Tuberculosis and Nephrotic Syndrome in A Child: Case Report

With all due respect to :
To be presented on February 5th 2014

CASE REPORT
TUBERCULOSIS AND NEPHROTIC SYNDROME

IN A CHILD
By :
Aldo Yustianto
Supervisor :
dr. Audrey M.I. Wahani, SpA(K)
DEPARTMENT OF CHILD HEALTH

MEDICAL SCHOOL OF SAM RATULANGI UNIVERSITY
PROF.DR.R.D.KANDOU GENERAL HOSPITAL
MANADO
2014
1
INTRODUCTION
Tuberculosis (TB) is an infectious disease that caused by Mycobacterium tuberculosis.
Tuberculosis usually attack lungs, but also spread to another organ inside the body. Lungs is
port dentree for more than 98% tuberculosis cases.1
Tuberculosis, especially pulmonary tuberculosis, is a problem not only in developing
countries but also in industrial country. Tuberculosis is one cause of high rates of morbidity and
mortality, both in developed countries and industrial countries. The World Health Organization
estimates there are about 8,6 million people fell ill with TB and 1,3 million died from TB. In
2012, an estimated 530.000 children become ill with TB and 74.000 HIV-negative children died
of TB. Over 95 % of TB deaths occur in low- and middle-income countries. The five countries
with the largest number of incident cases in 2012 were India (2 2.4 million), China (0,9 1,1
million), South Africa (0,4 0,6 million), Indonesia (0,4 0,5 million) and Pakistan (0,3 0,5
million). India and China alone accounted for 26% and 12% of the global cases, respectively.2
WHO annual report on global TB control 2013 said Indonesia include in the data of
high-burden countries for TB, in 2012 the number of new TB cases in Indonesia is 322.882
people, TB death rate around 67.000/years and incidence about 185/100.000 population.2
Nephrotic syndrome (NS) is a common childhood disease.3 The incidence of NS in
children ranging from 2-7 cases out of 100.000 children aged less than 16 years.4 In Indonesia is
estimated to 6 cases per year out of every 100.000 children less than 14 years. The majority
(90%) NS in children is a primary nephrotic syndrome that is suspected cause by
immunological disorders.5,6
Based on the response to steroid therapy, NS differentiated into steroid sensitive (SSNS)
and steroid resistant (SRNS). Steroid-resistant nephrotic syndrome represent a heterogeneous
group of kidney disorders that are resistant to immunosuppressive agents and tend to progress
to terminal renal failure.5 Most SRNS histopathologic picture show non minimal lesion is focal
segmental glomerulosclerosis (FSGS) and diffuse mesangial proliferation (DMP). The response
to steroid treatment is an important indicator for the prognosis of NS. Although presentation of
SRNS relatively small but 50% of patients SRNS will develop into terminal renal failure within
1-4 years.7,8
Long-term prognosis of nephrotic syndrome during their 20 years showed only 4-5%
will be a terminal kidney failure. In many long-term study found that the response to steroid
2
treatment is more often used to determine prognosis compared with the pathological picture
anatomi.8
The following report is a case of Tuberculosis and Nephrotic Syndrome in a child who
was treated at the Pediatric Department of the Prof. Kandou General Hospital Manado.
CASE REPORT
SK, an Indonesian girl, Minahasanees, 12 years and 2 months old, lives in Amurang, was
admitted to the Department of Child Health, Prof.Dr.R.D. Kandou General Hospital Manado on
January 14th, 2014 with chief complaint was swelling in all body d fever since 2 weeks before
admission to hospital.
History of illness (allo and autoanamnesis from patient and her mother)
Patients present with swelling of the whole body since 10 days before admission to hospital.
Initially perceived swelling of the face, but the longer reaches the stomach and legs. Patients
were then treated at the hospital Kalooran, Amurang and treated there for 5 days. Patients was
said suffering from kidney disease. Her complaints swelling is not reduced so the patient was
referred to the Prof. Dr.R.D.Kandou hospital. Patient also accompanied by a fever since 2
weeks before entering the hospital. Intermittent fever and felt down with medicine. Patients had
treatment to the clinic, but until now they still occasionally got a fever.
Previously, patients had never experienced such swelling on his eyelid or his whole
body. Vomiting experienced by patients but rarely. There is no presence of cough and cold.
History of sore throat earlier denied by the patient and his mother.
Until now, the patient is still have a good appetite and eat as usual. But her body weight
does not increase. History of reddish urination denied and during treatment at hospital at
Kalooran hospital, patients do not experience an increase in blood pressure. Patients defecation
as usual every 2-3 days, urination was normal.
Her neighbour had suffered from lung disease with symptoms of persistent cough but
her mother didnt know whether he got treatment for 6 months or not.
History of prenatal care and birth
3
During the pregnancy, her mother has regular antenatal care and she had tetanus toxoid
immunization twice. This patient was born with normal labour, aterm, birth weight 3.500 gram
History of experienced illness

