NEPHROTIC SYNDROME

Dinesh Kumar P
Demographic details
• Name
• Age -
a) Nephrotic syndrome is common in 2-6 yrs whereas nephritic syndrome is
common in 4-10 yrs (school going children as they are exposed to infections
more)
b) Congenital NS – seen at birth or before 3 months of life .
c) Infantile NS – seen from 3 months to 1 year .
• Sex
a) NS – Male > female – 2 : 1
b) UTI – female > males due to ascending infections, but in infants male = female
due to major route of infection is hematogenous .
• Birth order , consanguinity
• Address
• Informant
• Reliability
Chief complaints –
Generalised swelling of the body
Puffiness of face
Decreased urine output

HOPI -
1.Generalised edema of the body –
Onset – Insidious
Duration
Order of progression – First the face followed by legs and then abdomen and even scrotal edema maybe seen in male
child – Indicates renal origin.
( In CCF – legs -> abdomen -> face ; In Hepatic Failure – Abdomen -> Legs -> face )
Relieved by medications ( oral drugs – steroids , rarely diuretics ; Iv medication - albumin infusion? ; ascitic tap – for
pressue symptoms ,peritonitis)

2. Puffiness of face – (Due to loose areolar connective tissue present and specific for renal origin)
Site – Periorbital , Onset – Early morning puffiness of face ,duration ,relieved by medications.

3. Decreased urine output – (Ask to mother if the urine output is less than usual either quantity or frequency)
Normal urine output – 1-2ml/kg/min
Low urine output (oliguria) - < 1 ml/kg/min or <500ml / day
Anuria - < 0.5 ml/kg/min

4. H/o hematuria/cola colored urine (To rule out AGN/ Nephritic on NS/ Nephrotic with renal
lesions)
5. H/o frothy urine(Early marker of NS)
5. H/o suggestive of UTI – increased frequency of urine, dysuria(painful/burning/crying
during micturition), foul smelling urine, nonspecific symptoms like nausea, vomiting,
fever with chills and rigors, vague suprapubic abdominal pain.
6. H/o thin stream of urine , ballooning of prepuce , dribbling of urine.(To rule out
phimosis ,obstructive uropathy like posterior urethral valves if present since birth)
7. H/o abdominal pain
Nature , frequency , site , severity , timing , aggravating and relieving factors
Flank pain/loin pain – ureteric colic / renal colic
Dragging pain – Hydronephrosis, Polycystic kidney disease
Suprapubic pain – UTI, cystitis, bladder calculi
Colicky pain at renal angle – Renal calculus
8. H/o swellings in the abdomen (Renal mass eg. Polycystic Kidney, Wilm’s tumor,
Hydronephrosis ; Urinary bladder distension)
H/o to rule out other causes of generalised edema :
H/o dyspnoea, chest pain, orthopnoea, PND, palpitations (CCF)
H/o jaundice, hematemesis, melena, flapping tremors, altered sensorium (Hepatic
Failure)
H/o reduced urine output (AKI)
H/o loss of weight, loss of appetite, skin changes, irritability (PEM/Kwashiorkor;
Malignancy)
H/o greasy stools (malabsorption)
H/o of rashes, prolonged fever and cough (measles and TB respectively, both these
conditions predispose to malnutrition)
H/o itching, insect bite, drug ingestion – (To rule out of allergy,anaphylaxis)
H/o prolonged steroid intake – Cushing’s syndrome
H/o suggestive of hypothyroidism
H/o to rule out secondary causes of NS –
H/o skin rash, joint pain – (SLE ,RA, other connective tissue disorders)
H/o drug intake/native medications/herbal medications – (Drug induced- gold and
other heavy metals,penicillamine, NSAIDs)
H/o jaundice , blood transfusion – (Hepatitis B)
H/o fever with chills – (Malaria)
H/o to rule out Post-streptococcal Glomerulonephritis(PSGN)
H/o Cola colored urine (hematuria)
H/o skin lesion in the recent past (Impetigo followed by PSGN)
H/o headache, vomiting, convulsions (hypertensive encephalopathy in PSGN)
H/o reduced urine output (PSGN >> NS)

