1

CLINICAL CASE REPORT

ACUTE NEPHRITIC SYNDROME (N0.9) IN A 10 YEARS OLD
BOY

Mirantika Audina
I4061172033
Supervisor
dr. Hilmi Kurniawan Riskawa, Sp.A, M.Kes

Pediatric Unit of Medical Education Course

Tanjungpura University
Kartika Husada’s Hospital
Kubu Raya Region
2018

Patient’s Identity
FA, An 10 years old boy with medical record
number 143336, was admitted in pediatric ward
of Kartika Husada’s Hospital for 3 days since
31st July 2018 till 2nd August 2018.
2
Subjective Findings
Present Complain
• Edema
History Of Present Ilness
• An 10 years old boy presented with edem for 4
years on his face. Edema firstly located on his
palpebra then it was spread to both of his fingers.
• Others complain such as fever, cough, dispnea,
headache, sore throat, dan abdominal pain was
denial. There was no complain both on his urination
or defecation.
• His appetite and drink was normal.
 3

Subjective Finding Objective Finding

 Past Illness History Vital Sign
He had similar complaint when he was 6 • General status: moderate sickness
years old • Awareness : compos mentis
• Blood pressure: 130/100
 Family History • Heart rate: 100 x/minutes, regular rhytm, palpable
There was no similar compain in his • Respiratory rate: 30x/minutes
family
• Temperature : 37 º C
• Spo2 : 98%
 Medical History
Nutritional Status
On the first day of his complain, he went • Weight : 28 kg
to a health center and was found blood on • Height: 134 cm
his urine (+++) on the examination. • BMI : 15,59
• Status : normal
 4

Objective Finding

 Eyes : Anemic Conjunctiva (-), icteric sclera (-), edema palpebra (+)
 Ear : mucus (-), tragus pain (-), deformity (-), hyperemic auricula(-), tympani membrane
intact
 Nose : mucus (-), hyperemic nasal mucosa (-)
 Mouth : Mucosa of the mouth dan lips moist, leukoplakia (-)
 Throat : hyperemic Pharyng (-)
 Neck : lymph node enlargement (-),
 Lung
• Inspection : Symmetric shape and motion, retraction subcostae
• Palpation : Same tactile fremitus of right and left lung
• Percution : Sonor in both lung fields
• Auscultation: bronchovesicular breath sound, wheezing (-/-), slime (+/+)
 Cor : Heart sound S1 and S2 single, regular, murmur (-) and gallop (-)
 5

Objective Finding

 Abdomen
• Inspection : Flat, no mass
• Auscultation: Bowel sound normal
• Percution : Timpani in all region of abdomen
• Palpation : Liver and spleen not palpable, there is no tenderness and ascites
 Anus and genitalia : were not examined
 Extremities : Warm, Capillary Refill Time < 3”, cyanosis (-), edema (+) et region digiti manus
dextra and sinistra
 Laboratory Finding 6

30th July 2018 31st July 2018

Urinalisis Complete Blood Examination
• Colour : yellow • Leukocyte : 11.500/mm3 (Normal : 5.000-17.000 /mm3 )
• Turbidity : clear • Eritrocyte : 4,55 juta/mm3 (Normal : 3.90-5.50 juta
• pH : 8 /mm3)
• Density : 1,010 • Hemoglobin : 11,6 g/dl (Normal : 11,5-13,5 g/dl)
• Leukocyte: (-) • Hematocryte : 35,2% (Normal : 34-40%)
• Protein : (-) • Trombocyte : 336.000/mm3 (Normal : 150.000-400.000
• Glucose : (-) /mm3)
• Keton : (-) • MCH : 25,6 pg (Normal : 23,1-28,2 pg)
• Bilirubin : (-) • MCV : 77,4 fl (Normal : 71,6-83,5 fl)
• Urobilinogen: normal • MCHC : 33,1 g/dl (Normal : 32,0-35,9 g/dl)
• Nitrit : (-) • %Limfosit : 41,6% (Normal : 20-80%)
• Blood : +++ • %Granulosit 30,4% (Normal : 40-65%)
 Laboratory Finding 7