She had several episodes of common cold and diarrhea.
Developmental milestones
Social smile : 3 months Standing : 12 months
Turning in prone position : 4 months Calling mama/papa : 12 months
Sitting : 9 months Walking : 14 months
Crawling : 10 months
History of feeding
Breast feeding : birth - 18 months
Formula milk : 6 - 12 months
Milk porridge : 8 - 15 months
Soft rice porridge : 9 12 months
Rice :12 months - now
History of Immunization
She received all the basic immunization.
Family Tree
4
= the patient
Social, economic and environment

He is the second child in the family. Her father was 36 years old, a primary school graduation,
works as a farmer. His mother was 40 years old, a junior high school graduation, works as a
housewife. Their house is a permanent house with toilet and bathroom inside the house, and has
2 rooms occupied by 4 adults and 4 children. The electricity source is from state power
company and drinking water from deep well. Garbage is buried at the backyard.
Physical Examination (February, 14th 2014)

General conditions : Moderately sick
Consciousness : E4M6V5
Body weight : 33 kg
Body height : 143 cm
Weight /age : CDC 2000 : 76,7 % (moderate malnutrition)
Length / age : CDC 2000 : 93,4 %
Weight / height : CDC 2000 : 91,6 %
Vital signs : Blood pressure : 120/70 mmHg
Pulse rate : 80 times/minute, regularly
Respiratory rate : 20 times/minute
Temperature : 36,50C
Skin : brown, turgor and muscle tone were normal
Head : oval shape, black hair, not easy to pulled out
Eyes : conjungtiva was not anemic , sclera was not icteric
pupil was isochor with diameter 3 mm, light reflex was normal, corneal
reflex normal, palpebral edema (+).
Ears : no secrete
Nose : no secrete,
Mouth : no cyanosis, tonsil T1/T1 without inflammatory sign, pharynx without
inflammatory sign, dry mouth mucous
Neck : no lymph node enlargement, trachea in the middle line
5
Chest : symmetrical respiratory movements, no retraction
Heart : normal rate, regular rhythm, no thrill, no murmurs
Lungs : symmetrical movements, symmetrical vocal fremitus, sonor on
both sides, no rales and no wheezing
Abdomen : flat, soft, liver and spleen were not palpable, normal bowel sound,
Extremities : Warm, not cyanosis, capillary refill time less than 2 seconds,
normal muscle tone, physiological reflexes normal,
pathological reflexes negative, tibial edema (+)
Genitalia : female, no abnormality.
Persentile for hypertension

P90 : 116/75
P95 : 120/79
P99 : 127/86
Crisis : > 180/120
Laboratory :
January 13th, 2014 (from Kalooran Hospital, Amurang)
Total protein : 6 g/dl LDL : 198 mg/dl
Albumin : 2.6 g/dl HDL : 23 mg/dl
Globulin : 3,4 g/dl Triglyseride : 154 mg/dl
Total cholesterol : 248 mg/dl
Urinalysis
Appearance : yellow
Leucocyte : 31 - 40/hpf
Erythrocyte : > 50/hpf
Epithel : 3 - 4/hpf Nitrit : (-)
Specific gravity : 1.015 PH : 7.0
Protein : +++ Keton : ++
Diagnosis:
Nephrotic syndrome
Suspect urinary tract infection
Suspect tuberculosis
Moderate malnutrition
6
Hypertension grade 1
Differential Diagnosis :
Acute glomerulonephritis
Treatment :
- Prednisone 3 x 20 mg (2 mg/kgBW/day)
(Postpone until tuberculin test was done and have a result)
- Captopril tab 3 x 10 mg
- Fluid Balance and diuresis
- Qualitative urinary protein & body weight every day
- Diet according to RDA:
o Fluid needed 70-85 ml/kgBW/day = 1575-1785 ml/day
o Calorie needed 47 kcal/kgBW/day = 1.645 kcal/day
o Protein needed 1 g/kgBW/day = 35 g/day
o Fat needed (30% from total calorie) = 494 kcal/day
o Salt needed : 1 g/day
Is given to the patient by:
Nephrisol milk 3 x 250 ml (@ 4 spoon milk powder in 200 ml water) =
= 750 ml/day (780 kcal, 15 g)
Daily meal 3 x 1 portion/day
Can be given 1 serving rice, 1 piece of fish or 1 egg or 1 slice of
chicken meat, vegetables and fruit (each portion contains 300 kcal, 5 g
protein)
Planning :
- CBC, lipid profile, total protein, albumin, globulin, electrolyte
- Chest X-ray, Mantoux test, BSR
- Regularly urinalysis, urine culture
- ASTO, complement C3
February, 15th 2014 (2nd day care)

Complain : palpebra edema decrease, fever (-)
7
General conditions : Look well, consciousness: alert (compos mentis)
Vital sign : Blood pressure : 120/80 mmHg

