious child (GCS 15). Blood pressure 140/100 mmHg (P95+12mmHg),
heart rate 95 beats per minute, regular, adequate volume. Respiratory rate
22 breaths per minute, body temperature 36,8 0C. Body weight (BW) on
admission was 24,5 kg, body height (BH) 129 cm, ideal BW 26 kg. There

were no swollen and neurological state within normal limit. Other physical
examination was unremarkable.
Laboratory examination revealed hemoglobin 12,5 gr/dl, MCV 76 fL,

MCH 26 pg, HCT 36%, LED 33, leucocytes 21.900/mm 3, platelet
371.000/mm3, random blood sugar 132 mg/dL, cholesterol 206 mg/dl,
ASTO: 607 iu/ml, albumin 3,6 g/dl, ureum 30 mg/dl, creatinine 0,56 g/dl,
SGPT 23, SGOT 31, CRP 0,5 mg/l, prokalsitonin 0,05 ng/ml, sodium 141
mmol/l, potassium 4,3 mmol/l, chloride 102 mmol/l. GFR 126,7
ml/minute/1,73m2. Urinalysis showed Color: Red, Leucocytes: (-), Protein:
300 (+3), Blood: 200 (+3), microscopic sediment: Erythrocytes: 1569/lpb,
Leucocytes: 5/lpb, Bacteria: 5, Crystal: 0
He was then diagnosed as Acute Post streptococcal
Glomerulonephritis and grade II Hypertension.
Patient was treated with furosemide 25 mg once daily (1
mg/kgBW/dose), captopril 6,25 mg three times daily (0,3-0,5
mg/kgBW/dose), ceftriaxone 2 gr once daily (100 mg/kgBW/dose) for 14
days, phenytoin maintenance dose 50 mg twice daily (2mg/kgBW/dose),
protein 1 g/kgBW/day, low salt diet 1 g/day, fluid maintenance based on
insensible water loss (IWL) + urine output a day, and then bedrest.
Monitoring of vital sign, diuresis, fluid balance and urinalysis regularly.
Observation was started on the second day of hospitalization.
Diagnosis
1. Acute Post Streptococcal Glomerulonephritis (N00.9)
2. Grade 2 Hypertension (I.12.9)
3. Post seizures due to Emergency hypertension
Problems
1. Acute post streptococcal glomerulonephritis
2. Hypertension
3. Seizure

4. Proteinuria
Management Planning
1. Acute post streptococcal glomerulonephritis with seizures,

hematuria, proteinuria, hypertension, increased of ASTO.
Diagnostic  24 hours urine collecting and daily urinalysis
 Qualitative protein urine measurements (dipstick)
 Quantitative protein urine measurement (Esbach)
 C3 complement measurements
Therapy  Ceftriaxone 2 gram once daily (100 mg/kgBW/dose)
for 14 days
Pediatric  Diet according to RDA (IBWxRDA) = 2080 kcal/day,
Nutrition solid food 3 times/day and snack 2 times/day, consist
Care of:
Carbohydrate = 1040 kcal
Protein = 1 g/kgBW/dayx24.5 kg = 24 g/day
Fat = 30%x2080 kcal = 624 kcal = 69 g/day
Low salt diet intake 1 gr/day
Monitoring  Vital signs (blood pressure)
 Fluid balance
 Weight monitoring
 Diuresis monitoring
 Adverse effect from treatment
 Adherence to treatment
Education  Parents were informed about patient’s condition,
drugs schedule, daily urine volume follow
up/monitoring.
 The possible cause of the condition
 The management for the condition

 Possible complications
 Prognosis of the condition
2. Grade 2 Hypertension
Diagnostic  Measurement of blood pressure based on age,
height and sex
Therapy  Captopril 0,3-0,5 mg/kgBW/dose (6,25 mg twice
daily)
 Furosemide 1 mg/kbBW/dose (25 mg once daily)
Monitoring  Observation sign of hypertensive crisis
 Blood pressure monitoring
 Urine output production
Education  Explain to parents about hypertension and inform
sign of hypertensive crisis.
OBSERVATION IN PEDIATRIC WARD, October 13th - 22th 2021
October 13th 2021 (1st observation day, 2nd days of hospitalization)

S  There was headache
 No swollen on eyelids, face and stomach
 There were no fever, cough, and difficulty of breathing
 There was vomit once, contained water, not projectile
 Urine redness
O Composmentis
Blood pressure : 130/90 mmHg
Respiratory rate : 24 breaths per minute, regular, adequate depth
Temperature : 36.7OC

Urine output : 2,72 ml/kgbw/hr
Fluid balance : negative (142 ml)
Actual BW : 24.5 kg
No swollen and neurological state was normal
Blood examination, October 13h 2021:
Calcium 9,4 mg/dl (6,8-10,2 mg/dl), Magnesium 1.92 mg/dl (1,5-2,5
mg/dl).
A  Acute Post Streptococcal Glomerulonephritis
 Grade II Hypertension
 Post seizures due to Emergency hypertension
P 1. Bed rest
2. Monitoring of vital sign, urine output, fluid balance, body weight
and abdominal circumference.
3. 6Ceftriaxone 2 g once daily (100 mg/kgBW/dose)
4. Furosemide 1 mg/kbBW/dose (25 mg once daily)
5. Captopril 0,3-0,5 mg/kgBW/dose (6,25 mg twice daily)
6. Phenytoin 2mg/kgBW/dose (50 mg twice daily)
7. Nutrition (2080 kcal/day) : solid food 3 times/day and snack 2
times/day, consist of:
Carbohydrate = 1040 kcal
Protein = 1 g/kgBW/dayx24.5 kg = 24 g/day
Fat = 30%x2080 kcal = 624 kcal = 69 g/day
 Low salt diet intake 1 gr/day
8. Education:
 The importance to prevent infection by personal hygiene and
keep environment sanitation.
 Parents were informed about patient’s current condition, drugs
schedule.
 The importance of patient to eat or drink in compliance with his
nutritional role.

14th October 2021 (2nd observation day, 3nd day of hospitalization)
S  There was headache (decreased)
 Urine redness
O Compos mentis
Temperature : 36,7OC
Actual BW : 24.5 kg
 Acute Post Streptococcal Glomerulonephritis
P 1. Bed rest

 Carbohydrate = 1040 kcal
 Protein = 1 g/kgBW/dayx24.5 kg = 24 g/day
 Fat = 30%x2080 kcal = 624 kcal = 69 g/day
8. Education:
schedule.
 The importance of patient to eat or drink in compliance with
his nutritional role
15 October 2021 (3rd observation day, 4th day of hospitalization)
th
S  There was headache (decreased)

 Urine redness
O Composmentis

Actual BW : 24.5 kg
C3 complement : 11,3 mg/dl (50-120mg/dl)
 Acute Post Streptococcal Glomerulonephritis
P 1. Bed rest
7. Nutrition (2080 kcal/day): solid food 3 times/day and snack 2
8. Education:
schedule.
 The importance of patient to eat or drink in compliance with
his nutritional role.