31st July 2018 1st August 2018

Serology chemical Complete blood examination
• SGOT : 21 u/l (Normal : ≤ 40 u/l) Colour : yellow
• SGPT : 8 u/l (Normal : ≤ 41 u/l) Turbidity : clear
• Ureum : 10 mg/gl (Normal : 15-45 pH : 6
mg/dl) Density : 1,010
• Creatinin : 0,48 mg/dl (Normal: L 0,9-
1,3 mg/dl, P 0,6-1,1 mg/dl) Leukocyte: (-)
• Cholesterol total : 114 mg/dl (Normal < Protein : (-)
200 mg/dl) Glucose : (-)
• Albumin: 3,9 g/dl (Normal : 3,4-4,8 Keton : (-)
g/dl)
Bilirubin : (-)
Urobilinogen: normal
Nitrit : (-)
Blood : +++
 8

Differential Diagnose Working Diagnose

 Acute Nephritic Syndrome

Acute Nephritic Syndrome
 Nephrotic Syndrome
 Therapy 9

Bed rest Venflon

Medicamentosa
Non-medicamentosa
Monitor of Diuresis Inj. Ampicillin 4 x 1 gr IV
Monitor of blood pressure/6 hours Oral Route
• Furosemid 2 x 20 mg tab
• Prednison 3-3-3 tab (3 x 15 mg)
• Captopril 2 x 6,5 mg tab
 Follow UP 10

Tgl S O A P
1/8-18 Edema (+) a/r face and Awareness: ompos mentis Nephrotic syndrome Venflon
(SD 6 HD 2) digiti manus dextra BP: 110/80 mmHg Inj. Ampicillin 4 x 1 gr IV
sinistra, fever (-), HR: 90x/mnt Oral Route:
cough (-), dyspnea (-), RR: 26x/mnt Furosemid 2 x 20 mg tab
urination (+) norma, T : 36,5oC, Prednison 3-3-3 tab (3 x 15 mg)
defecation (-) the latest Weight : 28 kg, Captopril 2 x 6,5 mg tab
day was 2 days ago edem palpebra (+), anemic conjungtive (-/-), S1S2 Bed rest
regular, murmur (-), gallop (-), crackles (-/-), Monitor of Diuresis
wheezing (-/-), soeple, timpani, bowel sound (+) N, Monitor of blood pressure/6 hours
abdominal pain (-), liver and spleen not palpable,
edem a/r digiti manus dextra sinistra (+)
2/8-18 Edema (+) a/r face and Awareness: ompos mentis Nephrotic syndrome Venflon
(SD 7 HD 3) digiti manus dextra BP: 120/90 mmHg Oral Route:
sinistra decreased, HR: 90x/mnt Ampicillin 3 x 1/2 tab
fever (-), cough (-), RR: 24x/mnt Furosemid 2 x 20 mg tab
dyspnea (-), urination T : 36,5oC, Prednison 3-3-3 tab (3 x 15 mg)
(+) norma, defecation Weight : 27,5 kg, Captopril 2 x 6,5 mg tab
(-) the latest day was 2 edem palpebra (+) decreased, anemic conjungtive Hospital free-days
days ago (-/-), S1S2 regular, murmur (-), gallop (-), crackles
(-/-), wheezing (-/-), soeple, timpani, bowel sound
(+) N, abdominal pain (-), liver and spleen not
palpable, edem a/r digiti manus dextra sinistra (+)
decreased
 Prognosis
 Ad vitam : dubia ad bonam
 Ad functionam : dubia ad bonam
 Ad sanactionam : dubia ad bonam
 12