H/o complications of NS
1.)H/o suggestive of infections (most common complication of NS ; due to
a) IgG loss, b) defective cell mediated immunity, c) treatment with steroids)
a)H/o fever ,abdominal pain with distension, foul smelling feces – Spontaneous
bacterial peritonitis (Strep pneumonia > Gram negative organisms)
b)H/o localised swelling with fever,redness,pain – Cellulitis
c) H/o cough, fever, fast breathing, chest retractions – Pneumonia
d)H/o itchy vesiculo-pustular rashes – Varicella

2.)H/o suggestive of thromboembolism (Cerebral vein thrombosis, Renal vein

thrombosis and Pulmonary artery thrombosis) such as -
H/o headache, vomiting, convulsions, altered sensorium, facial weakness,
hemiplegia ; decreased urine output ; hemoptysis, breathlessness
Thrombosis risk due to-
a) loss of anti-thrombin 3
b) Protein C , Protein S (defective fibrinolysis)
c) Increased platelet aggregation
d) Increased fibrinogen synthesis from Liver (compensatory for albumin loss)
3. H/o lethargy , easy fatiguability (Due to loss of transferrin)
4. H/o suggestive of hypothyroidism(Due to loss of Thyroid-binding globulin)
5. H/o convulsions , tetany (hypocalcemia – due to decrease in Vitamin D synthesis
and excretion of Vitamin D binding globulin)
6. H/o moon facies, purple striae over abdomen, short stature, GI bleeding,
polyphagia, polydipsia, polyuria – due to steroid toxicity (drug induced)

Past history –
H/o similar illness in the past (In MCNS – recurrence common ; identify if relapse ,
frequent relapse, steroid dependence, steroid resistant)
Elaborate past medical history with duration of therapy , drug name , remission
achieved , relapse present ?
H/o jaundice, blood transfusion – Hep B
H/o prolonged fever, abdominal distension, painful swelling of digits (For infective
endocarditis which predispose to NS)
H/o gum bleeding and bone pain (Leukemia/Lymphoma predispose to NS)
H/o sore throat, skin lesions – (predispose to PSGN , mostly skin lesions like
Impetigo, scabies)

ANTENATAL HISTORY – As usual

Oligohydramnios ?(seen in newborn with renal anomalies)
Increased placental weight ? (Congenital NS – Finnish type , poor prognosis)

NEONATAL HISTORY - As usual

Umblical cord catheterisation done ? (Renal artery thrombosis)
H/o delayed passing of urine (more than 48 hours)

DIETARY HISTORY – feeding problems, loss of appetite, craving for salt?

GROWTH AND DEVELOPMENTAL HISTORY – growth retardation is seen in

chronic renal failure patients and in steroid toxicity.
FAMILY HISTORY –
H/o similar illness in the family – Hereditary nephritis, Congenital NS, Infantile
Polycystic Kidney Disease, Cystinosis, Nephrogenic Diabetes Insipidus
H/o contact TB – predisposes to malnutrition => generalised edema

IMMUNIZATION HISTORY –
Whether immunised upto age ? BCG scar present ?
Pneumococcal conjugate vaccine (PCV) – 6th , 10th and 14th weeks to prevent
pneumococcal infections since complement mediated capsular attack (alternative
pathway) is deficient in NS .
Varicella vaccine – 15th month , 4-6 years (common infection in NS)

SOCIOECONOMIC HISTORY - Education levels of the parents are important

since it is a recurring disease and needs long term treatment adherence.

SUMMARY OF HISTORY – eg. 6 year old , male child with generalised edema
for 5 days. He had 2 episodes in the past and has taken medications for
the same.
 EXAMINATION

General Examination –
Consciousness , orientation – irritable or altered sensorium in renal failure
Appearance-
Sick-looking child (AGN)
Well-looking child (nephrotic syndrome)
Generalised hemihypertrophy (nephroblastoma and medullary sponge kidney)
Stature- Short stature in Chronic Renal Failure(CRF), steroid toxicity(delayed bone age),
Turner's syndrome (associated with renal anomalies like Horse-shoe kidney, Ectopic kidney,
Duplex ureters, etc) and Rickets.

Built and nourishment - poorly nourished in CRF and NS of long duration.