18th October 2021 (6th observation day, 7th day of hospitalization)
S  There was no headache
 No vomit, no abdominal pain.
 Urine yellow color
O Composmentis
 Urine output: 3,4 ml/KgBW/hour
 Fluid balance: positive (100 ml)
Hemoglobin 12,8 gr/dl, MCV 69 fL, MCH 25 pg, HCT 35%, leucocytes
5.060/mm3, platelet 545.000/mm3, random blood sugar 130 mg/dL,
albumin 4,1 g/dl, ureum 60 mg/dl, creatinine 0,66 g/dl, SGPT 29,
SGOT 41, sodium 135 mmol/l, potassium 3,5 mmol/l, chloride 92
mmol/l.
Color: dark yellow, Leucocytes: 70 (+1), Protein: 30 (+1), Blood: 200
(+3), Microscopic sediment: Erythrocytes 296/lpb, Leucocytes: 8/lpb,
Bacteria: 27, Crystal: 0.
A  Acute Glomerulonephritis Post Streptococcus

P 1. Bed rest
11
3. Ceftriaxone 2 g once daily (100 mg/kgBW/dose)
8. Education:
schedule.
nutritional role
21th October 2021 (9nd observation day, 10th day of hospitalization)

O Composmentis

Hemoglobin 13,5 gr/dl, MCV 68 fL, MCH 28 pg, HCT 36%, leucocytes
6.870/mm3, platelet 566.000/mm3, random blood sugar 111 mg/dL,
albumin 4,2 g/dl, ureum 80 mg/dl, creatinine 0,44 g/dl, SGPT 36,
SGOT 50, sodium 136 mmol/l, potassium 3,6 mmol/l, chloride 87
mmol/l.
Color: dark yellow, Leucocytes: (-), Protein: 30 (+1), Blood: 200 (+3)
Microscopic sediment: Erythrocytes 175/lpb, Leucocytes: 7/lpb,
Bacteria: 15, Crystal: 2.
P 1. Bed rest
14
3. Ceftriaxone 2 g once daily (100 mg/kgBW/dose)

8. Education:
schedule.
nutritional role
22th October 2021 (10th observation day, 11th day of hospitalization)

O Composmentis
P 1. Bed rest

7. Education:
schedule.
nutritional role
PROGNOSIS
Quo ad vitam : Bonam
Quo ad sanationem : Bonam
Qua ad functionem : Bonam
SUMMARY OF HISTORY OF ILLNESS AND HOSPITALIZATION
Prior to observation by candidate
th
Local Board Examination,
Admission ER “W” Makassar, November 11 2021 Page 21
Hospital Adopted as a Case
October,12th 2020 October,13th 2020
PE: General Condition: Moderately ill, CM, BP: 140/100
History of seizure since 1 days before mmHg, HR: 95 bpm, RR: 22 tpm, T: 36,80C
Dark-colored urine since 3 days before admission
Laboratory: hemoglobin 12,5 gr/dl, MCV 76 fL, MCH 26
There was cough 1 weeks before
History edema in face and eyelid 3 days before pg, HCT 36%, leucocytes 21.900/mm3, platelet
History of recurrent respiratory tract infection 371.000/mm3, random blood sugar 132 mg/dL,
PE: General Condition: moderately ill, CM, BP: cholesterol 206 mg/dl, ASTO: 607 iu/ml, albumin 3,6
180/120 mmHg, HR: 95 bpm, RR: 22 tpm, T: g/dl, ureum 30 mg/dl, creatinine 0,56 g/dl, SGPT 23,
36,70C SGOT 31, CRP 0,5 mg/l, prokalsitonin 0,05 ng/ml,
Laboratory : hemoglobin 12,2 gr/dl, MCV 74 fL,
sodium 141 mmol/l, potassium 4,3 mmol/l, chloride
MCH 25 pg, HCT 33%, leucocytes 16.500/mm3,
platelet 174.000/mm3, random cholesterol 133 102 mmol/l. GFR 126,7
mg/dl, albumin 3,3 g/dl, Urinalysis showed Red, Leucocytes: (-), Protein: 300
Urinalysis showed dark yellow, Leucocytes: (+1), (+3), Blood: 200 (+3), microscopic sediment:
Protein: (+3), Blood: (+2), microscopic sediment: Erythrocytes: 1569/lpb, Leucocytes: 5/lpb, Bacteria: 5,
Erythrocytes: 0-5/lpb, Leucocytes: 0-17/lpb, Crystal: 0
Bacteria: 0.
Diagnosis: Diagnosis:
Acute Nephritic Syndrome Acute Post streptococcal Glomerulonephritis
Grade II Hypertension Grade II Hypertension
Post seizure due to Emergency Post seizure due to Emergency hypertension
hypertension
Therapy
Therapy
Bed rest Furosemide 25 mg once daily (1
Nifedipine sublingual 0,1 mg/kgBW/dose), captopril 6,25mg three times
mg/kgBW/dose = 2,5 mg daily (0,3-0,5 mg/kgBW/dose), ceftriaxone 2 gr
ceftriaxone 2 gr once daily (100 once daily (100 mg/kgBW/dose) for 14 days,
mg/kgBW/dose) phenytoin maintenance dose 50 mg twice daily
(2mg/kgBW/dose), protein 1 g/kgBW/day, low
salt diet 1 g/day, fluid maintenance

During observation by candidate
“W” Hospital
“W” Hospital “W” Hospital
October 18th - 22th 2021
October 13th – 14th 2021 October 15th – 17th 2021
7th- 11th day of hospitalization
2 - 3rd day of hospitalization
nd
4 - 6th day of hospitalization
th
 Headache  Headache (decreased)  No headache

 Reddish urine  Dark yellow urine  Yellow urine
 BP : 140/100 mmhg  BP : 110/80 mmhg  BP : 110/70 mmhg
 Actual BW : 24,5 kg  Actual BW : 24,5 kg  Actual BW : 24,5 kg
 Urine output: 2,72  Urine output: 2,8  Urine output : 3,4 ml/kgbw/hour
ml/kgbw/hour ml/kgbw/hour  Urinalysis: Dark yellow,
 Calcium 9,4 mg/dl,
 Calcium 9,4 mg/dl, Leucocytes: 70 (+1), Protein: 30
Magnesium 1,92 mg/dl. (+1), Blood: 200 (+3),
Magnesium 1,92 mg/dl.
 C3 Complement : 11,3 Microscopic sediment:
mg/dl Erythrocytes 296/hpf,
Leucocytes: 8/hpf
 Hemoglobin 12,8 mg/dl, MCV
69 fl, MCH 25 pg, leucocyte
5.060/uL, platelet 455.000/uL
Diagnosis: Acute Glomerulonephritis Post Streptococcus + Grade II Hypertension +

