DR - ERLIN Fix

TIMELINE
Sept 3rd 2018 Sept 6th 2018 Sept 7th 2018 Sept 12th 2018 Sept 13th 2018
Initial
Patient
examination Initial Last
admitted to Reporting
by observation observation
Hospital
candidate
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PATIENT’S RECORD
Candidate: dr. Erlin
I. IDENTITY
Patient Identity
Register number : 00.50.61.XX
Name of patient : YCS
Gender : Male
Date of birth : April 26th, 2010 (8 years 4 months old)
Date of Admission : September 3rd, 2018
Date of Examination : September 6th, 2018
Parental Identity
FATHER MOTHER
Name : NS GL
Age : 44 years old 37 years old
Occupation : Goverment employee Goverment employee
Education : Bachelor degree Bachelor degree
II. HISTORY
(Autoanamnesis and alloaanamnesis was taken from parents, physician
and medical records on Sept 6th, 2018 at 14.00 AM in pediatric ward)
Chief complaint : Dark colored urine
Additional complaint : Swollen on the eyelids
Headache
Patient was admitted to hospital on September 3rd 2018 with chief

complaint dark colored urine, swollen on the eyelids, and hypertension.
Patient was referred from A hospital and was hospitalized for 5 days with
the same complaint but there were no clinical improvement and then he
was referred to B hospital.
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2.1 HISTORY OF PRESENT ILLNESS
Two weeks prior to admission, patient got swollen that appears in
the eyelids especially in the morning. One week prior to admission that
symptoms accompanied by dark colored urine. A day prior to admission
patient got headache. There was no history of head and abdominal trauma.
Patient did not receive nor underwent any medication that could change
urine color. Patient did not have complaint of pain in urination, vomitting,
seizure or loss of consciousness. Patient did not suffered by shortness of
breath and fever. There was no complaint about defecation pattern.
Patient had good appetite. According to information given by his parents,
patient have good food portion and take meals three times daily regularly.
A month prior to admission, patient got fever, cough and sore
throath. The symptoms got relieve without any medication. There was no
history of skin infection. Before admitted to B hospital, patient had
hospitalized in A hospital for 5 days and got eritromycin tablets, captopril
tablets and furosemide tablets. Because of there was no clinical
improvement and then he was referred to B hospital.
2.2 HISTORY OF PREVIOUS ILLNESS

There was no history of swelling, kidney disease, urine color and urinary
infection before.
2.3 HISTORY OF ILLNESS IN THE FAMILY

There were no family history of kidney disease or receive kidney dialysis.
Only patient had this complaint in his family.
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Family tree
Family member
No Name Relationship Sex Age Description
with patient
1. NS Father M 44 years Healthy
2. GL Mother F 37 years Healthy
3. LHS Child M 15 years 6 months Healthy
4. YCS Child M 8 years 4 months Patient
2.4 PERSONAL AND SOCIAL HISTORY

A. History of antenatal care :
During pregnancy, patient mother’s had 9 times antenatal examination at
the the private hospital and got Tetanus Toxoid (TT) immunization twice.
She was otherwise healthy during the pregnancy.
B. History of labor :
Patient was full term baby and delivered by sectio caesaria because of
prolonged second stage of labour, in a general hospital by obstetrician.
Birth weight was 3300 grams, birth length 48 cm. He immediately cried
after birth.
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C. History of postnatal
The patient had never experienced any cyanotic or yellowish skin color.
The patient was breastfed and brought for routine control and
immunization at private hospital.
D. History of feeding
The patient was given breastmilk exclusively from birth until six months old
and continued until 2 years old, he never given milk formula. Milk porride
was given at 6 months old, and then changed to refined porridge from 8
months old to 10 months old. Soft porridge rice was given from 12 months
old to 14 months old. After 14 months old patient take home meat 3 times
daily, that contain rice with fish or chicken, or eggs with vegetables and
fruits.
Conclusion: There is no history of abnormal feeding
E. Developmental milestone
Patient’s growth and development examination was conducted in the
private hospital until 9 months old and the result was normal. According to
mother, his growth and development history is equal as his peers. Patient
was able to sit without support by the age of 6 months old, to stand by age
of 9 months old, and to walk at the age of 12 months. His parents did not
clearly remembered other developmental status. Right now patient is on
third grade elementary school and can follow school lesson well. His
activity is like any other child on his age and never failed in his educational
degree. He has many friend, gets along well with them, and do activities
like his peers.
Conclusion: Patient had appropriate growth and developmental.
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F. History of vaccination
Patient received basic immunization according to ages. Patient got Bacille
Calmette Guerin (BCG) immunization with scar (+) in right arm, Polio 5
times, Diphteria Pertussis Tetanus (DPT) 4 times, Hepatitis B 5 times, and
Measles twice, DT once and Td once.
Conclusion: Patients received basic and booster immunization
appropriate to his age.
G. History of basic needs

Physic-biomedic :
The patient received adequate primary needs (food, clothes and shelter).
He received a home meal three times a day. When he gets sick, his parent
took him to the nearest health facility in the area
Emotional needs :
The patient received sufficient affection from parent and other family
members. All members of his family strongly support the treatment
provided for the cure of the patient.
Mental stimulation :
Patient loves to play with other kids of the same age. Patients went to first
grade elementary school. Patients have many friends and easy to
socialized with new friends.
Conclusion: Patient received adequate affection, care, and stimulation
from his family.
H. SOCIAL ECONOMIC CONDITION AND ENVIRONMENT