Pulse rate : 84 x/minute
Respiration rate : 24 x/minute
Temperature : 36,3C.
Head : oval shape, black hair, not easy to pulled out
Eyes : conjungtiva was not anemic , sclera was not icteric
pupil was isochor with diameter 3 mm, light reflex was normal, corneal
reflex normal, palpebral edema (+).
Ears : no secrete
Nose : no secrete,
Mouth : no cyanosis, tonsil T1/T1 without inflammatory sign, pharynx without
inflammatory sign, dry mouth mucous
Neck : no lymph node enlargement, trachea in the middle line
Chest : symmetrical respiratory movements, no retraction
Heart : normal rate, regular rhythm, no thrill, no murmurs
Lungs : symmetrical movements, symmetrical vocal fremitus, sonor on
both sides, coarse bronchovesicular breath sound, with rales and no
wheezing
Abdomen : flat, soft, liver and spleen were not palpable, normal bowel sound,
Extremities : Warm, not cyanosis, capillary refill time less than 2 seconds,
normal muscle tone, physiological reflexes normal,
pathological reflexes negative, tibial edema (+)
Genitalia : female, no abnormality.
Fluid balances : her mother not recorded

Diuresis in 24 hours : her mother not recorded
Qualitative urine protein : +++
Laboratory :
Complete Blood Count :
8
Haemoglobin : 11.8 g/dl
Haematocrit : 32.3 %
Leukocyte : 8.600/mm3
Thrombocyte : 295.000/mm3
Total protein : 5.8 g/dl
Albumin : 2.6 g/dl
Globulin : 3.2 g/dl
Lipid profil
Total Cholesterol : 266 mg/dl
LDL : 182 mg/dl
Electrolyte :
Sodium : 125 mEq/l
Potassium : 4.25 mEq/l
Chloride : 92.2 mEq/l
Urinalysis :
Appearance : yellow
Erythrocyte : 10-15/hpf
Epithel : 8-10/hpf Nitrit : (-)
Protein : +++ Keton : +
Diagnosis:
Nephrotic syndrome
Treatment :
9
- Nephrisol milk 3 x 250 ml/day
- Daily meal 3 x 1 portion/day
Planning :
- Chest X-ray, Mantoux test, BSR
- Regularly urinalysis, urine culture
- ASTO, complement C3
February, 16th 2014 (3rd day care)

Complain : palpebra edema decrease, got fever last night

Physical examination : BB : 33 kg
Palpebral edema decrease, pitting edema on extremities (-)
Others examination in normal limited
Fluid balances : + 3 cc per day

Diuresis in 24 hours : 1,26 cc/kgBW/hour
Diagnosis:
Nephrotic syndrome
10
Treatment :
- Paracetamol tab 3 x tab
Planning :
- Urine culture, regularly urinalysis
- Chest X-rays, Mantoux test
- Waiting for ASTO and complement C3 result
February, 17th 20th 2014 (4th 7th day care)
Complain : palpebra edema decrease, fever (-)

Palpebral edema decrease, pitting edema on extremities (-)
Fluid balances : between - 280 until - 850 cc per day

Diuresis in 24 hours : > 1,5 cc/kgBW/hour
Laboratory :
11
ASTO : < 200 (normal)
C3 : 150 mg/dl (normal)
Diagnosis:
Nephrotic syndrome
Treatment :
- Furosemide pulv 2 x 15 mg
Planning :
- Chest X-rays, Mantoux test
February, 21st 2014 (8th day care)

Complain : palpebra edema (-), fever (-)

Palpebral edema (-), pitting edema on extremities (-)
12

Qualitative urine protein : (-)
Laboratory :
Urinalysis :
Appearance : yellow
Erythrocyte : 6 - 7/hpf
Epithel : 2 - 4/hpf Nitrit : (-)
Protein : +++ Keton : (-)
Diagnosis:
Nephrotic syndrome
Treatment :
Planning :
- CBC, lipid profile, total protein, albumin, globulin, electrolyte, ureum, creatinin
13
- Waiting for Mantoux test
February, 22nd 2014 (9th day care)

Complain : edema (-), fever (-)

Qualitative urine protein : ++
Laboratory :
Total protein : 8.2 g/dl
Albumin : 3.4 g/dl
Globulin : 4.8 g/dl
Lipid profil
LDL : 251 mg/dl
HDL : 33 mg/dl
Electrolyte :
Sodium : 137 mEq/l
Chloride : 97 mEq/l
Renal function
Ureum : 57 mg/dl
Creatinin : 1,1 mg/dl
Liver function
14
AST : 14 U/l
ALT : 9 U/l
Urinalysis :
Appearance : yellow
Erythrocyte : 10-15/hpf
Epithel : 8-10/hpf Nitrit : (-)
Protein : +++ Keton : +
Diagnosis:
Nephrotic syndrome
Treatment :
Planning :
- Regularly urinalysis
- Waiting for Mantoux test, urine culture
February, 23rd 2014 (10th day care)

15

Diuresis in 24 hours : 0.9 cc/kgBW/hour
Scoring system for TB

- Contact 0
- Nutrition 1
- Cough 0
- Fever > 2 weeks 1
- Lymphadenopathy 0
- Mantoux test 3
- Chest X-rays 1
- Joint swelling 0
TOTAL 6 (positive TB)
Laboratory :
Mantoux test : positive (13 mm)
Diagnosis :
Tuberculosis
Nephrotic syndrome
Treatment :
- Antituberculosis drugs
o Rifampicin 1 x 300 mg
16
o Isoniazid 1 x 150 mg
o Pyrazinamid 1 x 450 mg
- Pyridoxin 1 x 25 mg
Planning :
- Sputum smear for acid-fast bacilli
- Waiting for urine culture
- Prednison will be given 2 weeks after antituberculosis drugs therapy
February, 24th 2014 (11th day care)


