East Avenue Medical Center

Department of Pediatrics

A CASE OF NEPHROTIC SYNDROME

Team G
General Data
• Informant: Mother
• Reliability: 95%
General Data
• A.B
• 4 y.o/Male
• Filipino
• Roman Catholic
• Single
• Tandang Sora Quezon city
• Admitted for the 1st time at EAMC last Dec 5, 2018
• CC: Tea-coloured urine
Prenatal History
• Mother was 26 y.o
• OB score of G3P3(3003)
• Prenatal care started at 16 weeks AOG at a local health center
• UTI at 28weeks AOG; unrecalled antibiotic x 7 days
• Preterm labor at 35 weeks AOG —> Dexamethasone x 3 doses
• Vaccinated with 1 dose of Tetanus toxoid
• No comorbidities
• Nonsmoker, non-alcoholic and denies elicit drug used
Natal History
• Preterm via normal spontaneous delivery at 35weeks
• Birthweight: 1.2kg, Ballards score and Apgar score unrecalled
• Assisted by an Obstetrician at a Hospital in Cavite
• (-)meconium (-)cord coil
• NICU for 5 days
• Birthrank 2/2
• Given Hep B, BCG vaccine and Vitamin K
Post Natal History
• Newborn Screening done
• No jaundice nor cyanosis
• Previous Hospitalization
• 2014 – 6 months old; Meningitis; Cavite District Hospital for 2 weeks
• Immunization
• BCG – 1
• OPV, DPT, Hep B, HiB – 3
• AMV – 1 dose
• Breastfed – 6 months
• Formula feeding: started at 6 months
• Solid food at 6 months old
• No known food and drug allergies
• No previous surgeries
• Development milestone at par with age
Family History
• Father: 33 yrs old, Filipino, unemployed
• Mother: 30 years old, Filipino, Cashier
• Household: Mother, 1 aunt, 7 uncles, 2 cousins
Heredofamilial disease
• (+) HPN – maternal
• (+) DM - Maternal
• (+)Asthma – Maternal
• Breast CA – maternal
• (-) thyroid disease
• (-) Heart Disease
• (-) Kidney problems
HPI
• 3 days prior to admission,
• Onset of intermittent fever (Tmax 39.8 C)
• Chills
• Epigastric pain, nonradiating
• 2 episodes of tea-colored urine
• Dysuria
• Took Paracetamol(Tempra) 250mg/5ml 3mL every 4 hours which provided temporary relief
• No cough, coryza, vomiting and changes in bowel movement.

• During the interim, symptoms still persisted.

• 1 day prior to admission
• Onset of facial edema associated with difficulty breathing upon lying down
• Patient sought consult at QCGH with Urinalysis result showed proteinuria of +3 and microscopic RBC of many/hpf. Patient was advised
to seek consult at our institution for further work up and management.
Physical Examination
Examined an awake, alert, afebrile, patient not in respiratory
distress with following vital signs:

T: 36.60C PR: 98bpm RR: 20cpm

BP: 90/60mmhg SpO2: 97% at room air
Ht:105 cm Wt:14kg BMI:16.3
(Z score 0) (Z score below -1) (Z score -2)

Skin: warm to touch, good turgor and mobility, (+) erythematous

maculopapular lesions with excoriation and crusts located on both lower
extremities, no jaundice
Physical Examination
HEENT: normocephalic, white sclera, pink palpebral conjunctivae,
(+) mild periorbital edema, no nasal discharge, moist lips and oral
mucosa, no tonsillopharyngeal exudate

Neck: (-) lymphadenopathies, no engorgement, supple

C&L: no retractions, equal chest expansion, equal tactile fremitus,

resonant over both lung fields, clear breath sounds
Physical Examination
CVS: Adynamic precordium, PMI 2cm in diameter within 5th LICS, distinct heart
sounds, no murmur

Abd: flat, non tender, NABS, (-) fluid wave test, (-) shifting dullness, soft, no
organomegaly noted

Back: no deformities, (-) KPS

Ext: (+) bipedal pitting edema, CRT <2s, strong pulses

NEUROLOGIC EXAMINATION
Cerebral: oriented, coherent

Cerebellar: well-coordinated by rapid alternating

movement, finger to nose, normal gait

Motor:
5/5 5/5
5/5 5/5

Sensory: can distinguish between pain from light

touch
Cranial Nerves
CN I: correctly identify scent of cologne
CN II: vision is 20/20, full peripheral vision
CN III,IV, VI: EOM full range, PERRLA
CN V: corneal reflex present, identifies light and sharp
touch to forehead and cheeks, clenches teeth
CN VII: symmetric facial expression
CN VIII: can hear spoken voice
CN IX,X: (+) Gag Reflex and swallowing
CN XI: can shrug shoulder against resistance
CN XII: tongue at midline upon protrusion