Social Economic :
The patient’s father and mother worked as a government employees.
Medical treatment cost is covered by national health insurance.
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Environment :
Patient lives together with his parents and his brother. The house were
permanent with aluminium roof, concrete wall, tile floor. The house
consists of four bedrooms, inhabited by two adult and two children.
Bathroom is inside the house. The source of electricity from the
government electric company. Water resource is from government water
company and refilled water.
Conclusion: Social economic condition in middle higher level, hygiene
and sanitation was good enough and ventilation was good.
PATIENT’S HOSPITAL ADMISSION SUMMARY

Prior to candidate’s initial observation (Sept 3rd 2018 - Sept 6th 2018)
Patient was admitted to hospital on Sept 3rd 2018 at 19.20 pm
with chief complaint dark colored urine, swollen on the eyelids, and
headache. Two weeks prior to admission, patient got swollen that appears
in the eyelids especially in the morning. One week prior to admission that
symptoms accompanied by dark colored urine. A day prior to admission
patient got headache. A month prior to admission, patient got fever,
cough and sore throath. The symptoms got relieve without any medication.
There was no history of skin infection. Before admitted to B hospital,
patient had hospitalized in A hospital for 5 days and got eritromycin tablets,
captopril tablets and furosemide tablets. Because of there was no clinical
improvement and then he was referred to B hospital.
On physical examination, body weight was 20 kg and body height
was 118 cm. Nutrition status was well-nourished (based on CDC 2000
stature for age and weight for age percentiles for boy aged 2-20 years).
Patient looked sick, compos mentis (GCS E4V5M6). Vital signs: blood
pressure was 120/80 mmHg, pulse 88 bpm (regular,normal pulse volume
and stregth), respiratory rate 24 times per minutes (regular,adequate) and
body temperature 36,80C (axilla). On head examination, conjungtiva was
not anemic and sclera not icteric. On eyes examination, there was eyelids
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swelling on both eyes, round isochor pupils, 3 millimetres in diametre with
normal light reflex. On mouth examination, tonsil T1/T1, tonsil and pharynx
were not hyperemic. There were no enlarged lymph nodes on the neck.
Chest examination found symetrical movement of chest wall, no retraction,
normal breath sound. Regular heart sound, no thrill or murmurs. Abdomen
looks flat, soft on palpation, normal bowel sound, liver and spleen were not
palpable. On extremities, there was no edema, capillary refil time less
than 2 seconds, warm, no cyanosis. There was no abnormality on
genitalia and scrotum examination, testicles palpables on both side.
Result of laboratories workup when admitted to hospital were
hemoglobin 11.2 g/dL, hematocrit 31.5%, leukocytes 10.200/mm3,
platelets 542.000/mm3, ureum 18 mg/dl and creatinin 0.8 mg/dl,
Glomerulus Filtration Rate 81 ml/minutes/1.73 m2, C3 <11 mg/dL, Sodium
135 meq/L, Potassium 3.6 meq/L, Chloride 99 meq/L, Total cholesterol
180 mg/ dL, ASTO 400 IU/ml, Albumin 3.86 g/L. Urinalysis: cloudy yellow,
pH 5, specific gravity 1.020, leukocytes 2-4/hpf, erytrocytes >50/hpf,
protein +2. Radiology examination lung and heart within normal limit.
Electrocardiography was sinus rhythm, no PR interval elongation.
Patient was diagnosed with acute post streptococcal
glomerulonephritis. Patient was treated by Cefixime 100 mg twice daily
orally. Patient was also given furosemide 20 mg twice daily (1
mg/kgBW/dose), captopril 6,5 mg three times daily (0,3 mg/kgBW/dose),
protein 1g/kgBW/day, and low salt diet 1 g/day. Monitoring of vital signs,
diuresis, and fluid balance regularly. Throat swab culture was still waiting
for result. During treatment on B hospital, eyelid swelling and blood
pressure were decreased, but there are still dark colored urine.
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III. PHYSICAL EXAMINATION
Examination was performed in the pediatric nephrology ward on
September 6th, 2018
General condition : looked sick, Compos mentis (GCS E4V5M6)
Anthropometric Status
Body weight = 20 kg
Ideal body weight = 22 kg
Body height = 118 cm
Nutrition status (CDC 2000 Stature for age and weight for age for boy
aged 2-20 years chart)
Weight/Height = 20/22 x 100% = 91 % (Good nutrition)
Weight/Age = 20/27 x 100% = 74 % (Underweight)
Height/Age = 118/130 x 100% = 90 % (Normal height)
Vital sign: blood pressure 110/70 mmHg, pulse 84 bpm (regular,full pulse),
respiratory rate 24 times per minutes (regular,adequate) and body
temperature 36,80C (axila).
Percentile of blood pressure based on age, height, and sex
P90 : 107/71 mm/Hg
P95 : 111/75 mm/Hg
P99 : 119/83 mmHg
Hypertension Crisis ≥ 180/120 mmHg
Skin : brown, efluoresensi (-), scar (-), multiple
hyperpigmentation (+) on arms, BCG scar
(+) on right arm, edema (-).
Head and Neck