Laboratory
Urine culture : no growth of organism

17
Diagnosis :
Tuberculosis
Nephrotic syndrome
Treatment :
Planning :
- Sputum smear for acid-fast bacilli
February, 25th 27th 2014 (12th 14th day care)


18
Fluid balances : - 540 cc per day
Laboratory
Lipid profil
LDL : 205 mg/dl
HDL : 27 mg/dl
Triglyseride : 256 mg/dl
Electrolyte :
Sodium : 137 mEq/l
Chloride : 97 mEq/l
Renal function
Ureum : 57 mg/dl
Creatinin : 1,1 mg/dl
Sputum smear for acid-fast bacilli : negative
Diagnosis :
Tuberculosis
Nephrotic syndrome
Treatment :
19
Planning :
February, 28th 2014 (15th day care)


Fluid balances : - 540 cc per day

Diagnosis :
Tuberculosis
Nephrotic syndrome
Treatment :
20
Planning :
- Discharge from hospital, control in pediatric clinic
DISCUSSION
Tuberculosis is a disease that is widely available in developing countries such as Indonesia,
both in children and in adults who also can be a source infection.9 Pulmonary TB is a disease of
lower respiratory tract infections caused by Mycobacterium tuberculosis.10
There are two things that are important in childhood TB, the TB infection and TB
illness. TB infection is when a child shows a positive tuberculin test without showing
symptoms and signs, and X-ray picture normal . TB is an illness when there are symptoms and
signs and X-ray picture abnormal in a child who has been infected with tuberculosis.11
The occurrence of TB disease in a person depends on the person's immune system is
able to suppress the bacterial multiplication. There are several factors that facilitate the
occurrence of TB infection and TB disease onset in children. These factors are divided into risk
factors for infection and progression of infection risk factors into disease.1 Risk factors for TB
infection include children exposed to adults with active tuberculosis (TB positive contact),
endemic areas, poverty, unhealthy environments and shelters.12 The risk for transmission of
germs from adults to children will be higher if the adult patient has a positive sputum smear,
extensive infiltrates or cavities in the upper lobes, much sputum production, and the
21
environment with bad air circulation. TB disease risk factors are age, malnutrition,
immunocompromised, malignancy, renal failure, and virulence of bacteria.12
Children are usually infected from a source of infection that generally is adult patients.
Children who are infected with TB, also called received TB infection, will form the immunity
so that the tuberculin test will be positif.10,12 Transmission is usually by air, by inhalation of
droplet nuclei containing TB bacilli. TB germs are inhaled reaches alveoli and quickly resolved
by nonspecific immunological mechanisms. Alveolar macrophages will fagocyt TB germs and
is able to destroy most of the TB germs. In a minority of cases, macrophages are not able to
destroy the TB germs and bacteria will replicate in macrophages. TB germs are kept proliferate
in macrophages, eventually will cause macrophages undergo lysis, and TB bacteria form
colonies in such places. The first location of the TB germ colonies in the lung tissue called the
primary focus Ghon.1
Starting from the primary focus of the TB, germs spread through lymph channels
leading to the regional lymph nodes, that is the lymph nodes which have channels to primary
focus location. This spread leads to inflammation in the lymph channels (lymphangitis) and in
the lymph nodes (lymphadenitis).1 If the primary focus lies in the lower or middle lobe, lymph
nodes to be involved are parahilus lymph nodes, whereas if the primary focus is located at the
apex of the lung , which will be involved are paratracheal nodes. Complex primary is a
combination of primary focus, enlarged regional lymph nodes (lymphadenitis) and inflamed
lymphatics (lymphangitis).1
After cellular immunity formed, the primary focus in the lung tissue usually have a
perfect resolution formed fibrosis or calcification after experiencing necrosis and
encapsulation. Regional lymph gland will also undergo fibrosis and encapsulation but healing is
usually not as perfect as a primary focus in the lung tissue. TB germs can stay alive and lived
for many years in the gland.1
In the colonies that had formed and then limited their growth by cellular immunity, the
bacteria remain alive in dormant form. This focus indirectly continue to be a disease, but it has
the potential to become the focus of reactivation, known as focus of Simon. Years later, when
the host immune system decreases, Simon's focus be able to experience reactivation of TB
disease in the related organ, such as meningitis, bone tuberculosis.1,13,14 During the incubation
period, before the formation of cellular immunity , can occur lymphogen and hematogenous
22
dissemination. At lymphogen deployment, germs spread to regional lymph nodes make a
primary form complexes but in hematogenous spread, TB germs come to the blood circulation
and spread throughout the body. The presence of hematogenous spread make tuberculosis
known as systemic disease.1
The most common hematogenous spread is in the form of occult hematogenic spread,
TB germs spread are sporadic and little by little so didnt cause symptoms.1 TB germs then will
reach various organs throughout the body. Target organ is an organ that has a good
vascularization, such as brain, bone, kidney, and lungs themselves, especially apex of the lung
or upper lobes of the lungs.1
Journey of TB in children through three important stages , namely : exposure , infection
and become ill. TB infection process does not directly provide symptom. The tuberculin test is
usually positive within 4-8 weeks after the initial contact with TB germs. Children exposed,
which usually have close contact with patients with smear-positive adult TB. 15 In these
circumstances, the tuberculin test was negative and have no symptoms and signs of TB also
chest radiograph were normal. Some children may have been exposed to infection by
Mycobacterium tuberculosis.11 In children if they become sick, not all of them show signs and
symptoms of TB disease. Clinical manifestations and abnormal chest X-ray picture of the TB
infection in children are more influenced by the immune status of the host rather than the
number of microorganisms.1,15 The risk of spread of infection is greatest in the first 5 years of
life, and 12-24 months after infection.5 To distinguish between illness caused by primary
infection and reactivation of latent TB is difficult, because the children were sick could have
been infected at all times in their life.15
23
Figure 2. Primary Tuberculosis Time-Table
Source : Rahajoe N1
Clinical manifestations of TB in children can be distinguished into systemic or general