Discussion
 13

 Patients present with edema complaints. Some diseases that can cause it are from kidney, liver, allergic
and malnutrition. In edema caused by heart disease is starting from both legs due to reduced backflow
due to impaired return to the cor, the influence of force and peripheral resistance on the high limbs,
especially the popliteal fossa and inguinal.
 Next is the liver organ. This swelling begins from the stomach due to fibrosis of the liver which aims to
bend the vein back and occur portal hypertension, a decrease in protein synthesis that occurs
hypoalbuminemia which enters intravascular osmotic which causes extravasation of fluid.
 In addition, allergies can also cause edema, but only in certain places which are non pitting edema and
do not last long.
 In malnutrition, swelling occurs throughout the body for no apparent reason and usually in the
kwashiorkor or marasmus kwashiorkor.
 In edema caused by kidney disorders is starting from the eyelids. It is because og the gravitation. Eyelid
is a network that contains a lot of connective tissue.

In this patient, edema starts from the eyelids
which continues to his fingers. This shows
that edema in these patients leads to kidney
disorders. To help establish a diagnosis, a
supporting examination is needed in the
form of a complete blood laboratory test,
complete blood chemistry and urinalysis
14
Result of Laboratory examination obtained:
• From the results of laboratory examination obtained proteinuri
(-), hematuri (+++), albumin 3.9 g / dl, urea 10 mg / dl,
creatinine 0.48 mg / dl, and total cholesterol 114 mg / dl. From
the results of history, physical examination and laboratory
examination, these patients obtained palpebral edema and edema
of digiti manus dextra sinistra, levels of albumin, cholesterol and
proteinuria within normal limits.
 15

Acute  Acute nephritic syndrome (ANS) is a collection of

glomerulonephritiis
is more general and clinical symptoms in the form of
more specific terms
of the
histopathological
process in the form Proteinuria
of glomeruli
proliferation &
inflammation due to Haematuria
immunologic
processes. In the
literature the terms
AGN and ANS are Edema
often
interchangeable.
Acute
Hypertension
glomerulonephritiis
is a more histological
term, whereas ANS
is more clinical. Oliguria
 16

Rest in bed, especially if there are complications that usually arise during the first week of the disease. After the
acute phase, it is not advisable to rest in bed, but activities such as before sick are not permitted. The duration of
treatment depends on the state of the disease. In the past, prolonged bed rest was recommended for months on
the grounds that proteinuria and microscopic hematuria had not disappeared. If urine laboratory abnormalities
are still found, further observations are made at the time of outpatient treatment. Resting too long in bed causes
the child to be unable to play and away from his friends, so that it can provide psychological burden.

Management of these patients is appropriate for the patient being treated, while bed rest can be done well.
Giving antibiotics to the SNA is still often contested. One party only gives antibiotics if the
culture breaks the throat or the skin is positive for streptococci, while the other party gives
it regularly on the grounds that negative cultures have not been able to get rid of
streptococcal infection.

Negative culture can occur because it has received antibiotics before entering the hospital
or due to a latent period that is too long (> 3 weeks). Medical therapy for penicillin groups
is given for eradication of germs, namely Ampicillin 50 mg / W every time they are given.
If there is an allergy to penicillin group, erythromycin can be given a dose of 30 mg / kg /
day.

Management in this patient is correct, namely Ampicillin 4x1 gr P.O. The

patient has a weight of 28 kg so the calculation of the dose is 50 (28) = 1400
mg for each time administration.

. The dose of 4x1 gr given to the patient is right because it is still in the
dosage range of Ampicilin.

In these patients, furosemide is
given to reduce edema. The dose of
furosemide is 1 -3 mg / kgbb, so the
dose calculation is 1-3 (28) = 28-84
mg, so the dose given is 2x20 mg iv
is appropriate, because it is in the
dose range of furosemide.
18
 In addition, to reduce blood pressure the patient is given
Captopril. The dose of captopril is (0.3-2 mg / kg / day) so the
dose calculation is (0.3-2) (28) = 8.4-56 mg / day. So giving
2x6.5 mg can still be tolerated because it is within the dose
range of captopril for children.