Head : mesocephal, black hair not easily removed, head
circumference 52 cm (normocephal)
Eyes : palpebra edema (+), conjungtiva anemic (-),
sclera icteric (-), corneal reflex +/+, round pupil, isocor,
diameter 3 mm, light reflex (+), strabismus -/-, normal
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movement, nistagmus -/- Palpebra edema +/+
Nose : no secretes, no flare
Ear : no secretes
Mouth : cyanosis (-), wet mucosa, atrophy of tongue papil (-)
Throat : tonsils T1/T1, tonsils and pharynx not hyperemic.
Neck : trachea in the middle, lymph node not enlarge.
Chest : symetrical shape, no retraction
Heart
Inspection : ictus cordis unseen
Palpation : ictus cordis palpable in left midclavicule line, 5th
intercostal space, no thrill
Percussion : left heart margin at the left midclavicularis line,
right heart margin at the right parasternal line,
upper heart margin at II-III intercostal space
Auscultation : heart rate frequency 96 bpm, regular, murmur (-)
Lung
Inspection : symetrical respiratory movement
Palpation : symetrical stem fremitus
Percussion : sonor at both lungs
Auscultation : normal, vesicular breath sounds, no rales, no
wheezing
Abdomen
Inspection : flat, no venectation
Palpation : soft, liver, kidney and spleen are not palpable, skin
turgor normal, no undulation, no suprapubic pain
abdominal circumference : 54 cm
Percussion : tympanic
Auscultation : normal bowel sound
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Spine : no deformity
Genitals : male, palpable bilateral testicles inside the scrotum.
Extremities : warm, no cyanotic, capillary refill time less than 2
seconds, normal muscle tone, spastic (-) pretibial
edema (-)
Muscle : good muscle tone
Neurology Status
Reflex : Normal physiology reflex, patology reflex (-)
Stiff neck : negative
Sensoric : normal limit
Motoric : strength of four body limbs was normal
Cranial nerves examination :
 NI = no olfactory problem
 N II = round, isochoric pupils, positives direct and indirect
light reflexes
 N III, IV, VI = no strabismus, normal movements of the eyeballs
 NV = no problem
 N VII = symmetrical nasolabialis sulci, no lagophtalmus
 N VIII = no hearing or balance problem
 N IX = clear articulations, can swallow well
 NX = uvula is central, no deviation
 N XI = can shrug shoulders and turn head against
resistance
 N XII = no tongue deviation
Fluid balance in 24 hours : +150 ml

Urine output : 960 ml/24 hour
Diuresis : 2 ml/kgBW/hour
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IV. RESUME
Patient was admitted to hospital on Sept 3rd 2018 with chief
complaint dark colored urine, swollen on the eyelids, and hypertension.
Patient was a referral from type C private hospital. Two weeks prior to
admission, patient got swollen that appears in the eyelids especially in the
morning. One week prior to admission that symptoms accompanied by
dark colored urine. One days prior to admission patient got headache and
hypertension. Two month’s prior to admission, patient got blister’s on the
arms, it’s swollen, redness and tender. He also got fever, the symptoms
relieved without any medication. Patient had already hospitalized for 5
days at type C private hospital but there were no improvement and then
he was referred to tertiary public hospital.
On physical examination, body weight was 20 kg and body height
was 118 cm. Nutrition status was well-nourished (based on CDC 2000
chart for boy aged 2-20 years). The patient looked moderately sick,
compos mentis (GCS E4V5M6). Vital signs: blood pressure was 110/70
mmHg, pulse 88 bpm (regular,full pulse), respiratory rate 24 times per
minutes (regular,adequate) and body temperature 37,20C (axilla). On head
examination there was edema on eyelid, conjungtiva not anemic. On
mouth examination, tonsil T1/T1, tonsil and pharynx were not hyperemia.
There were no enlarged lymph nodes on the neck. On extremities, there
was no edema.
Result of laboratories workup when admitted to hospital were
hemoglobin 11.2 g/dL, hematocrit 31.5%, leukocytes 10.200/mm3,
platelets 542.000/mm3, ureum 42 mg/dl and creatinin 0.9 mg/dl,
Glomerulus Filtration Rate 72.1 ml/minutes/1.73 m2, Sodium 135 meq/L,
Potassium 3.6 meq/L, Chloride 99 meq/L, Total cholesterol 180 mg/ dL,
ASTO 400 IU/ml, Albumin 3.86 g/L. Urinalysis: cloudy yellow, pH 5,
specific gravity 1.020, leukocytes 2-4/hpf, erytrocytes >50/hpf, protein +3.
Radiology examination lung and heart within normal limit.
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Electrocardiography was sinus rhythm, no PR interval elongation. The
throat swab culture were still waiting for result.
Patient was diagnosed with acute post streptococcal
glomerulonephritis. Patient was treated with antibiotic (Cefixime), diuretic
(furosemide), antihypertensive (captopril) protein diet according to the
RDA, low salt diet, maintenance fluid based on IWL and urine output.
Monitoring of vital signs, diuresis, fluid balance regularly.
V. DIAGNOSIS
Acute glomerulonephritis post streptococcus (ICD 10 N00.9)
VI. PROBLEM
Prognosis problem in 8 years and 4 months old boy with acute
glomerulonephritis post streptococcus and Hypertension.
VII. MANAGEMENT PLAN

1. Working plan diagnosis
- Waiting for throat swab culture
2. Medical plan therapy

- Antibiotic cefixime 100 mg 2 times daily per oral
- Anti hypertensive 6.25 mg 3 times daily per oral
- Furosemide 20 mg 2 times daily per oral (1 mg/kgBW/dose)
3. Pediatric Nutrition Care
- Assesment of nutritional status
Body Weight : 20 kg, Ideal Body Weight = 27 kg
Body Height : 118 cm
Nutrition status : well-nourished ( according to CDC 2000 chart)
- Nutritional needs ( based on RDA)
Calories = 90 kkal/kgBW/day x 20 kg = 1800 kkal/day
Protein = 1 g/kgBW/day x 20 = 20/day
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Fat = 30 % x 1800 kkal = 60 g/day
Fluid (IWL + urine of the day before) = 1360 mL/day
- Nutritional route
Nutrition is given orally
- Determination of food type
Solid food and side dishes 3x1 portion(@500kkal, 5g protein,20g
fat) consist of :
3/4 glass of rice, side dish (medium fish 100 grams), vegetable
and fresh fruit
Snack 2 x 150 kkal
Water 1400 mL
Low salt diet 1 g/day
- Monitoring and observation
Monitoring of acceptabillity, tolerance and effectivity
4. Monitoring and evaluation