Post seizures due to emergency hypertension
 Bed rest
 Monitoring of fluid balance, blood pressure, body weight, and abdominal circumference.
 Furosemide 25 mg once daily (1mg/kgBW/dose), captopril 6,25mg three times daily (0,3-
0,5 mg/kgBW/dose), ceftriaxone 2 gr once daily (100 mg/kgBW/dose) for 14 days,
phenytoin maintenance dose 50 mg twice daily (2mg/kgBW/dose)
 Nutrition: solid food 3 times/ day, snack 3 times/day, consist of: Energy 2080 kcal/day
(Carbohydrate 1040 kcal/day, Protein 1 g/kgBW/day ≈ 24 gram/day, Fat 30% of total
calorie (624 kcal) = 69 gram/day, Low salt diet 1 gr/day)
 Education

P
R
O
B
CASE ANALYSIS A 9-year-6-months old boy
L
E Actual BW: 24,5 kg
M Ideal BW: 26 kg
Hypertension Proteinuria Seizures Edema BH: 129 cm
Weight-for-Height: 94% (good nourished)
D
I History taking
A Physical examination Grade II hypertension
Laboratory finding
G
Ayoob R, Scwaderer A. Acute Kidney
N Injury and Atypical Features
During Pediatric Poststreptococcal
O Glomerulonephritis. Int J Nephrol.
S 2016;3:1-5 (LoE 2B)
Acute Glomerulonephritis Post Streptococcus
I
S Post Seizure due to
emergency hypertension
T
H Hypertensive encephalopathy
Antibiotic Antihypertension Adequate nutrition & Antiseizures secondary to acute post-
E Observation streptococcal glomerulonephritis
R Hossain A., et al. Comparative Paediatr Indoens. 2012 (LoE 2B)
Dagan R, Cleper R, Davidovits Nur S, Albar H, Daud D. Hypertensive
Efficacy of Calcium Channel
M, Trieman LS, Krause I. Post-
A infectious glomerulonephritis in Blocker and ACE Inhibitor in Prognostic Factor for encephalopathy secondary
P pediatric patient over two the Treatment of Acute Mortality in Pediatric to acute poststreptococcal
decades: severity-associated Hypertension in Acute Post Indones. Acute Pediatri glomerulonephritis Paediatr
Y features. IMAJ. 2016;18:336- Streptococcal Poststreptococcal Indoens. 2012 (LoE 2B)
40 (LoE2B) glomerulonephritis. Urology &
Glomerulonephritis.
Nephrology Open Access
P Journal volume 3 Issue 2016;56:155-70.(LoE 2B)
4.2016.. (LoE 1B)
R
O
G Response to treatment and complication Prognosis :
N
Hadiwijaya A, Albar H, Rauf S, Daud D. Prognostic Factor of Ureum Quo ad vitam : Bonam
O and Creatinine Serum of Acute Post Streptococcal Glomerulonephritis
S in Children. AJHR. 2015;3:151-5.( LoE2B) Quo ad sanationem : Bonam
Dagan R, Cleper R, Davidovits M, Trieman LS, Krause I. Post-infectious
I glomerulonephritis in pediatric patient over two decades: severity-associated Quo ad functionam : Bonam
features. IMAJ. 2016;18:336-40 (LoE2B)
S

DISCUSSION
Glomerulonephritis is a general term that is used to explain several
kinds of kidney disease that have glomerular proliferation and
inflammation because of an immunological process. Acute Post
Streptococcal Glomerulonephritis (APSGN) is the most common cause of
acute glomerulonephritis on children. Acute Post Streptococcal
Glomerulonephritis (APSGN) is marked by sudden onset of combined
symptoms of gross hematuria, periorbital swelling, hypertension, and
1,2
previous streptococcal infection.
Acute Post Streptococcal Glomerulonephritis (APSGN) is a
Glomerular disease that is mediated by the immunity complex with the
activation of alternative complement pathway caused by previous acute
pharyngeal infection or skin infection by group A β-hemolytic
streptococcus.2 Latent period between infection and the onset of APSGN
therapy and the prognosis of APSGN is mostly good, with 6-8 weeks
period of recovery.3,4
It is usually acquired from history taking information that there are
pyoderma (3 weeks) caused by group A β-hemolytic streptococcus strain
2,49,55,57,60 or there are presence of pharyngitis (1-2 weeks) caused by
group A β-hemolytic streptococcus strain 1,3,4,12,25,49. Clinical
manifestation usually varies from asymptomatic form either sporadic
endemic. Although rare, APSGN can show severe renal disorder with
rapid progressive Glomerulonephritis.3-5
The incidence of APSGN has increased in the low social economic
group, this is associated with bad hygiene and the long distance of
medical service location. Acute Post Streptococcal Glomerulonephritis
(APSGN) can occur in all ages, but occurred more often in children,
usually at the age of 2-6 years, and rarely occurred on children younger
than 2 years, and older than 25 years. The study in Indonesia indicated
that the age distribution of APSGN is 2.5 years to 15 years with the

average age of 8.45 years with the male children and female children ratio
of 1.4 : 1.4,5
Acute Post Streptococcal Glomerulonephritis consists of 3 phase.
The latent phase, acute phase, and recovery phase. The latent phase is a
phase between in the occurrence of streptococcal infection until the
appearance of clinical symptoms. Clinical symptoms usually appear 7-14
days after upper airway tract infection or 3-6 weeks after pioderma. The
acute phase is a phase where the patient starts to show symptoms of
Nephritic Syndrome such as proteinuria, hematuria, azotemia, oligouria,
and hypertension. The recovery phase is indicated with the improvement
of clinical symptoms and laboratory results.6-8
The diagnostic criteria of APSGN according to the Nephrology
consensus of IPS (Indonesian Pediatric Society) is : (1) if there are
encounters of hypertension, edema, and oligouria symptoms which is the
typical symptoms of APSGN, (2) if the laboratory examination for
supporting clinical diagnosis have results of increased anti-streptolysin
titer O and decreased C3 accompanied with the presence of total
erythrocyte, hematuria or proteinuria, (3) Diagnosis is established if there
are findings of group A β-hemolytic streptococcus on the microbiological
culture examination.5 According to Papanagnau et al 9, if there are
nephritic symptoms like proteinuria, hematuria, hypertension, edema, and
oligouria on a child, the diagnosis of APSGN can be established.
Based on the information acquired from the history taking of this
patient, there are complains history of seizures. He had cough and sore
throat since 1 week ago, and there was skin lessions 3 weeks before
admitted to the hospital. There was of dark colored since urine 3 days
before admitted. There was history of edema in face and eyelid 3 days
before and then from vital sign we found there was hypertension. From
laboratory examination there were increased of ASTO 607 IU/ml (<200
IU/ml), decreased of C3 Complement : 11,3 mg/dl and urinalysis showed
reddish colored urine, Leucocytes: (-), Protein: 300 (+3), Blood: 200 (+3),