Pallor - anaemia (in CRF) is usually normocytic normochromic, due to loss of transferrin in NS.
Icterus –
Cyanosis –
Clubbing – Present in bacterial endocarditis
Pedal edema – bilateral pitting , fast edema (less than 40sec) , localised or generalised , Grade
of edema?
Generalised lymphadenopathy is seen in patients with leukaemia, lymphoma, SLE and
infectious mononucleosis
Vital Signs -
1.Pulse - Conditions associated with renal impairment:
Radiofemoral delay – Coarctation of Aorta
Absence of pulses – Takayasu disease
2. Blood pressure- Hypertension seen in AGN and usually absent in NS , adverse effect
of steroid therapy .
SBP = 90 + ( 2 x age in yrs)
DBP = 55 + ( 2 x age in yrs)
Hypertension is said to be present if systolic and/or diastolic pressure are
equal to more than 95th percentile for that age and sex on IAP chart for
atleast 3 different occasions.
Separate cuffs should be used for children of different ages. A cuff of the
appropriate size covers two-thirds of the length of the arm on which it is tied,
with the inflatable bladder covering the entire circumference of the arm with
no overlapping. If a big size cuff is used, it may give a falsely low value. If the
cuff is too small ,it may give a falsely high value. The cuff should be inflated
rapidly and deflated slowly.
3. Temperature – Fever due to infections like peritonitis, cellulitis , pneumonia
4. Respiratory rate – Fast breathing , Chest indrawing – pneumonia
Dyspnoeic – due to generalised edema with pressure symptoms
ANTHROPOMETRY

1. Weight – serial measurements are taken to look for response

to treatment and weight maybe initially increased due to
edema.
2. Height/length-decreased in CRF , steroid toxicity, rickets
3. Weight for height/length
4. Head circumference-microcephaly in CRF
5. Midarm circumference
6. Abdominal girth – For response to treatment.
 Head to toe examination

1. Head – HC , fontanelles – microcephaly maybe seen in Chronic Renal Failure

2. Hair – Normal
2. Face - puffiness of face and dysmorphism-
Cushingoid facies – Moon face with fish mouth, prominent flushed cheeks, double
chin and buffalo hump.
Potter facies – Widely spaced eyes, depressed nasal bridge, receded chin and ears
asymmetrical, low set, floppy and posteriorly rotated. (Potter’s syndrome –
Bilateral renal agenesis)
3. Eyes –
a) Buphthalmos, cataracts(subcapsular cataracts in steroid toxicity), intellectual
disabilities, aminoaciduria (Lowe's syndrome or oculocerebrorenal syndrome)
b) Aniridia (nephroblastoma)
c) Retinopathy (hypertensive nephropathy)
d) Retinitis pigmentosa (Laurence-Moon-Biedl syndrome)
4.Nose –
5. Ears – pre-auricular sinus is associated with renal anomalies.
6. Oral cavity-tonsillitis may be associated with acute nephritic syndrome.
7. Chest -
8. Skin – pyoderma(AGN), evidence for bee sting,
cafe-au-lait spots (neurofibromatosis associated with renal artery stenosis),
maculopapular rash (vasculitis), purpura and Henoch-Schonlein purpura (HSP),
butterfly rash and malar rash (systemic lupus erythematosus),
angiokeratoma (Fabry's disease), tuft of hair (spina bifida=> neurogenic bladder)

9. Nails - dystrophic nails (nail patella syndrome associated with congenital NS)
10. Extremities and skeletal system – short stature, bowing of legs, genu valgum and
costochondral beading (rickets) ; arthropathy in SLE, RA and HSP
11. Spine- Sacral agenesis (neuropathic bladder) and meningomyelocele (bladder
dysfunction)
12. External genitalia – phimosis, ulcer, swelling, scrotal/vulval edema(NS), bilateral
cryptorchidism
Cushingoid facies
Henoch Schonlein Purpura SLE

Café au lait spot Angiokeratoma – Fabry’s disease

ABDOMEN EXAMINATION
After obtaining consent , examined in supine position with hips and knees flexed
and abdomen is exposed from xiphisternum to pubic symphysis( theory- upto
midthigh)
Importance of abdominal examination – To demonstrate fluid collection and look
for signs of peritonitis.