- Vital sign monitoring
- Weight monitoring
- Nutrition monitoring
- Urinalysis monitoring
- Diuresis and fluid balance monitoring
5. Education
Educate parents about the disease, complication that can happen,
planning and side effect of therapy, follow up, and prognosis.
Family participation is very important for disease improvement of
thepatient.
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VII. FOLLOW UP
September 7th 2018(1stobservation day, 5th day of hospitalization)

S fever (-), swelling (+) on eyelids, oral intake (+), dark colored urine (+)
O General condition : looked ill, compos mentis
Blood pressure : 110/80 mmHg Respiratory rate : 22 cpm
Pulse : 78 bpM Temperature : 36.4oC (axilla)
Body weight : 20 kg BSA : 0.8 /m2
Fluid balance : +150 mL Diuresis : 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
Thorax : symmetrical movement, no retraction
Cor : normal S I-II, murmur (-), gallop(-)
Pulmo : broncovesicular sound, rales -/-, whezzing-/-
Abdomen : flat, soft, normal bowel sound, liver and spleen were
not palpable, Abdominal circumference:
: 54 cm, ascites (-)
Genitalia : male, normal, edema (-)
Extremities Warm, lower limb edema (-), capillary refill time
< 2 seconds, cyanotic (-)
Laboratory :
Urinalysis : Glucose :-
Color : Clear, yellow Ketone :-
Specific gravity : 1.015 Urobilinogen : -
pH :5 Bilirubin :-
Leukocyte : 5-10/hpf Blood : +5
Nitrite :- Erythrocyte : >50 /hpf
Protein :+2 Epitel : 2-3 / hpf
Throat Swab:
Streptococcus Sanguinis
Sensitif: ceftriaxone, levofloxacin,
linezolid, vancomysin
Resistent: eritromicin, clindamycin,
tetracycline, azithromycin, claritromicin
A Acute Poststreptococcal Glomerulonephritis (N00-09)

P Therapeutic :
- Cefixime 100 mg two times a day orally
- Captopril 6.25 mg three times a day orally
- Furosemide 20 mg two times a day orally
Monitoring and evaluation :
Fluid balance, diuresis
Body weight monitoring
Pediatric nutritional care
Solid food and side dishes 3x1 portion (@400 kcal, 5 gr protein, 5 gr fat),
consist of: ¾ glass of rice ( 100 gram), 1 sousage ( 50 gram), 1 glass of broccoli
( 100 gram), 2 pieces of sweet orange ( 110 gram)
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Milk 2 x 200 mL (@250 kcal, protein 5g, fat 6g)
Mineral water 1450 ml
Nursing care :
Same as before
September 8th 2018(2ndobservation day, 6th day of hospitalization)

S fever (-), swelling (+) on eyelids decrease, oral intake (+), dark colored urine (+)
Pulse : 84 bpM Temperature :36,7oC (axilla)
Body weight : 20 kg BSA : 0.8 /m2
Fluid balance : -487 mL Diuresis : 3.8 mL/kg/hr
Cor : normal S I-II, murmur (-), gallop (-)
Pulmo : broncovesicular sound, rales -/-, whezzing -/-
P Therapeutic :

Fluid balance, diuresis.
Same as before
Nursing care :
Same as before
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September 9th 2018(3rdobservation day, 7th day of hospitalization)
S fever (-), swelling decrease on eyelids, good oral intake (+),dark colored urine
(+)
Blood pressure : 100/60 mmHg Respiratory rate : 24cpm
Pulse : 80 bpm Temperature : 36,2oC (axilla)
Body weight : 20 kg BSA : 0.8/m2
Fluid balance : +180 mL Diuresis : 2,93 mL/kg/hr
Cor : normal SI-II, murmur (-), gallop(-)
P Therapeutic :


Same as before
Nursing care :
Same as before
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September 10th 2018 (4thobservation day, 8th day of hospitalization
S fever (-), swelling (-) on eyelids, good oral intake (+), dark colored urine (+)
Body weight : 21 kg BSA : 0,89/m2
Fluid balance : +46mL Diuresis : 1.2 mL/kg/hr
Eyes : palpebral edema (-)
Cor : normal SI-II, murmur (-), gallop (-)
P Therapeutic :
Same as before
Nursing care :
Same as before
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S fever (-), swelling (-) on eyelids, good oral intake (+), dark colored urine (-)
Eyes : pink conjunctiva, anicteric sclera,
normal form, secretions -/-, nasal lobe breathing(-)
Nose : normal form, secretions - /-
Ear : wet mouth mucosa, T1 / T1 tonsils are not hyperemic,
Mouth : pharynx is not hyperemic
lymph node enlargement (-), JVP not increase
Neck : symmetrical movement, no retraction
Thorax : normal SI-II, murmur (-), gallop (-)
Cor : broncovesicular sound, rales -/-, whezzing -/-
Pulmo : flat, soft, normal bowel sound, liver and spleen were
Abdomen : not palpable, Abdominal circumference:
58 cm, ascites (-)
: male, normal, edema (-)
Genitalia : Warm, lower limb edema (-), capillary refill time
Extremities < 2 seconds, cyanotic (-)
P Therapeutic :
Same as before
Nursing care :
Same as before
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S fever (-), swelling (-) on eyelids, good oral intake (+),dark colored urine (-)
Eyes : palpebral edema (-), facial edema (-)
Cor : normal SI-II, murmur (-), gallop (-)
: 57,5 cm, ascites (-)
P Therapeutic :
Same as before
Nursing care :
Same as before
IX. PROGNOSIS
Ad vitam : ad bonam
Ad functionam : ad bonam
Ad sanationam : dubia ad bonam
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CASE ANALYSIS
Glomerulonephritis is a general term used to describe various types of kidney