microscopic sediment: Erythrocytes: 1569/hpf, Leucocytes: 5/hpf,
Bacteria: 5, Crystal: normal.
Multicenter studies in Indonesia shows that there are 46-100% of
microscopic hematuria, while there are microscopic hematuria ranging
from 84-100%. Macroscopic hematuria usually occurs in first week and
can last a few weeks. Microscopic hematuria can occur longer, usually
disappearing in 6 months, so microscopic hematuria is sometimes
encountered even when the clinical symptoms has disappeared. 3-5 Yu et
al10 reports symptoms and clinical signs obtained from children with
APSGN (table 1). The most common symptoms is gross hematuria
(66.7%) and the most common clinical sign is hypertension (48.1%).
Table 1. Symptoms and Clinical Signs on APSGN.10

Clinical Symptoms % Clincal Signs %
Edema 51,9 Hypertension 48,1
- Facial edema 33,3 CVA Knock pain 7,4
- Edema generalisata 66,7 Hepatomegaly 3,7
Gross hematuria 33,3 Rales 42,3
Only micro hematuria 18,5
Decreased urine output 40,7
Fever 11,1
Headache 18,5
Vomit 40,7
Dyspnea 11,1
Abdominal Pain 18,5
Seizures 3,7
Decreased Consciousness 3,7
APSGN most commonly occurs in children two to 12 years of age

11,12
, with the clinical onset one to three weeks following Group A
streptococcal (GAS) positive pharyngitis or three to six weeks after GAS
impetigo11,12. Because post infectious nephritic syndrome is
indistinguishable from different antecedent infectious etiologies, diagnosis
of APSGN relies on documentation of preceding GAS infection. 13

In this patient is preceded with a history of recurrent respiratory
tract infection and history skin lessions 3 weeks ago. It is compatible with
the study conducted by Sepahi et all in Iran on 94 children with APSGN
that has previous infection, consisting of 92 children with upper airway
tract infection (painful swallowing or Pharyngitis) and 2 children with a
history of skin infection.14
Group A beta hemolytic streptococcus infection in the body can

cause the antibody response that can be proved with increased Anti-
streptolysin titer O (ASTO). Although ASTO is more commonly used,
evaluations shows that other serological test can increase the possibilities
of a positive test up 95-96% if the patient doesn’t produce high levels of
antibody on one or more extracellular enzyme. 12,13 In this patient we found
ASTO level was increased 607 IU/ml (< 200 IU/ml). ASTO is increase in
10-14 days after infection and the highest escalation happened 3 weeks
after streptococcal infection and will eventually decrease. 14
Other Clinical manifestation of APSGN is edema and hypertension.

Edema is found on 85% cases, especially on the periorbital area (76,3%),
the face, extremities even the entire body. The edema usually occurred
suddenly where it is visible the first time on the periorbital area primarily
while waking up in the morning and disappears in the afternoon after the
patient have conducted several activities. This edema is caused by a
retention of Sodium and water caused by a damage in the glomerulus that
causes excessive fluid. 15,16
In the Fourth Report, “normal blood pressure” was defined as SBP

and DBP values <90th percentile (on the basis of age, sex, and height
percentiles). For the preadolescent, “prehypertension” was defined as
SBP and/or DBP ≥90th percentile and <95th percentile (on the basis of
age, sex, and height tables). For adolescents, “prehypertension” was
defined as BP ≥120/80 mm Hg to <95th percentile, or ≥90th and <95th
percentile, whichever was lower. HTN was defined as average clinic

measured SBP and/or DBP ≥95th percentile (on the basis of age, sex, and
height percentiles) and was further classified as stage 1 or stage 2 HTN.
There are still no data to identify a specific level of BP in childhood that
leads to adverse CV outcomes in adulthood. Therefore, the subcommittee
decided to maintain a statistical definition for childhood HTN. The staging
criteria have been revised for stage 1 and stage 2 HTN for ease of
implementation compared with the Fourth Report. For children ≥13 years
of age, this staging scheme will seamlessly interface with the 2017 AHA
and American College of Cardiology (ACC) adult HTN guideline.*
Additionally, the term “prehypertension” has been replaced by the term
“elevated blood pressure,” to be consistent with the AHA and ACC
guideline and convey the importance of lifestyle measures to prevent the
development of HTN (see Table 2).34
Table 2. Updated Definitions of BP Categories and Stages
In this patient we found blood pressure 140/100 mmHg with 50 th

percentile 93/56 mmHg, 90th percentile 107/69 mmHg, 95th percentile
110/72 mmHg and 95th+12mmHg percentile 122/84 mmHg. It means that this
patient has grade II hypertension. Hypertension is found in up to 90% of
patients and 10% may have neurological symptoms, but only few present
hypertensive encephalopathy (HTE). 7% of children with
glomerulonephritis showed clinical presentations of encephalopathy. The
clinical presentation includes acute lethargy, confusion, visual impairment
(including blindness) and seizures. Seizures may be the main symptom

that occurs as a focal crisis, a generalized crisis or a focal crisis with
secondary tonic/ clonic generalization.35
The predominant trend in pediatric antihypertensive management is

towards increasing reliance on angiotensin converting enzyme inhibitors
and calcium channel blockers because of their general effectiveness, low
incidence of adverse reactions and potential specific benefit in patients
with renal disease. There was an obvious difference between the effects
of two investigated antihypertensives. Nifedipine reduced both systolic BP
and diastolic BP much earlier than captopril (p <0.05). The time required
for BP to become below 95 th percentile in this study was much higher in
Captopril group than in Nifedipine group. There was also a significant
difference regarding the duration of antihypertensive therapy (p<0.05).
Captopril had to be given for almost double time than that of Nifedipine
(p<0.005). It is obvious from the study that Nifedipine controlled BP earlier,
much less costly and reduced the duration of hospital stay than captopril.
For the control of hypertension in AGN patients, Nifedipine is a better
drug.35(Level of evidence 1B, recommendation A). But in this case
captopril is used as an antiproteinuria therapy and antihypertension.
Proteinuria can also be found on APSGN patients qualitatively

ranging from negative proteinuria to +2, rarely up to +3. On this case, early
presentation of the disease shows that there are qualitative proteinuria on
APSGN varying from a few weeks until a few months after the clinical
Symptoms disappeared. With 6 months as the limit, if proteinuria is still
found for more than 6 months, then it is called persistent proteinuria that
shows the possibility of a Chronic Glomerulonephritis that needs renal
biopsy.17
Serum Complement is mostly decreased on APSGN, because it

also has a role on the antigen-antibody process after streptococcal and
britogenic infection. Among the complement systems in the body,
Complement C3 is the most examined complement. The level of C3 on