• Inspection:
Shape – distended , flanks full
Umbilicus is in midline, everted and transverse in shape – Ascites
All quadrants move equally with respiration
Skin- normal/stretched/shiny
Any visible scars/sinuses/dilated veins/visible pulsations/visible peristalsis/mass –
ascitic tap ; renal biopsy scar at the back ; purple striae in Cushing’s syndrome.
Renal angle – free / full
Hernial orifices - free
External genitalia : normal
• Palpation:
- Warmth , tenderness – peritonitis
- Liver and spleen palpable? , any organomegaly (If ascites present, palpation by dipping
method)
Hepatosplenomegaly seen in malaria, syphilis, SLE, Juvenile RA, Subacute bacterial
endocarditis.
- Any renal mass? (Polycystic kidney, hydronephrosis, Wilm’s tumor, renal vein thrombosis)
- Fluid thrill present/absent.
- Renal angle tenderness ( renal stones ) / suprapubic tenderness (UTI)

Absence of anterior abdominal wall muscle - prune belly syndrome

• Percussion:
- Liver span
- Shifting dullness?

• Auscultation:
Bowel sounds: Normal bowel sounds heard
No Venous hum/ Bruit (Bruit maybe heard over renal arteries due to thrombosis or
stenosis)
OTHER SYSTEM EXAMINATION –

• Cardiovascular System – S1, S2 heard , no murmurs.

Cardiac failure may be seen in patients with acute nephritic syndrome.
Anasarca may also be seen in CCF.
Pericardial effusion may be present in association with anasarca.
Pericardial rub is seen in uraemia.

• Respiratory System – Normal vesicular breath sounds heard.

Look for fast breathing , chest retractions – pneumonia.
Right sided pleural effusion common due to anasarca.
Type of respiration - may be thoraco-abdominal in presence of ascites.
Kussmaul’s breathing in metabolic acidosis.
Basal crepitations may be present in the presence of CCF.
• Central Nervous System – No focal neurological deficit.
Hemiplegia, blindness and convulsions due to thromboembolism may be seen in
nephrotic syndrome.
Hypertensive encephalopathy is a complication of AGN.
Flapping tremor and delirium may be seen in uraemia.
In CRF, peripheral neuropathy may be seen.

Diagnosis - A case of nephrotic syndrome –

• First episode/relapse/frequent relapse
• Steroid sensitive/dependent/steroid resistant
• Any complications of NS – infections mainly UTI and peritonitis,
thrombo-embolic events, specific proteinuria – anemia, hypothyroidism,
hypocalcemia, etc .
• Any complications due to steroid therapy – hypertension, Vit D
deficiency (Rickets – more common than stunting) , Cushingoid facies , GI
bleeding, etc .
• Malnutrition? Developmental delay? Immunized upto age?
MANAGEMENT –

Investigations –
1. CBC – anemia(CRF , loss of transferrin in NS) , leucocytosis (infections) / leukopenia(S/E of
cyclophosphamide)
2. ESR – Tuberculosis
3. CRP – Sepsis
4. Urine routine – Sugar, Albumin, Deposits – casts , cells
(Hematuria - >5 RBC/High Power Field , microscopic hematuria can persist upto 2 years whereas
persistent gross hematuria is hematuria for > 2-4 weeks.)
5. Urine C/S – for UTI
6. Spot urine protein: creatinine ratio (Single test/Best test to diagnose NS )
Interpretation - <0.2 – Normal , 0.2 – 2.0 – Nephritic range proteinuria
> 2.0 – Nephrotic range proteinuria

7. 24 hour urine protein - >40mg/m2/hr , > 1g/m2/day ,

>= 3.5g/day , 3+ 4+ dipstick => indicates nephrotic syndrome.
8. Liver Function Tests –
a) Serum proteins – serum total proteins are decreased, albumin- <2.5g% , A:G ratio reversed . IgG
decreased and IgM increased .
b) Lipid profile – s.cholesterol - >200mg% (Due to lipoprotein lipase excretion and increased
compenstory synthesis of B-lipoproteins) ;
VLDL ,LDL increased , HDL maybe normal, decreased or increased.
9. Renal Function Tests – (For AKI – seen in PSGN > NS , usually seen in NS
following severe intravascular volume depletion due to diuretic therapy)
a) Blood urea – Normal : 7-20mg/dl
b) Serum creatinine – Normal : <1 mg/dl
c) Electrolytes
10. C3 levels (<80mg% - reduced C3 levels – PSGN ) , ASO titre - >333 Todd units
(>250 Todd units in adults) , Throat swab => PSGN
11. Thyroid function tests – TSH , free T3 , free T4 (hypothyroidism in NS)
12. Chest X ray – pleural effusion , tuberculosis
13. Mantoux , CBNAAT - tuberculosis
13. USG Abdomen –
a)Ascites , pleural effusion
b)Kidney, Ureter, Bladder (KUB- For hydronephrosis , signs of chronic renal failure
like loss of cortico-medullary junction , hydroureter)
14. X-rays of long bones – Rickets
Other investigations for secondary causes of NS –
HBsAg – Hep B
ANA , RF – SLE , R.A
Peripheral smear – Malaria
TREATMENT –
• Initial episode- prednisolone 60 mg/m2/day (or 2 mg/kg/day) should be given
daily for 6 weeks in two or three divided doses,
followed by 40 mg/m2/day (1.5 mg/kg/day) on alternate days for 6 weeks.
Prednisolone tab – 5mg