disease that experience proliferation and inflammation in the glomerulus due to an
immunological process. Post-streptococcal acute glomerulonephritis is defined as a
form of gromerular inflammation which histopathologically shows glomerular
proliferation and inflammation preceded by infection with Streptococcus Group A B-
hemolyticus and characterized by nephritic symptoms such as hematuria. edema,
hypertension, oliguria that occurs acutely.1,2,3
Acute post streptococcal glomerulonephritis (APSGN) is an immunological

disease due to circulating or in-situ antigen antibody reactions in the glomerulus.
APSGN was initially preceded by a pharyngeal infection 1-2 weeks earlier, or a skin
infection (pyoderma) 3 weeks earlier.4,5 This disease arises after upper respiratory
tract (URT) infections caused by APSGN bacterial infection with nephritogenic type
strains 1, 3, 4, 12, 18, 25 and 49, while strains 2, 49, 55, 61 and 57 cause skin
infections.6,7 The risk of developing APSGN is 10-15% after infection with this
bacteria. In a multicentre study in Indonesia showed that infection through URT was
45.8% while based on previous skin infections 31.6%.6,7
APSGN may occur sporadically or epidemically. The incidence of APSGN
was increased in the low social economic group, this is associated with bad hygiene
and the long distance of medical service location. APSGN can occur in all ages, but
usually more often in children at the age 2 to 6 years, and rarely occurred in children
younger than 2 years old, and older than 20 years.8,9 The study in Indonesia
indicated that the age distribution of APSGN is 2.5 years to 15 years with the
average age of 8.46 years with the male to female children ratio is 1.4:1.10
There are 3 phase in APSGN, which consist of latent phase, acute phase,
and recovery phase. The latent phase is a phase between the occurrence of
streptococcal infection until the appearance of clinical symptoms. Clinical symptoms
usually appears 7-14 days after upper respiratory tract infection or 3-6 weeks after
skin infection. The acute phase is a phase where the patient starts to show
symptoms of nephritic syndrome such as proteinuria, hematuria, azotemia, oliguria,
and hypertension. The recovery phase is indicated with the improvement of clinical
symptoms and laboratory results. Supportive therapy and the prognosis of APSGN is
mostly good, with 6-8 weeks period of recovery.5
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The pathogenesis of APSGN is not known clearly. There are 3 prevailing
theories about the mechanism of immune complex injury to the glomeruli. The first
theory is that there is formation of Group A Streptococcus (GAS) antigen and
antibody complexes in the circulation with subsequent trapping in the glomeruli. The
second theory is that there is first deposition of GAS antigens into glomerular
components with subsequent antibody binding in situ, resulting in immune complex
formation. The third theory is that some GAS antigens in the serum resemble
components of the glomerular basement membrane, commonly referred to as
molecular mimicry, leading to the generation of cross-reacting antibodies and the
formation of complexes in the glomeruli. Evidence supporting and contradicting each
of these theories has included the patterns of complement pathway activation
(contrary to the first theory) and similarities to other GAS-induced diseases
(supporting the third theory), but it is currently thought that GAS antigen deposition
with in situ immune complex formation is most likely. The exact antigen leading to
immune complex formation also remains somewhat elusive. Two of the leading
candidate antigens are nephritis-associated plasmin receptor and streptococcal
pyrogenic exotoxin B. With strong evidence for both antigens from differing parts of
the world, there may not be a single antigen that causes APSGN. 11
There is a common pathway of inflammatory response in the glomerulus,
which results in many of the clinical signs and symptoms of the disease. The
presence of immune complexes leads to complement deposition, leukocyte
infiltration, and proliferation of the structural mesangial cells of the glomerulus. This,
in turn, diffusely impairs capillary perfusion, resulting in a reduction of glomerular
filtration, although not always to the degree that is detectable by an increase in
serum creatinine level. With this decrease in filtration, water and sodium are retained,
leading to an increase in extracellular volume and fluid overload. In addition, by
products of metabolism normally filtered in the urine, such as potassium, urea, and
organic acids, may also accumulate.6,12
The diagnostic criteria of APSGN according to the Nephrology consensus of
Indonesian Pediatric Society is : (1) if there are encounters of hypertension, edema,
and oliguria 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
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of group A β-hemolytic streptococcus on the microbiological culture examination.4
According to Papanagnou et al13, if there are nephritic symptoms like proteinuria,
hematuria, hypertension, edema, and oliguria on a child, the diagnosis of APSGN
can be established.
In this case, boy, 8 years and 4 months old came to the hospital with chief
complaint, got swollen that appears in the eyelids especially in the morning, dark
colored urine one week prior to admission and headache a day prior to admission.
patient have good food portion and take meals three times daily regularly. A month
prior to admission, patient got fever, cough and sore throath. The symptoms got
relieve without any medication.
On physical examination upon admission patient looked sick, compos
mentis (GCS E4V5M6). Vital signs: blood pressure was 120/80 mmHg, On eyes
examination, there was eyelids swelling on both eyes. Result of laboratories workup
when admitted to hospital were hemoglobin 11.2 g/dL, hematocrit 31.5%, leukocytes
10.200/mm3, platelets 542.000/mm3, ureum 18 mg/dl and creatinin 0.8 mg/dl,
Glomerulus Filtration Rate 81 ml/minutes/1.73 m2, C3 <11 mg/dL, Sodium 135
meq/L, Potassium 3.6 meq/L, Chloride 99 meq/L, Total cholesterol 180 mg/ dL,
ASTO 400 IU/ml, Albumin 3.86 g/L. Urinalysis: cloudy yellow, pH 5, specific gravity
1.020, leukocytes 2-4/hpf, erytrocytes >50/hpf, protein +2. Radiology examination
lung and heart within normal limit. Electrocardiography was sinus rhythm, no PR
interval elongation.
The clinical symptoms of APSGN vary greatly from asymptomatic to specific
clinical symptoms. Asymptomatic form is more common than symptomatic form.
Clinical manifestations of acute glomerulonephritis in Indonesia also show similar
results. Of the 45 patients with acute glomerulonephritis at the Cipto Mangunkusumo
General Hospital in Jakarta, the clinical signs were a history of acute upper
respiratory infections (80%), history of skin infections (31.1%), anuria or oliguria
(68.9%), hematuria (64,4%), swelling (86.7%), hypertension (86.7%). 5 Wong et al12
reported various symptoms and clinical signs commonly found in children with
APSGN. There was a decrease in complement levels of C3 (93%), haematuria
(87%), hypertension (72%), renal function disorder (67%) and massive proteinuria
(44%).12,14
23
Damage to the glomerular capillary wall results in haematuria and albuminuria.
Symptoms of macroscopic haematuria occur in the first week and persist for several
days, but may occur for several weeks, whereas microscopic haematuria may last
longer, this usually disappears within 6 months. Proteinuria can be found
qualitatively in APSGN patients ranging from negative to +2, rarely to +3. 10,12 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.6 On this case, early presentation of the disease shows that there were