ADSGN decreases during the acute phase as much as 80-92% cases,
then it returns to normal after 8 weeks of the symptoms' appearance. On
this patient complement C3 level was decreased (11,3 mg/dl). Qian et al18
found that In the past 2 years, a total of 78 patients were admitted to their
department with APSGN. They were found that 3 of those patients had
normal plasma C3 levels. In fact, other infectious agents can also cause
acute glomerulonephritis, so the diagnosis can be broader to be called
post-infectious glomerulonephritis. Normal C3 has been well described in
some 10% of such patients. We need to notice this during our clinical
work. Welch19 said in his article that the importance of a timely
measurement of C3 cannot be overstressed in APSGN because the
hypocomplementemia is evanescent, typically normal in six to eight weeks.
But the first plasma C3 levels of these three patients were gotten at the
fifth day, third day, sixth day from the symptoms, the time points seemed
to be suitable, and they were all in the normal range. Thus, the importance
of a timely measurement of C3 cannot be overstressed not only because
of the hypocomplementemia is evanescent but also the C3 level will not
always decrease absolutely. We currently believe that the pathogenesis of
APSGN is due to multi streptococcal antigen and a host antibody response
to the formation of soluble complexes, which cannot be removed by the
glomeruli and activate the complement system. Some studies19,20 indicate
that an alternative pathway of complement activity is the most important
prognosis of APSGN. We also observed strong endocapillary deposit of
C3 shown by immunofluorescence, suggesting that an alternative
complement pathway is involved in the leading cause of morbidity. Further
studies are required to determine why acute phase C3 levels still remained
within the normal range.18
Oliguria is a condition that is rarely encountered on APSGN (5-

10%) with the urine production of less than 0.8 ml/kg body weight/ hour.
On this patient, there are no findings of decreased urine volume. Daily

diuresis is above 1 ml/kg body weight/ hour. Oliguria can become anuria
that shows severe glomerular damage with a bad prognosis. 4
Decreased kidney function can occur in patients with APSGN.

Decreased kidney function occurs due to glomerular inflammation thereby
decreasing glomerular function in filtration process. Pathological findings
of renal tissue are found in endothelial diffuse hypercellular and mesangial
cells with polymorphonuclear cell infiltration of the glomerulus. Capillary
endothelial hypercellularity leads to a reduction in capillary lumen which
correlates with the severity of renal insufficiency. The study by Chung et
al, found that this hypercellularity is more due to infiltrate infiltration
reducing the capillary lumen further. This causes the reabsorption process
in the proximal tubules to decrease. This situation eventually causes the
reabsorption process in the distal tubules to increase and water and salt
retention occurs so that the amount of urine production decreases and
oliguria occurs until anuria is reversible when given adequate early
handling. 23
In a multicenter study in Indonesia, it was reported that acute renal

injury (AKI) occurred in 10% of APSGN patients, 19 In AKI patients, the
diagnosis was made by anamnesis, physical examination, and
investigation. Acute kidney injury is diagnosed after diuresis reduction,
elevated serum urea and creatinine levels. Acute post streptococcal
glomerulonephritis itself is one of the main causes of AKI. Acute kidney
injury is a condition in which there is sudden decrease in renal function,
characterized by high serum urea, creatinine and renal inability to regulate
fluid and electrolyte homeostasis.21
The decrease of renal function varies depending on the severity of

acute renal impairment. The term of AKI is accompanied by various
factors that affect the stage of acute renal impairment called RIFLE (Risk –

Injury - Failure - Loss - End stage kidney disease). Acute renal injury in
these patients is determined by a decrease in LFG > 25% or serum
creatinine increased by 1.5 times the initial condition or urine output <0.5
ml/kg/hour for 12 hours. Acute kidney injury usually at this stage are still
irreversible, so further decline in kidney function can be prevented. 22,23
Management of AKI is directed at underlying diseases such as

conservative therapy, while preventing life–threatening complications, and
if necessary renal transplantation can provide support for recovery of
kidney function. Conservative therapies are fluid restriction, low-salt diet
and protein. The goal of therapy is conservative to prevent excess fluid,
acid-base electrolyte abnormalities, uremia, and hypertension. In this
patient, AKI was treated conservatively. 24,25
Supportive therapy in APSGN includes bed rest, nutrition, as well

as symptomatic therapy for edema, hypertension, and renal impairment. In
acute kidney injury fluid restriction, nutrients with adequate protein and
salt. In this case, the patient is given furosemide due to excess fluid.
Nutrition is given with a diet containing calories according to RDA, protein
1 g/kg/day and restriction of salt 1 g/day.
Education plays an important role in APSGN management. Patients

and families need to be explained about the course of the disease and its
prognosis. Families need to know and understand that although perfect
cure is expected at 95%, there is still a small chance of a persistent and
even worsening disorder of about 1 - 5%. It should also be described later
monitoring plan, in the form of urinalysis every 2 weeks for the first 2
months, then every month for 6 months, continued every 3 - 6 months until
hematuria and proteinuria disappear. C3 levels that return to normal after
8-10 weeks describe a good prognosis.26
Based on the results of the study, in general APSGN cured

perfectly, although there is a risk of permanent interference. Kidney

function of this patient was normal, with urea at the time of the initial
diagnosis was 30 mg/dl, creatinine 0,56 mg/dl, glomerulus filtration rate
(GFR) 126,7 ml/minutes/1.73 m2. Patients respond well to the treatment,
this can be seen from the improved symptoms. At the end of monitoring
still found microscopic hematuria, so the need for further observation
every 4 – 6 weeks during the first 6 months.
Hadiwijaya, et al" Out of the 95 patients as sampled, there were 90