or non-specific manifestations and organ-specific manifestations or local.16 Most children do
not show signs or symptoms for several time. The most common systemic symptom is fever.
Fever in TB patients was found about 40-80% of cases. Fever usually not high and intermittent
periods long enough. Anorexia, weight loss (fall, remain, or rise but not according to the
growth charts), and malaise (tired, lethargic, weak) is another systemic manifestations.11
This patient got a fever since 2 weeks before admission to hospital, her fever is not too
high. She also complain about her body weight that does not increase eventhough she ate as
usual.
Prominent respiratory manifestations are sometimes not found in most cases of
childhood TB. Chronic cough is a common symptom in adult pulmonary TB, but the symptoms
of chronic cough in children is more often caused by asthma. Recurrent cough may arise
because children with TB decreased body immunity, so prone to recurrent acute respiratory
infections.12 Cough can occur because of irritation by the enlargement of gland and presses the
bronchi. In older children, the symptoms can be as in adults, such as cough with phlegm and
can also occur hemoptisis.1,11,16 Symptoms of shortness rarely found except in a state of severe
pain, such as miliary TB and pleural effusion.11
24
Specific clinical manifestations depending on the affected organs. In the lymph nodes
are commonly affected are the lymph nodes of the anterior or posterior Colli, can also occur in
the axillary, inguinal, submandibular, and supraclavicular. Affected glands are usually multiple,
unilateral, non-tender, no heat on the touch, and can be closer to each other (confluence). When
TB germs affect on nerve tissue membranes, the symptoms usually associated with cranial
nerve disorders, headache, loss of consciousness, stiff neck, and seizure.11
Routine investigations commonly performed to determine the presence of
Mycobacterium tuberculosis infection is Tuberculin test (Mantoux test). Tuberculin test is a test
that can detect the presence of infection in the absence of the manifestation of the disease, may
be negative due to anergy or severe energy shortage protein. 1,17 Tuberculin test is not able to
determine the presence of active TB. 1 From investigations found a positive tuberculin test with
13 milimetres in diameter.
Bacteriological examination cab be obtained by direct microscopic examination of
smear, culture of M. tuberculosis bacteria from sputum, gastric lavage, cerebrospinal fluid,
pleural fluid, or tissue biopsy and biomolecular techniques (PCR).1
We found a negative result in sputum smear for acid-fast bacilli in this patient. This
condition can happen especially in children because the small number of germs that can be
found in children (paucibacillary) and the difficulty to collect specimen (sputum).1
Radiographic examinations should be conducted on every child suspected of TB,
because TB is occurs primary more than 95 % in the lung parenchyma, whereas X-rays in other
organs performed in accordance existing clinical picture.1 Tuberculosis in childhood is not
always typical, the radiological abnormalities can also be found in other disease. Conversely a
normal chest radiograph can not rule out the diagnosis of TB if clinical and other investigations
support.1,17 Suspicion towards TB appears if we found enlargement hilar node, paratracheal and
mediastinal, atelectasis, consolidation, pleural effusion, cavities, emphysema, and miliary
picture. Primary complexes are more common in lung radiographic of infants and young
children than adult.1,17
Examination of chest X-rays obtained perihiler impression seemed infiltrates, hilar
impression slightly thickened, bronchovaskular pattern looks normal. With conclusion suspect
primary tuberculosis.
25
Definitive diagnosis of TB is confirmed by the discovery of the TB bacteria in sputum
examination, gastric lavage, cerebrospinal fluid, pleural fluid or tissue biopsy. In children there
are some difficulty because of lack of germs and the difficulty of specimen collection. So to
overcome this IDAI and Department of Health, supported by the WHO using the scoring
system.1
Figure 3. Scoring System to Diagnose Tuberculosis In Children