qualitative proteinuria varying for a few weeks after the symptoms disappeared.
Based on the information acquired from the history taking of this patient, there
are complains like dark-colored urine. The urinalysis test obtained visible dark brown
colored urine with >50 erythrocyte / high power field on microscopic examination.
The complain of dark-colored urine on this patient is preceded with a history of sore
throat a month before admission. It is compatible with the study conducted by Sepahi
et al15 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
child with a history of skin infection.
Decrease in C3 complement is found in 80 - 90% of cases in the first two
weeks because the component plays an important role in the process of antigen -
antibody after infection with streptococcus nephritogenic strains. C3 level in APSGN
decreased during the acute phase, then normalized after 4 - 8 weeks of symptom
onset.6 Srisawat et al15, in a retrospective study of 36 patients with acute
glomerulonephritis, consist of 8 patients with APSGN and 28 patients with non
streptococcal AGN acquired there was a significant difference in the level of
complement C3, where in APSGN patients obtained low levels of complement C3
whereas in patients with non streptococcal AGN obtained normal levels of C3
(p<0.05). On this patient, the examination of C3 resulted in decreased C3 which was
11 mg/dL.
A throat swab culture examination will assist in the diagnosis of APSGN.
Result of throat swab culture in this patient is still waiting for the result. Throat swab
culture examination has a sensitivity of 97% and a specificity of 99%. But positive
culture is found in only 20 - 25% of cases, except during epidemics. Streptococcus
pyogenes is a species of Gram - positive bacteria. These bacteria are bacteria in the
form of cocci, non - motile. Streptococcus pyogenes is the main species that holds
24
the Lancefield group A antigen, and is often called Group A Streptococcus (GAS).
Group A streptococcus in the blood usually results in a small zone of beta –
hemolysis, so it is called GABHS. Streptococcus pyogenes causes many diseases in
humans, ranging from mild skin infections to life - threatening systemic disease.
Infection usually begins in the throat or skin. Streptococcal infection of beta
hemolyticus group A on the body will result in an antibody response that can be
proved by the increase in Anti Streptolysin Titer O (ASTO). Streptococcal hemolytic
exotoxins can cause oxygen stability and immunogenic produced by most strains of
group A. The main function of Streptolysin Titer O is to make hemolysis (in red blood
cells). This titer is of significant value if it is > 200. ASTO is the most frequently
examined serological reaction, because it can easily be titrated. This titer increases
70% - 80% in APSGN. The increase in ASTO begins on days 10 to 14 after
streptococcal infection and peak levels at weeks 3 to 5 and begins to fall by 2 to 6
months. The ASTO titer in post - infection skin infection by Streptococcus is rarely
increased and occurs in only 50% of cases.6,10,16 On this patients, ASTO result
increased to 400 IU/ml.
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,
and 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. 1,17
Hypertension occurs on 32 to 70 % of APSGN patients. 8 The elevation of
blood pressure is caused by excessive fluid leading to a disturbance in the renin
angiotensin and aldosterone system (RAAS).18,19 Generally, hypertension occurred
on the first week and disappeared along with the disappearance of other clinical
symptoms. Mild hypertension is found on most cases (diastolic blood pressure of 80-
90 mmHg). Severe hypertension can also occur, such as encephalopathy
hypertension (4-50%) with symptoms like headache, seizures, decreased
consciousness, nausea and vomitus.5 The study of Kumar et al20, on children with
APSGN at the age of 3 to 12 years in India, edema occurred on 100% cases and
hypertension is found on 80% of the cases.
25
On this patient, palpebral edema is also found 3 days before admission. On
the vital sign examination at the beginning of the patient’s admission, it is found that
there are an increased blood pressure which is 120/80 mmHg. Based on the curve
from The Task Force on Blood Pressure Control in Children by age and sex, the
patient’s blood pressure is above the 95th – 99th percentile + 5mmHg.
Management of APSGN patients includes eradication of bacteria, supportive,
diet, and education. Bacterial eradication is necessary for all APSGN patients with
penicillin antibiotic groups. Antibiotics do not affect the severity of glomerulonephritis,
but reduce the likelihood of the spread of Streptococcal infection. Antibiotics are
given only if there is evidence of active infection. 10 The study by Driel et al18 reported
the results of a meta - analysis that there was no significant difference between
cephalosporin, macrolide, carbapenem and sulfonamide antibiotics in cases of
Streptococcus sp bacterial infection compared with penicillin. The antibiotic therapy
given to this patient is oral erythromycin then was shifted to cefixime. The duration of
antibiotics in this patient is planned for 10 days.
Supportive therapy for APSGN patients include bed rest, nutritional
management, symptomatic therapy for swelling, hypertension, and kidney disorder.
Bed rest could lower the degree and duration of gross hematuria, but does not affect
the course of the disease or long term prognosis. Swelling is treated through fluid
restriction and administration of diuretics. Hypertension is treated in accordance to
the degree of hypertension. Nutritional management is done through diet containing
adequate calorie, protein according to Recommended Dietary Allowances (RDA),
and natrium.6 Salt restriction as much as 0,5-1 g/ day. Fluid and salt restriction dan
administration of loop diuretic are the first line therapy to treat fluid overload and
hypertension. He et al21, in a systematic review of 10 randomized control study
founds that low salt diet on children as long as ≥ 2 weeks could lower blood pressure
both systolic an diastolic. Administration of furosemide in hypertension accompanied
by edema gives a better result compared to reserpin. During treatment, fluid
management, diet management, and administration of furosemide are done to the
patients. After inducted as a case, swelling and elevated hypertension found during
hospital admittance were no longer found.
Education plays an important role in treatment of APSGN. Patients and family
needs to be explained about the course of the disease and prognosis. Family also
need to know and understand although chance of total recovery is as high as 95%,
26
there is small risk of persistent anomaly or even worsening of condition
approximately as much as1-5%. Plan of further observation also needs to be
explained, including regular blood pressure measurement, urine analysis every 2
weeks during the first 2 months, and afterwards every 6 months, continued by every
3-6 months until hematuria and proteinuria resolved. Level of C3 that returns to
normal after 8-10 weeks is indicative of good prognosis.22
Dagan23 et al, in study of 125 patients with Streptococcal infection was
established by elevated anti-streptolysin O titers (ASTO) in 109 (85%), while throat
culture was positive in 39 (31.2%). Histopathological findings in fie specimens were
compatible with post infectious glomerulonephritis, which are diffuse proliferation of
glomerular cells, deposits of immunoglobulin G and C3 along with sub-epithelial
dense deposits (hump-like) on electron microscopy (EM). Two specimens showed