(94.7%) cured, and 5 (5.2%) patients died. Multivariate analyses indicated
that serum ureum levels <119 mg/dl is an independent prognostic factor
for APSGN outcomes in children (p=0.032, OR 1.021, and CI 95% 1.002-
1.041). There is a significant difference both in early ureum levels to
outcome with p=0.003 and in early creatinine levels to outcome with
p=0.02. As for conclusion that serum ureum is an independent prognostic
factor for APSGN, where serum ureum levels <119 mg/dl and creatinine
levels <1.3 mg/dl have a good prognosis. There is no significant
correlation between the outcome and sex (p=0.961), nutritional status
(p=1.000), and age (p:0.108). (Level of evidence 2B, recommendation B)
Dagan, et al, A total of 125 patients with Streptococcal infection

was established by elevated anti-streptoliysin O titers (ASTO) in
109(85%), while throat culture was positive in 39 (31.2%). Complement C3
levels were significantly lower in 84 patients with azotemia (31.9 + 28.6
mg/dl) compared with 36 patients with normal renal function (53.2 + 46
mg/dl, p=0.01). At last follow-up (mean 42 months) all examined patients
(100 of 125) had normal renal function, microscopic hematuria present in
29 (30%), 6 had hypertension, and 1 had proteinuria (Level of
evidence 2B, recommendation B).
Ayoob et al28 after review of Inpatient and outpatient records from

17 children with APSGN, most of them were males (64.7%) with mean age

of 8 years, all of the children examined had a current or preceding
pharyngitis but none had a documented skin infection. Acute kidney injury
was seen in 94% of all cases, and thrombocytopenia in 18% were treated,
APSGN manifestation was rarely seen as severe nephritis. All patients
had C3 <80mg/dL that normalized on follow-up. The mean value of GFR
was 44.5+22.9 mL/min/1.73m' that improved to 105+19,4 on follow-up.
(Level of evidence 2B, recommendation B)
Nur,et al29 from 86 children with APSGN that were admitted in

pediatric ward Wahidin Sudirohusodo hospital, Makassar, 82 (95,3%)
survived and 4 (4.7%) died. Fifty-three (61.6%) patients were male and 33
(38,4%) were female. Subjects ages ranged from 3.42 to 14,67 years, with
a mean age of 9.36 years. Multivariate analysis revealed serum creatinine
level >1,5 mg/dL to be an independent prognostic factor for mortality in
children with APSGN (AOR 15.43; 95%CI 1.31 to 1817, p=0,03). (Level of
evidence 2B, recommendation B).
The prognosis of this patient, ad vitam and ad functionam bonam

because the patient showed a good response of the treatment where there
was clinical improvement, although the urinalysis was not improved. Ad
sanationam dubia ad bonam. Most APSGN patients recover but there is
still a possibility of risk of chronic renal impairment and the risk of
recurrence of illness. The best indicator for the recovery of
glomerulonephritis disease is the return of C3 levels to normal levels. This
generally occurs within 6 to 8 weeks. This persistent reduction in C3 levels
is useful as a guide, as it may be a sign that acute glomerulonephritis is
actually a chronic process of interference such as rapid progressive
glomerulonephritis, which is less than 5%. Urinary sediment disorders will
remain visible for months or even years most patients even though edema
and hematuria are not visible. However, patient still experience
microscopic hematuria, which was expected to improve. Microscopic
hematuria can persist for 6 months to 1 year after the infection heals. 30,31

Appendix 1 LIST OF ABBREVIATIONS

AKI Acute Kidney Injury
APSGN Acute Post streptococcus Glomerulonephritis
ASTO Anti-streptolysin Titer O
BAC Below arcus costa
BCG Bacill Calmette Guerin
CA Cronological Age
C3 Complement 3
CRT Capillary refill time
DPT Difteri Pertusis Tetanus
GCS Glasgow coma scale
GFR Glomerulus Filtration Rate
gr gram
HA Height Age
Hb Hemoglobin
Hib Hemophillus influenzatipe B
Hpf Huge power field
Ht Hematocrite
IPS Indonesia Pediatric Society
IV intravenous
kcal kilo calori
kgBW kilograms body weight
MCH Mean Cospuscular Hemoglobin

MCHC Mean Cospuscular Hemoglobin
Concentration
MCV Mean Cospuscular Volume
Meq/L miliEquivalent per liter
Mg milligram
mL milliliter
mm millimeter
MMR measless, mumps, rubella
MPH Mid Parental Height
Posyandu Pos Pelayanan Terpadu
Puskesmas Pusat Kesehatan Masyarakat
PSC Pediatric Symptom Checklist
RDA Recommended Dietary Allowance
µg/dL microgram per desi Liter

Appendix 2 Head circumference
Examination date : October, 12th 2021
Name :M
Age : 9 years 6 months
Head circumferences 51 cm (normal: 49 cm – 55 cm)

Appendix 3 Growth Chart Examination date : October, 12th 2021

M/BOY/9 YEARS 6 MONTHS
949XXX
MPH
HA CA
 Body weight: 24,5 kgs

 Ideal body weight: 26 kgs
 BH: 129 cms
 Weight-for-height: 24,5/26 x 100% =94%
 Height-for-age (H/A): 129/136 x 100% = 94,8%
39
 Weight-for-age (W/A): 24,5/30 x 100% =82%

 Height Age : 9 years 6 months
 Father’s height : 163 cm
 Mother’s height : 155 cm
Appendix 4.Pediatric Symptom Checklist
 Genetic potential height : 144 – 161 cm (<P3 – P50, CDC-NCHS 2000 chart)
 Midparental height : 152,5 cm

Emotional and physical health go together in children. Because parents are often
the first to notice a problem with their child’s behavior, emotions or learning, you
may help your child get the best care possible by answering these questions.
Please mark under the heading that best fits your child.
Never Sometimes Often

child’s behavior (0) (1) (2)
1. Complains of aches/pains √
2. Spends more time alone √
3. Tires easily, has little energy √
4. Fidgety, unable to sit still √
5. Has trouble with a teacher √
6. Less interested in school √
7. Acts as if driven by a motor √
8 Daydreams too much √
9. Distracted easily √
10. Is afraid of new situations √
11. Feels sad, unhappy √
12. Is irritable, angry √
13. Feels hopeless √
14. Has trouble concentrating √
15. Less interest in friends √
16. Fights with others √
17. Absent from school √
18. School grades dropping √
19. Is down on him or herself √
20. Visits doctor with doctor finding nothing √
wrong
21. Has trouble sleeping √
22. Worries a lot √
23. Wants to be with you more than before √
24. Feels he or she is bad √
25. Takes unnecessary risks √
26. Gets hurt frequently √
27. Seems to be having less fun √
28. Acts younger than children his or her age √
29. Does not listen to rules √
30. Does not show feelings √
31. Does not understand other people’s feelings
32. Teases others √
33. Blames others for his or her troubles √
34. Takes things that do not belong to him or √
her
35. Refuses to share √
Examination date
ociety) : October, 13th 2021
Name :M
Age : 9 years 6 months
Total Score :2
past 10 days, how much of a problem has your teen had with