Source : Rahajoe N1
Scores of TB in these patients was 6 which is support for diagnosis TB and Tuberculin
test was positive with 13 milimetres in diameter so the patient was diagnosed pulmonary
tuberculosis and treated with antituberculosis drugs.
Antituberculosis chemotherapy is the main principle of therapy in all cases, including
pulmonary tuberculosis and miliary tuberculosis. The main current drug is rifampicin,
isoniazid, pyrazinamide, ethambutol, and streptomycin. The second line are
paraaminosalicylate, ethionamide, thioacetazone, fluorokinolon, aminoglycosides and
capreomycin, cycloserine, betalactam inhibitor, clarithromycin, linezolid, thioacetazone. The
therapy is divided into two phases, namely the intensive phase (first 2 months) and the
continuation phase. In intensive phase we use at least 3 kinds of drugs (rifampicin, isoniazid,
pyrazinamide) and 2 kinds of drugs in the continuation phase (rifampicin and isoniazid). At
26
both pulmonary TB and extrapulmonary TB including miliary tuberculosis, given four different
drugs (rifampicin , isoniazid , pyrazinamide , and ethambutol or streptomycin).1
These patients are given 3 kinds of Antituberculosis Drugs, there are isoniazid 1 x 300
mg, rifampicin 1 x 300 mg, and pyrazinamide 1 x 500 mg, also given vitamin B 6 1 x 25 mg.
Rifampicin, isoniazid and pyrazinamide given for 2 months.
Table 3. Antituberculosis drugs and dosage
Source : Rahajoe N1
The number of children with TB are much, resulting in high cost of treatment, therefore
prevention of TB infection is one of the important efforts that must be made. Prevention is done
by controlling the risk factors of TB infection. Besides taking medication compliance and
supervision necessary to resistency ie by way of DOTS (directly obeserved teratment) with
supervisors taking medication. Also searching and checking the source of infection, adults
around him, nutritional adequacy, BCG immunization and chemoprophylaxis important to
prevention.1
The most important thing in the management of TB is adherence to medication. TB
patients have demonstrated improvement usually a few weeks after the treatment so they feel
healed and did not continue treatment. An effort to improve the regularity is the direct oversight
of the treatment. One component of the program requires that a person who oversees the patient
takes the medication (PMO).1 In this case, the mother served as PMO for the patient.
27
Nephrotic syndrome (NS) is a disease of the glomerulus which is characterized by
symptoms of massive proteinuria (40 mg/m2 BSA/hour or 50 mg/kg/day), hypoalbuminemia
(<2.5 g/dl), edema, and hypercholesterolemia (> 200 mg/dl). 3,6 Sometimes accompanied by
symptoms of hematuria, hypertension, and decreased of renal function. 6 NS is a chronic disease
that is common in childhood with the incidence ranging from 2-7 cases per 100 thousand
children under the age of 16 years every year.3 Wila Wirya reported 6 children suffering from
NS among 100 thousand children under the age of 14 years per year in Jakarta. NS can affect
all ages, but primarily affects children aged 2-6 years.6,7
In NS, increasing permeability of the glomerular capillary wall resulted in proteinuria
and hypoalbuminemia. The cause of increased permeability of the glomerular capillary can not
be explained clearly until now.20
Edema is a major clinical manifestation, edema usually through and distributed
following the gravitation.4 NS patients usually come with palpebral edema or pretibial edema.
When more severe NS will be accompanied by ascites, pleural effusions, and genital edema. 6,20
Children with NS have problems in regulating the body's water balance, which causes fluid
retention, which may lead to edema. Another complaint is the urine can also be found muddy
color or it could be hematuria. Sometimes accompanied by oliguria.6,8
Investigations are important in NS such as urinalysis, which found massive proteinuria
(40 mg/m2 BSA/hour), or protein and creatinine ratio of more than 2 mg/dl in urine, or with
dipstick urine examination more than 2+.5,8 Other findings in the urinalysis is an increase in