typical fidings on light microscopy without hump-like deposits on EM. Follow-up data
were available in 116 patients (92.8%). Mean duration of follow-up was 42 months
(median 13). At the last visit all patients had normal renal function, microscopic
hematuria was present in 29 (30%), and 1 had nonnephrotic proteinuria. Blood
pressure measurements were available in 100 patients, 6 of whom (6%) had
elevated levels. No signifiant diffrence in clinical and laboratory fidings during the
acute phase of the disease was noted between patients with high blood pressure
and patients without hypertension. Complement levels were normal at the end of the
follow-up. (Level of evidence 2B, recommendation B)
Hadiwijaya24 et al, in a study of 95 children with acute post-streptococcal
glomerulonephritis (APSGN) to assess patient outcomes, 90 children (94.7%) were
cured and 5 children (5.2%) died. Urea levels <119 mg / dl at early of the
examination were independent prognostic factors for the outcome of children with
APSGN (p = 0.032; OR 1.021, and 95% CI 1.002-1.041). Creatinine levels <1.3 mg /
dL at the start of the examination were also associated with outcomes of pediatric
patients with APSGN (p = 0.02) but sex (p = 0.961), nutritional status (p = 1.00), and
age (p = 0.108) does not correlate with patient outcomes (Level of evidence 2B,
recommendation B)
Ayoob25 et al, 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 of preceding pharyngitis but had not documented
skin infection. APSGN manifestation was rarely seen as severe nephritis. All patient
27
had C3 <80 mg/dl that normalized on follow-up. (Level of evidence 2B,
recommendation B)
Ugwu26 et al, in a study of 20 patients (13 male and 7 female) with acute
glomerulonephritis were seen during the three-year period follow up. Seventeen
(85%) of the patients were in the school-going age group (>5 years to 10 years). The
most common symptom/sign noted was oliguria/anuria and edema seen in 80% of
the patients. Seventy percent of the patients had cola-colored urine, while 55% had
hypertension. The outcome of the management of these patients showed 14 (70%)
of the patients recovered fully while three (15%) had persistent hematuria and two
(10%) had persistent proteinuria. Ninety-five percent of the patients recovered from
the acute illness and one patient (5%), a boy aged nine years old, died. (level of
evidence 2B, recommendation B)
Prognosis ad vitam and functionam in this child is ad bonam, ad sanationam
is dubia ad bonam. Education is important in the treatment of APSGN. Patient and
the patient family should be given explanation regarding the cause of the disease
and the prognosis. Patient needs to be reminded for control within first week after
given the permit for outpatient care. Drugs for this patient needs to be administered
until the next scheduled control. In patients with APSGN, patient needs to measure
blood pressure and conduct an urinalysis to assess hematuria and proteinuria
gradually. Education in this patient includes nutritional care that still require low salt
diet and adequate protein nutrition and visit a doctor as soon as possible if upper
respiratory tract infection occurs.
28
REFERENCES
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NA, Subandiyah K, Prasetyo RV, Alatas H, Tambunan T, dkk, penyunting.
Kompendium nefrologi anak. Jakarta : BP IDAI. 2011. h.57-61.
2. Lurn G. Glomerulonephritis. Dalam: Hay W, Levin M, Sondheimer J, editor.
Current diagnosis and treatment pediatrics. 19th Ed. United States of America:
McGraw Hill. 2009. h.656-7.
3. Pan CG, Avner ED. Acute post streptococcus glomerulonephritis. In: Kliegman
RM, Stanton BF, St Game lll JW, Schor NF, Berman RE, editor. Nelson
Textbook of Paediatrics. Edisi ke-19 .Elsevier Saunders: Philadelphia. 2011. h.
1783-94.
4. 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
5. Albar H, Rauf S. The profile of acute glomerulonephritis among Indonesian
Children. Paediatrica Indonesiana. 2005;45;264-9.
6. Cunningham MW. Pathogenesis of group A streptococcal infections.
ClinMicrobiol Rev. 2000;13:470-91.
7. Gunasekaran K, Krishnamurthy S, Mahadevan S, Harish BN, Kumar AP. Clinical
Characteristic and Outcome of Post Infectious Glomerulonephritis in Children in
Southern India: A Prospective Study. Indian J Pediatr. 2015;10:46-51.
8. Rodriguez B, Mezzano S. Acute postinfectious glomerulonephritis. In: Avner ED,
Harmon WE, Niaudet P, Yashikawa N,editors. Pediatric nephrology. 6 th edition.
Berlin: Springer; 2009. Pg. 743-55.
9. Smith JM, Faizan MK, Eddy AA. The child with acute nephritis syndrome. In:
Webb N, Postlethwaite R,editors. Clinical paediatric nephrology. 3 rd edition. New
York:Oxford;2003. Pg. 367-80.
10. Eison T, Ault B, Jones DP. Post streptococcal acute glomerulonephritis in
children: clinical features and pathogenesis. Pediatr Nephrol. 2011;26:165-80.
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11. Rodriguez- Hurbo B, Batsford S: Pathogenesis of poststreptococcal
glomerulonephritis : a century after clemons von Pirquet. Kidney Int 71, 2007:
1094 -104.
12. 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 Oct;49:850-5.
13. Papanagnou D, Kwon NS. Acute glomerulonephritis in emergency medicine.
Updated e Medicine Emergency December. 2010;12:1-18.
14. Madaio MP, Harrington JT. The diagnosis of glomerular diseases: acute
glomerulonephritis and the nephrotic syndrome. Arch Intern Med. 2001;161:25-
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15. 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.
16. Srisawat N, Aroonpoonsul L, Lewsuwan S, Kanjadabach T, Avihingsanon Y, et
al. The clinicopatholgy and outcome of post infectious glomerulonephritis. J Med
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17. Long SS, Pickering KL, Prober GC. Streptococcus pyogenes (group A
streptococcus). In: Gerber M. Principles and practices of pediatric infectious
disease. 3rd Ed. Churcilllivingstone :Elseviers science; 2008.p.700-10.
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antibiotics treatments for group A staphylococcal pharyngitis. The Cochrane
Database of Systematic Reviews. 2013.8:12-9.
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Prasetyo RV, Alatas H, Tambunan T, dkk, editor. Kompedium nefrologi anak.
Unit Kerja Koordinasi Nefrologi Ikatan Dokter Anak Indonesia. Jakarta: Badan
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children with special reference to presentation. Curr Pediatr. 2011;15:89-92
21. He FJ, MacGregor GA. Importance of salt in determining blood pressure in
children: meta-analysis of controlled trials. Hypertension J. 2006;48:861-9.
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23. 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
24. Hadiwijaya A, Albar H, Rauf S, Daud D. Prognostik factor of ureum and creatinin
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2015;3:151-5.
25. Ayoob R, Scwaderer A. Acute kidney injury and atypical features during pediatric
post streptococcal glomerulonephritis. Int J Nephrol. 2016;3:1-5.
26. Ugwu M. Acute glomerulonephritis in children of the Niger delta region of Nigeria.
Saudi J Kidney Dis Transpl. 2015;26:1064-9.
EVIDENCE BASED REFERENCES
23. 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
24. Hadiwijaya A, Albar H, Rauf S, Daud D. Prognostik factor of ureum and creatinin
serum of acute post streptococcal glomerulonephritis in children. AJHR.
2015;3:151-5.
25. Ayoob R, Scwaderer A. Acute kidney injury and atypical features during pediatric
post streptococcal glomerulonephritis. Int J Nephrol. 2016;3:1-5.
26. Ugwu M. Acute glomerulonephritis in children of the Niger delta region of
Nigeria. Saudi J Kidney Dis Transpl. 2015;26:1064-9.
31