In the past 10 days, how much of a problem has your teen had with
PHYSICAL FUNCTIONING (problems with ) Never Almost SomeOften Almost

Never times Always
1. Walking more than one block 0 1 2 3 4
2. Running 0 1 2 3 4
3. Participating in sports activity or exercise 0 1 2 3 4
4. Lifting something heavy 0 1 2 3 4
5. Taking a bath or shower by him or herself 0 1 2 3 4
6. Doing Chores around the house 0 1 2 3 4
7. Having hurts or aches 0 1 2 3 4
8. Low energy level 0 1 2 3 4
EMOTIONAL FUNCTIONING (problems with ) Never Almost Some Often Almost
Never times Always
1. Feeling afraid or scared 0 1 2 3 4
2. Feeling sad or blue 0 1 2 3 4
3. Feeling angry 0 1 2 3 4
4. Trouble sleeping 0 1 2 3 4
5. Worrying about what will happen to him or 0 1 2 3 4
her
In the past 10 days, how much of a problem has your teen had with
SOCIAL FUNCTIONING (problems with ) Never Almost Some Often Almost

Never times Always
1. Getting along with other teens 0 1 2 3 4
2. Other teens not wanting to be his or her friend 0 1 2 3 4
3. Getting teased by other teens 0 1 2 3 4
4. Not able to do things that others teens his or 0 1 2 3 4
her age can do
5. Keeping up with other teens 0 1 2 3 4
In the past 10 days, how much of a problem has your teen had wth
SCHOOL FUNCTIONING (problems with ) Never Almost Some Often Almost

Never times Always
1. Paying attention in class 0 1 2 3 4
2. Forgetting things 0 1 2 3 4
3. Keeping up with schoolwork 0 1 2 3 4
4. Missing school because of not feeling well 0 1 2 3 4
5. Missing school to go to the doctor or hospital 0 1 2 3 4

Physical function 56,25
Emotion function 80
Social function 80
School function 45
REFERENCES
1. Lurn G. Glomerulonephritis. Dalam: Hay W. Levin M, Sondheimer

editor. Current diagnosis and treatment pediatrics. Edisi ke-19.

United
States of America: McGraw Hill 2009. h.656-7.
2. Pan CG, Avner ED. Acute post streptococcus glomerulonephritis.
Dalam: Kliegman RM, Stanton BF, St Game III JW, Schor NF,
Berman
RE, editor. Nelson Textbook of Paediatrics. Edisi ke-19 Elsevier
Saunders: Philadelphia; 2011. h. 1783-94.
3. Rauf S, Albar H, Aras J, Umboh A, Widiasta A. Pabuti A dkk
Glomerulonefritis akut pasca streptokokus. Rauf S, Albar H, Aras J.
editor. Konsensus glomerulonefritis akut pasca streptokokus. Unit
Kerja Koordinasi Nefrologi Ikatan Dokter Anak Indonesia. Jakarta:
Badan Penerbit Ikatan Dokter Anak Indonesia; 2012. h. 1-17
4. Albar H. Rauf S. The profile of acute glomerulonephritis among
Indonesian Children. Paediatrica Indonesiana. 2005;45:264-9.
5. Dagan R. Cleper R, Davidovits M, Sinai-Trieman L. Krause I Post
streptococcal acute glomerulonephritis in pediatric patients over two
decades: severity-associated features. Pediatr Nephrol.
2011;26:165-
80.
6. Eison T Ault B. Jones DP. Post streptococcal acute
glomerulonephritis in children: clinical features and pathogenesis.
IMAJ. 2016, 18:336-40.
7. Cunningham MW. Pathogenesis of group A streptococcal
infections.
Clin Microbiol Rev. 2000;13:470-91.
8. Noer MS. Glomerulonefritis akut pasca streptokokus. In : Noer MS,
Soemyarso NA, Subandiyah K,Prasetyo RV, Alatas H, Tambunan
T,
dkk, penyunting. Kompendium nefrologi anak. Jakarta : BP IDAI,
2011. h.57-61
9. Papanagnou D, Kwon NS. Acute glomerulonephritis in emergency
medicine. Updated e Medicine Emergency December 2010:1-18.
10. Yu R, Park SJ, Shin JI, Kim KH. Clinical patterns of acute post
streptococcus glomerulonephritis: a single center's experience. J
Korean Soc Pediatr Nephrol. 2011;15:49-57.
11. Sepahi AM, Shajari A, Shakiba M. Acute glomerulonephritis: a 7
years follow up of children in center of Iran. Acta Med
Iranica 2011;6:375-8.
12. Eison T, Ault B, Jones D, et al. Post-streptococcal
glomerulonephritis in children: Clinical features and pathogenesis.
Pediatr Nephrol 2011;26:165–80.
13. VanDeVoorde R. Acute poststreptococcal glomerulonephritis: the
most common acute glomerulonephritis. Pediatr Rev 2015;36:3–
14. Blyth CC, Robertson PW. Anti-streptococcal antibodies in the
diagnosis of acute and post streptococcus disease: streptokinase