Reflexes: 2+ Biceps, Triceps, Patellar and Achilles reflex

Primary Impression
• NEPHROTIC SYNDROME

RULE IN
Edema
Proteinuria
Hematuria (tea-colored urine ,TNTC on
Microscopy)
Differential Diagnoses
 Acute Poststreptococcal Glomerulonephritis (APSGN)

RULE IN RULE OUT

Edema Hypertension

Hematuria Renal insufficiency

Skin infection (erythematous lesions

on both lower extremities)
Nonspecific:
Abdominal pain
 Acute Pyelonephritis

RULE IN RULE OUT

Fever

Abdominal pain

Hematuria, Pyuria

Dysuria
Heart Failure

RULE IN RULE OUT

Edema Unremarkable CVS examination

Difficulty Breathing

Abdominal pain
Diagnostic Plan
 CBC
 2D Echocardiography
 Complement C3 level
 Mantoux Test
 SGPT/ALT
Diagnosis of nephrotic syndrome is confirmed by the following:
 24 hour urine protein
 Urinalysis, spot urine protein:creatinine ratio
 Serum albumin
 Serum creatinine
 Serum cholesterol
 Serum electrolytes
• Renal biopsy should be considered:
MCNS less likely
gross hematuria
hypertension
renal insufficiency
hypocomplementemia
age <1 yr or >12 yr
Therapeutic Plan
Definitive: Corticosteroid therapy
 Prednisone 20 mg/tab TID (AD: 0.95mkD) for 4-6 weeks , followed by alternate day
prednisone for 8 weeks to 5 months

Supportive:
 Furosemide 20 mg IVTT q 12h
 Dietary salt restriction <1500mg daily
Supportive:
 Elevate scrotum with pillows
 Fluid restriction
 Low fat diet
 Avoid going to crowded areas
Course in the Wards
2nd Hospital Day

(+) Noted decrease in periorbital CBC with PC Low salt, low fat diet
swelling Therapeutics:
(-) fever UA 1. Cefuroxime (75) 350 mg
TIV every 8 hours
Conscious, coherent, not in TPAG
distress Monitor VS Q4 and record
BP 90/60 C3, ASO
CR 98 bpm
RR 20 cpm Na, K, Cl, Ca
T 36.6 °C
O2 Sat 98% 24 hr urine CHON

No retractions, symmetrical
chest expansion, normal breath
sounds
Adynamic precordium, normal
heart sounds, no murmur
Flabby, soft, nontender abdomen
Full pulses, (+) grade 1 bipedal
edema
 URINALYSIS
Color Dark Yellow
CBC with PC Transparency Turbid
Hgb 107 Sp. Gr. 1.030
Hct 0.35 L pH 6.0
RBC 5.9 L Glucose -
MCV 59.8 Protein +3
MCH 18.2 Ketones -
MCHC 305 Blood -
RDW 15 Leukocytes +2
Platelet 564 Nitrite -
WBC 8.5 RBC TNTC
Neutrophils 0.42 WBC 25-30
Lymphocytes 0.49 Bacteria Numerous
Monocytes 0.06 Epithelial Cells Few
Eosinophils 0.02 Mucus threads Many
Basophils 0.01 A. urates Few
Cast -
Total Cholesterol: 5.98 mmol/L (0 – 5.18) H
HDL: 0.76 mmol/L (1.04 – 1.55) L Creatinine 1.11 mg/dL
LDL: 4.32 mmol/L (2.49 – 3.96) H BUN 42.58 mg/dL
VLDL: 0.90 mmol/L (0.77 – 1.02)
Triglycerides: 1.98 mmol/L (1.70 – 2.25) Sodium 135
Total Protein 40.00 g/L (60-80 g/L) L Potassium 4.56
Albumin 24 g/L (38-45 g/L) L
Globulin 16 g/L (22-35 g/L) L Calcium 2.06
A/G Ratio 1.5 (1.29 – 1.75) Chloride 103.30
3rd Hospital Day

(+) Noted decrease in periorbital Still for KUB Utz Low salt, low fat diet
swelling Continue medication:
(-) fever Awaiting C3 results 1. Cefuroxime (75) 350 mg
TIV every 8 hours
Conscious, coherent, not in
distress Monitor VS Q4 and record
BP 100/60
CR 87 bpm
RR 20 cpm
T 36.8 °C
O2 Sat 98%

No retractions, symmetrical
chest expansion, normal breath
sounds
Adynamic precordium, normal
heart sounds, no murmur
Flabby, soft, nontender abdomen
Full pulses, (-) edema
Anatomy
 Overview
 Retroperitoneal, paired
organs
 Posterior abdominal wall,
largely under cover of
costal margin