urine specific gravity and pH, leukosituria, double refractile lipoid bodies and cylinders
hyaline, may also be accompanied by microscopic hematuria. In blood tests obtained
hypoalbuminemia (<2.5 g/dl), with a ratio of albumin and globulin were reversed,
hypercholesterolemia (> 200 mg/dl), increased erythrocyte sedimentation rate and normal
levels of complement C3. Urea and creatinine levels are generally normal unless they obtained
a decrease renal function.7,21
The etiology of NS in children can be divided into 3 groups, congenital nephrotic
syndrome, primary/idiopathic nephrotic syndrome and secondary nephrotic syndrome
following the systemic illness.8 The large majority (>90%) is primary (idiopathic); a secondary
cause, e.g. amyloidosis, systemic lupus, henoch schonlein purpura, IgA nephropathy, and
infection with human immunodeficiency virus, hepatitis B and C is seen rarely.3,6 Most
28
idiopathic nephrotic syndrome in children (80-90%) is a minimal change nephrotic syndrome.
It said congenital nephrotic syndrome when symptoms arise within the first 3 months of life. In
primary nephrotic syndrome, etiology is still unknown. Called the primary as the result of
abnormalities in the glomerulus itself without any other cause. Primary nephrotic syndrome
often found in children. Secondary nephrotic syndrome, as a result of a metabolic disease,
infection, toxins or allergens, and neoplasms.5
Diagnosis of NS in this patient is made by anamnesis, physical examination and
laboratory investigations. The most common clinical manifestations of NS is a comprehensive
and distributed edema following gravity. Just as in this patient, we found that the patient had
swelling on his eyelid since 10 days before admitted to the Prof. Dr. R. D. Kandou hospital
Manado. And initially, the patient had a swelling all over the body and was hospitalized for 5
weeks at hospital at Amurang city. At first the swelling arising in the eyelid, followed by the
face, abdomens and legs. Swelling of the face is more severe in the morning and decreases at
night.
On physical examination we obtained systolic and diastolic pressure were high, no
breathing difficulty and no fever. In NS, blood pressure is generally normal or low, but 21% of
patients had high blood pressure that is temporary. This situation is caused by the excessive
secretion of renin, aldosterone secretion and other vasoconstrictor, as the body's response to
hypovolemia.22 Examination of the head obtained edema of the eyelids. On examination there
were no abnormalities in the chest and abdomen. There was a pitting edema on the extremities.
From the laboratory investigation revealed hypoalbuminemia (2.6 g/dl), hiperkolesterolnemia
(248 mg/dl), proteinuria (++), microscopic hematuria (>50/hpf) and qualitative positive urine
tests showed ++. Microscopic hematuria was found in 20-23% of cases of NS, whereas
macroscopic hematuria are rare.3 Examination of ASTO level have been conducted and the
results were normal.
In any patient who has been diagnosed with NS, before starting steroid treatment, we
have to do the tuberculin test. If the result is positive, give isoniazid prophylaxis for 6 months,
and if found to be a tuberculosis, give anti-tuberculosis regiments and prednison will be given 2
weeks after antituberculosis drugs therapy. This patient have positive Mantoux test with
induration 13 milimetres in diameter and get 6 points in scoring system for tuberculosis so this
patient will get prednison 2 weeks after she starts antituberculosis drugs.1
29
The response to steroids provide prognostic value that is more meaningful than the
picture of biopsy in patients with nephrotic syndrome. Response to steroid therapy is an
indicator that the patient has a good prognosis.23
Patients with nephrotic syndrome should receive regular follow-up and a dick in a long
time to prevent relapse. Measurement of body weight and urine tests should be monitored
regularly. This observation is also to prevent the occurrence relaps.24
30
Attachment
BB = 33 x 100 % = 76,7 % (moderate malnutrition) BB = 33 x 100 % = 91,6 %