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TIMELINE

Patient was admitted to hospital on September 3rd 2018 with chief

2.2 HISTORY OF PREVIOUS ILLNESS

2.3 HISTORY OF ILLNESS IN THE FAMILY

2.4 PERSONAL AND SOCIAL HISTORY

G. History of basic needs

H. SOCIAL ECONOMIC CONDITION AND ENVIRONMENT

PATIENT’S HOSPITAL ADMISSION SUMMARY

Head and Neck

Fluid balance in 24 hours : +150 ml

VII. MANAGEMENT PLAN

2. Medical plan therapy

4. Monitoring and evaluation

September 7th 2018(1stobservation day, 5th day of hospitalization)

A Acute Poststreptococcal Glomerulonephritis (N00-09)

September 8th 2018(2ndobservation day, 6th day of hospitalization)

Monitoring and evaluation :

Monitoring and evaluation :

Pediatric nutritional care

A Acute Poststreptococcal Glomerulonephritis (N00-09)

A Acute Poststreptococcal Glomerulonephritis (N00-09)

A Acute Poststreptococcal Glomerulonephritis (N00-09)

Glomerulonephritis is a general term used to describe various types of kidney

Acute post streptococcal glomerulonephritis (APSGN) is an immunological

1. Noer MS. Glomerulonefritis akut pasca streptokokus. In : Noer MS, Soemyarso

EVIDENCE BASED REFERENCES

23. Dagan R, Cleper R, Davidovits M, Trieman LS, Krause I. Post-infectious

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