• Diuretics can be used if edema is not resolving by steroids or if pressure

symptoms are present – Furosemide 1-2mg/kg (only oral forms are given to
prevent hypovolemic shock and AKI)
• If no response to diuretics or contraindicated ,
then albumin infusion = 5% albumin 10-20 ml/kg
Monitoring –
Daily weight monitoring , monitoring of BP , urinary dipstick for proteins till
remission (Nil/Trace).
ADVICE –

• Salt restriction - no additional salt in the form of chips, pickles and daily salt
requirements should be given in the food ( Normal salt consumption – 15g/day
reduced to 5g/day).
• Normal protein intake of 1.5-2 g/kg/day is recommended . Eggs must be
included in the diet - high quality protein.
• Foods that can be advised are idly, idiappam with sugar, egg white, rice kanji,
and curd rice.
• Avoid chocolates (it contains some heavy metals)
• Total fluid intake: should be restricted to the urine output plus insensible fluid
loss. Insensible fluid loss is the amount of fluid lost through the skin and
respiratory tract.
It is calculated as 30 ml/kg in young children and 20 ml/kg in older children.
Treatment for relapse –
If Relapse- prednisolone 2 mg/kg/day should be given till remission i.e till 3 daily
urine samples negative for proteins, followed by 1.5 mg/kg/day on alternate
days in a week for 4 weeks.

Treatment for frequent relapses ,steroid dependence and steroid

resistant cases –
• Long term alternate day prednisolone (0.5 – 0.7 mg/kg)
• Second line drugs for NS => Cyclophosphamide, Levamisole, Cyclosporine,
Mycophenolate mofetil.

Cyclophosphamide - 2 mg/kg/day , duration - 8-12 weeks

Contraindications – Infections , White blood cell count. <5000/mm3

Levamisole - 2-2.5 mg/kg on alternate days for 6-36 months.

Case discussion

Q1) What is Nephrotic Syndrome?

Nephrotic syndrome is characterized by
a) Massive proteinuria (>40mg/m2/hr , > 1g/m2/day , >= 3.5g/day , 3+ 4+ dipstick ,
urine Protein:Creatinine >2 )
b) Hypoalbuminemia (<2.5 g%)
c) Edema
d) Hyperlipidemia (S.cholesterol > 200mg%)

Q2) What is the pathogenesis of NS?

• The patients with nephrotic syndrome have an inherent susceptlbility to develop T-
ccll dysfunction. The released lymphokine (IL-2) causes a decrease in the heparan
sulphate sialoprotein and hence the anionic charge of the glomerular basement
membrane (GBM). This leads to massive proteinuria.
Q3) D/D of generalised edema in children

1. Nephrotic Syndrome
2. Congestive Cardiac Failure
3. Acute Kidney Injury (Hypovolemia ; AGN ,Drug induced eg: Aspirin,
Indomethacin, Aminoglycosides, Amphotericin B , RPGN ; Obstructive
uropathy eg: Posterior urethral valves)
4. Acute Liver Failure – Leptospirosis (Weil’s disease); Hep B,C ; Drug induced
– NSAIDs
5. Protein energy malnutrition (Kwashiorkor)
6. Hypothyroidism
7. Anaphylaxis
8. Malignancy
9. Connective tissue disorders eg: SLE, RA
10. Cushing’s disease (steroid induced)
• Q4) Classification of NS

According to Age -
1. Congenital nephrotic syndrome-presents at birth or before 3 months of life
• Primary type can be of Finnish type or non-Finnish type. It carries poor prognosis
• Secondary to in utero infections such as congenital syphilis, toxoplasmosis and
CMV disease. It is less common.
2. Infantile nephrotic syndrome-onset between 3 months and 1 year of age.
3. Childhood nephrotic syndrome-onset between 2 and 8 years.
4. Adult (pubertal)