 For the patient's diet, the amount of salt given needs to be
The important thing to note is the
restriction of fluids, giving enough
calories in the form of
carbohydrates. If acidosis occurs,
sodium bicarbonate should be given
and if hyperkalemia is given Ca
glukonas or Kayexalate to bind
potassium. In this patient, electrolyte
correction is not needed.
19
considered. When edema is severe, food without salt is given,
whereas if edema is mild, the administration of salt is limited to
0.5-1 g / day. Protein is limited if the level of urea is increased,
which is as much as 0.5-1 g / kg / day. Fluid intake must be
taken into account properly, especially in people with oliguria
or anuria, namely the amount of fluid that comes in must be
balanced with expenditure, meaning fluid intake = the amount
of urine + insensible water loss (20-25 ml / kg / day) + the
amount of fluid requirements in each temperature rise from
normal (10 ml / kg / day).

 Treatment for these patients was given full dose steroids
according to ISKDC (International Study on Kidney Diseases
in Children) given prednisone 60 mg / m2LPT / day or 2 mg /
kgBW / day (maximum 60 mg / day in divided doses to induce
remission). 9-11. In this patient had a BB 28 kg and TB 134
cm, so that the dose of prednisone given was 60 (1,020) =
61,25 mg / day. However, this patient is given a dose of 45 mg /
day because the dose of rounding to 45 mg is still in a safe dose
of prednisone which is a maximum of 60 mg / day
20
The prognosis in this patient is good if the
treatment process goes well. According to Ranjit
and Kamrul, most patients with
glomerulonephritis will heal, but 5% of them
experience a course of disease that rapidly
deteriorates the formation of cracks in the
glomerular epithelium. Diuresis will return to
normal on the 7-10th day after the onset of the
disease, with the disappearance of swollen blood
pressure will gradually return to normal
 REFERENCE 21

 Kliegman B, Jenson S. Nelson textbook of pediatric. Edisi ke-18. Philadelphia: Saunders; 2007.
 Betz CL, Sowden LL. Pediatrik. Edisi ke-5. Jakarta: EGC; 2009.
 Partini PT, Djajadiman G, Yulia A. Sindrom nefrotik sekunder pada anak dengan limfoma hodkin. Sari Pediatri. 2006; 8(1):37-42.
 Anderson S, Komers R, Brenner BM. Renal and systemic manifestations of glomerular disease. Dalam: Brenner BM, editor. Brenner and rector's the kidney.
Edisi ke-8. Philadelphia: Saunders Elsvier; 2008.

 Siddall EC, Radhakrishnan J. The pathophysiology of edema formation in the nephrotic syndrome. Kidney Int. 2012; 82:635–642.
 Rondon-Berrios H. New insights into the pathophysiology of edema in nephrotic syndrome. Nefrol. 2011; 31:148–54
 Carapetis JR, Steer AC, Mullolans EK. The Global burden of group A streptococcal diseases. The Lancet Infectious Diseases. 2005;5: hlm. 685–94.
 Iturbe BR, Mezzano S. Acute post infectious glomerulonephritis. Dalam : Avner ED, Hormon WE, Niaudet P, Yoshikawa N, penyunting. Pediatric Nephrology,
Sixth Completely Review, Updated and Enlarged Edition. Berlin Heidelberg: Springer-Verlag; 2008; hlm. 743–55.

 Lombel RM, Gipson DS, Hodson EM. Treatment of steroid-sensitive nephrotic syndrome: new guidelines from KDIGO. Pediatr Nephrol. 2013; 28(3):415-26.
 Hodson EM, Willis NS, Craig JC. Corticosteroid therapy for nephrotic syndrome in children. Cochrane Database Syst Rev. 2007; (4):CD001533
 Debbie SG, Susan FM, Lynne Y, Shashi N, William ES, John D, et al. Management of childhood onset nephrotic syndrom. Pediatrics. 2009; 124(2):747-57.
 Yoshizawa N, Yamakami K, Fujino Metal. Nephritis associated plasmin receptor and acute poststreptococcal glomerulonephritis characterization of the antigen
and associated immune response. J Amer Soc Nephrol. 2004; 15: 1785–93.
 22

 TERIMAKASIH