versus streptolysin 0 and deoxyribonuclease B. Pathology.
2008;38:152-6.
15. Long SS, Pickering KL, Prober GC. Streptococcus pyogenes (group
A
streptococcus). In: Gerber M. Principles and practices of pediatric
infectious disease. Edisi 3. Churcill livingstone: Elseviers science;
2008.h.700-10
16. Lurn G. Glomerulonepritis. In: Hay W. Levin M, Sondheimer J,
editor.Current diagnosis and treatment pediatrics. Edisi 19. United
States of America : McGraw Hill; 2009.h.656-7.
17. Kumar GV. Clinical study of post streptococcal acute
glomerulonephritis in children with special reference to presentation
Curr Pediatr. 2011;15:89-92
18. Qiant et al, Acute Post-streptococcal Glomerulonephritis with
Normal. HK J Paediatr (new series) 2014;19:188-191
19. Range Complement C3 Level: Three Case ReportsCemerlic-
Zecevic E, Macanovic M: The complement activation system in
acute poststreptococcal glomerulonephritis. Med Arh 1991;45:17-
21.
20. Hisano S, Matsushita M, Fujita T, Takeshita M, Iwasaki H:
Activation of the lectin complement pathway in post-streptococcal
acute glomerulonephritis. Pathol Int 2007;57:351-7.
21. Van Driel ML, De Sutter AI, Keber N, Habraken H, Christiaens T.
Different antibiotics treatments for group A staphylococcal
pharyngitis. The Cochrane Database of Systematic Reviews,
2013.8:12-9.
22. Alatas H. Gagal ginjal akut. Dalam: Noer MS, Soemyarso NA,
Subandiyah K, Prasetyo RV, Alatas H, Tambunan T, dkk, editor.
Kompedium nefrologi anak. Unit Kerja Koordinasi Nefrologi Ikatan
Dokter Anak Indonesia. Jakarta: Badan Penerbit Ikatan Dokter
Anak Indonesia; 2012.h. 207-14.
23. Chung WY, Kim YJ. Expression of Ki-67 antigen using monoclonal
antibody MIB-1 in children with post-streptococcal
glomerulonephritis. Pediatr Nephrol. 2000;14:389–92.
24. Behera MR, Patnaik L, Sahu SK. Clinical profile and immediate
outcome of acute post-infectious glomerulonephritis in children: a
hospital-based study. J Evolution Med Dent Sci. 2016;5:5529-33
25. Gunasekaran K. Krishnamurthy S. Mahadevan S, Harish BN,
Kumar AP. Clinical characteristics and outcome of post-infectious
glomerulonephritis in children in southern India: a prospective
study. Indian J Pediatr. 2015;82:1-8.
26. Wong W, Lennon DR, Crone S, Neutze JM, Reed PW. Prospective
population-based study on the burden of disease from post-
streptococcal glomerulonephritis of hospitalised children in New
Zealand: epidemiology, clinical features and complications. J
Paediatr Child Health, 2013;49:850-5.

27. Shah GS, Yadav SP Clinical profile and outcome of acute
glomerulonephritis in a tertiary care centre in the Eastern Nepal.
JIOM. 2014;36:29-33.
28. Hadiwijaya A. Albar H, Rauf S, Daud D. Prognostic Factor of Ureum
and Creatinine Serum of Acute Post Streptococcal
Glomerulonephritis in Children. AJHR. 2015;3:151-5.
29. Dagan R. Cleper R, Davidovits M, Trieman LS, Krause I. Post-
rectious glomerulonephritis in pediatric patient over two decades:
severity-associated features. IMAJ. 2016;18:336-40
30. Ayoob R, Scwvoob R. Scwaderer A. Acute Kidney Injury And
Atypical Features During Pediatric Poststreptococcal
Glomerulonephritis.IntJNephrol. 2016,3:1-5.
31. Nur S, Albar H, Daud D. Prognostic Factor for Mortality in Pediatric
Acute Poststreptococcal Glomerulonephritis. Pediatr Indones.
2016;56:155-70. 20 Hoy WE, White AV, Dowling A, Sharma SK,
Bloomfield H, Tipiloura BT, et al. Post-streptococcal
glomerulonephritis is a strong risk factor
for chronic kidney disease in later life. Kidney International.
2012;81:1026-32
32. Harambat J, van Stralen KJ, Kim JJ, Tizard EJ. Epidemiology of
chronic kidney disease in children. Pediatr Nephrol. 2012;27:363-
73.
33. Yap HK, Isaac Desheg Liu, Kar Hui Ng. Pediatric Nephrology on
the Go. Third Edition. 2015. Singapore : Children’s Kidney Center.
34. Flynn, JT. et al. Clinical Practice Guideline for Screening and
Management. American Academy of Pediatrics. Volume 140,
number 3, September 2017:e201.
35. Hossain A., et al. Comparative Efficacy of Calcium Channel Blocker
and ACE Inhibitor in the Treatment of Acute Hypertension in Acute
Post Streptococcal glomerulonephritis. Urology & Nephrology Open
Access Journal volume 3 Issue 4.2016
EVIDENCE BASED SURVEILLANCE REFERENCES
Hadiwijaya A, Albar H, Rauf S, Daud D. Prognostic Factor of Ureum

and Creatinine Serum of Acute Post Streptococcal Glomerulonephritis
in Children. AJHR. 2015;3:151-5.
Dagan R, Cleper R, Davidovits M, Trieman LS, Krause I. Post-

infectious glomerulonephritis in pediatric patient over two decades:
severity-associated features. IMAJ. 2016;18:336-40

Ayoob R, Scwaderer A. Acute Kidney Injury And Atypical Features
During Pediatric Poststreptococcal Glomerulonephritis. Int J Nephrol.
2016;3:1-5
Nur S, Albar H, Daud D. Prognostic Factor for Mortality in Pediatric
Indones. Acute Pediatri Poststreptococcal Glomerulonephritis.
2016;56:155-70.
Hossain A., et al. Comparative Efficacy of Calcium Channel Blocker

and ACE Inhibitor in the Treatment of Acute Hypertension in Acute
Post Streptococcal glomerulonephritis. Urology & Nephrology Open
Access Journal volume 3 Issue 4.2016.
(Level of evidence 1B, recommendation A)

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Long Case Report

Acute Post Streptococcal Glomerulonephritis

Nur Liya Abd. Kadir

Local Board Examination

INDONESIAN COLLEGE OF PEDIATRICS

October 12th October October November

Patient was Patient was Final

PARENT’S IDENTITIES : Father Mother

Initial observation by candidate began on November 12 th 2019

PATIENT’S HISTORY (Alloanamnesis from the mother)

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History of illness in the family

Patient’s personal and social history

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e) Growth and developmental history

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Mental stimulation needs

h) Family socio-economy history/environment/ housing

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PATIENT’S HOSPITAL ADMISSION SUMMARY

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Laboratory examination revealed hemoglobin 12,5 gr/dl, MCV 76 fL,

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1. Acute post streptococcal glomerulonephritis with seizures,

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OBSERVATION IN PEDIATRIC WARD, October 13th - 22th 2021

October 13th 2021 (1st observation day, 2nd days of hospitalization)

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S  There was headache (decreased)

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21th October 2021 (9nd observation day, 10th day of hospitalization)

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22th October 2021 (10th observation day, 11th day of hospitalization)

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SUMMARY OF HISTORY OF ILLNESS AND HOSPITALIZATION

Prior to observation by candidate

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 Headache  Headache (decreased)  No headache

Diagnosis: Acute Glomerulonephritis Post Streptococcus + Grade II Hypertension +

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Table 1. Symptoms and Clinical Signs on APSGN.10

APSGN most commonly occurs in children two to 12 years of age

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Group A beta hemolytic streptococcus infection in the body can

Other Clinical manifestation of APSGN is edema and hypertension.

In the Fourth Report, “normal blood pressure” was defined as SBP

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Table 2. Updated Definitions of BP Categories and Stages

In this patient we found blood pressure 140/100 mmHg with 50 th

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The predominant trend in pediatric antihypertensive management is