According to Etiology -
1. Primary nephrotic syndrome-idiopathic, responsible for about 90% of cases of
childhood nephrotic syndrome.
2. Secondary nephrotic syndrome-causes are amyloidosis, vasculitis, SLE, post-
infectious glomerulonephritis and hepatitis B nephropathy.
According to histology –
Q5) Complications of NS –
Q 6. Differences between Nephrotic syndrome and AGN
Q7) Indications of Renal biopsy in NS –

a)Age of onset below 1 year and above 8 years

b)Secondary nephrotic syndrome (SLE and HSP)
c) Features of AGN like :
Persistent haematuria (microscopic or gross)
Low C3 levels ,hypertension, renal failure not due to
hypovolaemia

d) Systemic disease or family history of renal disease

e) Not responding to steroids.
f) Frequent relapses, steroid dependence, steroid resistant.
g) After the initiation of treatment
• To evaluate the efficacy of treatment
• To detect the transformation of MCNS to significant changes like FSGN
Q8) What is underfill and overfill hypothesis?
The underfill hypothesis and the overfill hypothesis are 2 opposite
theories which have been proposed as mechanisms causing nephrotic
edema.

• The underfill hypothesis is based on the fact that nephrotic-range

proteinuria leads to a fall in the plasma protein level with a
corresponding decrease in intravascular oncotic pressure. This leads to
leakage of plasma water into the interstitium, generating edema.
As a result of reduced intravascular volume, there is increased secretion of
vasopressin and aldosterone, which results in increased sodium and water
retention by the tubules. Sodium and water retention therefore occur as a
consequence of intravascular volume depletion.

• This hypothesis does not fit the clinical picture of some patients with
edema caused by nephrotic syndrome who have clinical signs of
intravascular volume overload, not volume depletion. Treating these
patients with albumin alone may not be sufficient to induce a diuresis
without the concomitant use of diuretics.
Also, reducing the renin– aldosterone axis with mineralocorticoid receptor
antagonists does not result in a marked increase in sodium excretion. With
the onset of remission of MCNS, many children will have increased urine
output before their urinary protein excretion is measurably reduced.

• The overfill hypothesis postulates that nephrotic syndrome is associated

with primary sodium retention, with subsequent volume expansion and
leakage of excess fluid into the interstitium. There is accumulating
evidence that the epithelial sodium channel in the distal tubule may
play a key role in sodium reabsorption in nephrotic syndrome.

• The clinical weaknesses of this hypothesis are evidenced by nephrotic

patients who present with an obvious clinical picture of intravascular
volume depletion: low blood pressure, tachycardia, and elevated
hemoconcentration. Furthermore, amiloride, an epithelial sodium channel
blocker, used alone is not sufficient to induce adequate diuresis.
Q9)What is nephritic on nephrotic syndrome?
• Primary glomerular diseases can present as acute nephritic
syndrome in some children and nephrotic syndrome in others.
• MPGN presents as nephritic syndromes in 15%-20% and
nephrotic syndrome in 60% of patients.
But minimal change disease always produces nephrotic
syndrome and crescentic nephritis(RPGN) always manifests as
nephritic syndrome.
Q10) Biochemical tests of urinary proteins –

• Heat coagulation test:

Take 10 mL of urine in a test tube and boil the upper part of the
tube. If turbidity appears, add six drops of 5% acetic acid. If turbidity
is due to the presence of phosphates, it will disappear.
If it persists, it indicates that proteins are present and are graded as
1+ to 4+ .
• Sulphosalicylic acid test:
Add 5-10 drops of 20% sulphosalicylic acid to 5 mL of urine and
examine for turbidity. Presence of turbidity indicates proteinuria and
is graded according to the increasing amounts of turbidity
as 1+ to 4+ .

• Heller’s test: To 3 ml of urine, few drops of conc. Nitric acid is added slowly
to get a white ring at the junction of 2 fluids indicating presence of
proteins.
• Dipstick : It is a method for qualitative assessment of proteinuria.
It tells directly by comparing with colour code given on bottle.
Development of green colour indicates presence of protein.
Proteinuria is graded from trace to 4+ on the basis of dipstick .
Q11) Differences between MCNS and NS with significant lesions.
Q12) Differences between congenital and infantile NS.