U 43 TB 36
TB = 143 x 100 % = 93,4 %

U 153
31
Patients chest X-rays
Mantoux test with 13 milimetres in diametre Patients picture
32
DAFTAR PUSTAKA
1. Rahajoe N, Basir D, Makmuri MS, Kartasasmita GB, editors. Pedoman Nasional

Tuberkulosis Anak. Edisi ke-2. Jakarta: UKK Respirologi PP IDAI; 2008.
2. World Health Organization. Global tuberculosis report 2013. WHO. 2013.
3. Sinha A, Bagga A. Nephrotic syndrome. Indian J Pediatr. 2012;79:1045-55.
4. Salloum AAA, Muthanna A, Bassrawi R, Shebab AAA, Ibrahim AA, Islam MZ, et al.
Long-term outcome of the difficult nephrotic syndrome in children. Saudi J Kidney Dis
Transpl. 2012;23:965-72.
5. Noer MS. Sindroma nefrotik idiopatik. In: Noer MS, Soemyarso NA, Subandiyah K,
Prasetyo RV, Alatas H, Tambunan T, et al, editors. Kompendium nefrologi anak. Jakarta:
BP IDAI, 2011; p.72-88.
6. Wirya W IGN. Sindroma nefrotik. In: Alatas H, Tambunan T, Trihono PP, Pardede SO,
editors. Buku ajar nefrologi anak. 2nd edition. Jakarta: BP FKUI, 2002; p.381-426.
7. Avner ED, Voght BA. Nephrotic syndrome. In: Kliegman RM, Behrman RE, Jenson HB,
Stanton BF, editors. Nelson textbook of pediatrics. 19th edition. Philadelphia: Elseviers
Saunders, 2011; p. 2190-5.
8. Alatas H, Tambunan T, Trihono PP, Pardede SO. Konsensus tatalaksana sindroma nefrotik
idiopatik pada anak. Jakarta: UKK Nefrologi IDAI, 2005. p.1-20.
9. LoBue PA, Iademarco MF, Castro KG. The Epidemiology, Prevention, and Control of
Tuberculosis in the United States, In : Fishman AP, editor. Fishmans Pulmonary Diseases
and Disorders, 4th edition. New York : The McGraw-Hill Companies;2008. h. 2447-57.
10. Dexter JR, Wilkins RL. Tuberculosis, In : Wilkins RL, Dexter JR, Gold PM, editors.
Respiratory Disease A Case Study Approach to Patient Care , 3rd edition. Philadelphia : F.
A. Davis Company; 2007. h.442-40.
11. Rahajoe NN. Masalah tuberkulosis anak saat ini.Dalam : Tatalaksana mutakhir penyakit
respiratorik pada anak. Jakarta :UKK Respirologi PP IDAI; 2004. h.12-23.
12. Nelson LJ, Wells CD. Global epidemiology of childhood tuberculosis. Int J Tuberc Lung
Dis.2004;8(5):636-47.
13. Moon MS. Tuberculosis of the spine. Controversies and a new challenge.
Spine.2007;15:1791-7.
33
14. Abernathy RS. Tuberculosis: An update. Pediatrics in Review. 2007;2(18):50-58.
15. Singh L, Mynak ML, Kumar L, Mathew JL, Jindal SK. Prevalence and risk factors for
transmission of infection among children in household contact with adults having
pulmonary tuberculosis. Arch Dis Child 2005;90:624-28.
16. American Thoracic Society (ATS ): Diagnostic standards and classification of tuberculosis
in adults and children. Am J Resp Crit Care Med 2000; 161:1376-95.
17. Curley C. Diagnostic standards and classification of tuberculosis in adults and children.
Am J Respir Crit Care Med 2000;(161).h.1376-95.
18. Otukesh H, Mojtahedzadeh M, Hoseini R, Fereshtehnejad SM, Riahi FA, Sadiqh N, dkk.
Management and outcome of steroid-resistant nephrotic syndrome in children. Iran J
Kidney Dis. 2009;3:210-7.
19. Seigneux S, Martin PY. Management of patients with nephrotic syndrome. Swiss Med
Wkly. 2009;139:416-22.
20. Trihono PP, Pardede SO, Alatas H, Sekarwana A, Rusdidjas, Noer SM, et al. In: Pudijiadi
AH, Hegar B, Handryastuti S, Idris NS, Gandaputra EP, Harmoniati ED, editors. Pedoman
pelayanan medis IDAI. Jakarta: BP IDAI, 2010; p.274-6.
21. Olowu WA, Adelusola KA, Adefehinti O.Childhood idiopathic steroid resistant rephrotic
syndrome in Southwestern Nigeria. Saudi J Kidney Dis Tranpl. 2010;21:979-90.
22. Hamasaki Y, Yoshikawa N, Hattori S. Cyclosporine and steroid therapy in children with
steroid-resistant nephrotic syndrome. Pediatr nephrol. 2009;24:2177-85.
23. Gipson D, Massengil SF, Yao S, Nagaraj S, Smoyer WE, Mahan JD, et al. Management of
childhood onset nephritic syndrome. Pediatrics 2009; 124:747-57.
24. Geier P, Jurencak R, Zaptelova J. Treatment of the first episode of nephrotic syndrome in
children. Pediatr Nephrol 2006; 21: 1779-80.
34

Tuberculosis and Nephrotic Syndrome in A Child: Case Report

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Tuberculosis and Nephrotic Syndrome in A Child: Case Report

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With all due respect to :

To be presented on February 5th 2014

TUBERCULOSIS AND NEPHROTIC SYNDROME

DEPARTMENT OF CHILD HEALTH

History of prenatal care and birth

History of experienced illness

Social, economic and environment

Physical Examination (February, 14th 2014)

Persentile for hypertension

February, 15th 2014 (2nd day care)

Vital sign : Blood pressure : 120/80 mmHg

Fluid balances : her mother not recorded

February, 16th 2014 (3rd day care)

Vital sign : Blood pressure : 120/80 mmHg

Fluid balances : + 3 cc per day

Vital sign : Blood pressure : 110/70 mmHg

Fluid balances : between - 280 until - 850 cc per day

February, 21st 2014 (8th day care)

Vital sign : Blood pressure : 110/75 mmHg

Fluid balances : + 320 cc per day

February, 22nd 2014 (9th day care)

Vital sign : Blood pressure : 100/70 mmHg

February, 23rd 2014 (10th day care)

Vital sign : Blood pressure : 100/60 mmHg

Fluid balances : + 960 cc per day

Scoring system for TB

February, 24th 2014 (11th day care)

Vital sign : Blood pressure : 100/60 mmHg

Fluid balances : + 290 cc per day

February, 25th 27th 2014 (12th 14th day care)

Vital sign : Blood pressure : 110/70 mmHg

February, 28th 2014 (15th day care)

Vital sign : Blood pressure : 110/70 mmHg

Fluid balances : - 540 cc per day

Clinical manifestations of TB in children can be distinguished into systemic or general

Figure 3. Scoring System to Diagnose Tuberculosis In Children

Table 3. Antituberculosis drugs and dosage

BB = 33 x 100 % = 76,7 % (moderate malnutrition) BB = 33 x 100 % = 91,6 %

TB = 143 x 100 % = 93,4 %

Mantoux test with 13 milimetres in diametre Patients picture

1. Rahajoe N, Basir D, Makmuri MS, Kartasasmita GB, editors. Pedoman Nasional

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