Key organ of urinary
 system
Filtration/ concentration
 of urine
Biochemical balance,
hormone production
 Structure - macro
 Enclosed in a strong fibrous capsule which passes over the
lips of the sinus and becomes continuous with the walls
of the calices.
 Kidney + capsule are surrounded by pararenal fat

Each kidney has superior and inferior poles, medial and
lateral borders/margins and anterior and posterior surfaces

Reddish-brown in colour when fresh – colour varies
 between cortex and medulla
 Measure ~12x6x3cm (left often slightly longer than right)
 Weigh ~130g each
Ovoid in outline but indented medially (the renal sinus)

 Structure - macro

 Hilum
 At the concave part of each kidney
 Renal vein exits (anteriorly)
 Renal artery enters (posterior to renal vein)
 Renal pelvis exits (posterior to artery)
 Structure - macro
 Renal pelvis
 Funnel-shaped
 Lined with transitional epithelium with a smooth
muscle and connective tissue wall
 Continuous inferiorly with ureter
 Divides into major and minor calyces
 Urine  collecting tubule  minor calyx 
major calyx  renal pelvis  ureters 
bladder
 Structure - macro

 Cortex
 Beneath capsule, extends towards the pelvis as
renal columns lying between pyramids of
medulla
 Apices of several pyramids open together
into a renal papilla, each of which projects
into a renal calyx
Structure - macro
 Strcuture - micro
 Nephrons
 Functional and histological subunit
 ~106 per kidney
 = glomerulus + tubules
 glomerulus
tuft of capillaries
surrounded by
 podocytes
projects into Bowman’s capsule
tubule system
epithelium continuous with
Bowman’s capsule
 proximal convoluted tubule  Loop of Henle  distal convoluted
tubule  collecting tubule and collecting duct
glomeruli and convoluted tubules are in cortex
ducts lie in the medulla
Structure - micro
Structure - micro
Structure - nephron
 Position and relations
 Lie in a mass of fat (perinephric fat) and fascia, retroperitoneally
against posterior abdominal wall
 Fatty renal capsule is covered by fibroareaolar tissue – the renal fascia Renal
 fascia
• encloses kidney, its surrounding fibrous and fatty capsules
helps maintain organ position
• superiorly, is continuous with fascia of inferior diaphragm
• medially the left and right fascia blend with each other anterior to
abdominal aorta and IVC
• posterior layer of fascia blends with fascia overlying psoas
 Extraperitoneal fat outside the renal fascia is located between
peritoneum of posterior abdominal wall and renal fascia
 Position and relations
Left Right
Posterior  Diaphragm (postero-superiorly)
 Quadratus lumborum (postero-laterall y)
 Psoas major postero-medially
 Transversus abdominis postero-laterall y
 Subcostal nerve and vessels
 Il iohypogastric andili oinguinal nervesdescenddiagonall y
across posterior surface
Anterior Lies with pancreas and · Superiorly related to
spleenin thestomachbed inferior surface of li
· Adrenal gland ver
· Stomach · Descending part of
· Spleen duodenum
· Pancreas (tail ) · Right coli c (hepatic)
· Jejunum fl exure li es anterior
· Descending colon to
· Posterior wall of omental lateral border and
bursa inferior
· Peritoneum pole
· Small intestine
(inferiorly)
· Peritoneum
Medial · L adrenal gland · Right adrenal glandÐ
wedgedbetween
superior pole andIVC
 Surface anatomy
 Superior poles protected by 11th and 12th ribs
 Extend from T12 to L3 vertebral bodies
 Move ~2cm superior-inferior during respiration
 Right – just below transpyloric plane, 5cm right of
midline. Inferior pole ~ finger-width superior to
right iliac crest
 Left – just above transpyloric plane, 5cm left of
midline.
 Arterial supply

 Renal arteries
 branches of aorta at L1/L2 lie behind pancreas
and renal veins
 Enter at hilum, giving rise to
 Anteriorly – apical, upper, middle and lower
segments
 Posteriorly – posterior segment
 No communication between segments
 Venous drainage

 Renal veins
 Communicate widely
 Eventually form 56 vessels that unit at the
hilum
 Drain into IVC
 Lymphatic drainage

 Para-aortic nodes at L1/L2

 Surface of upper kidney drains through
diaphragm into nodes in the posterior
mediastinum
 Innervation

 Sympathetic
 Preganglionic cells in spinal cord T12/L1 
fibres to thoracic and lumbar splanchnic nerves
 Postganglionic cells in coeliac, renal and
superior hypogastric plexuses
 Vasomotor function
 Development
 Arises from mesoderm
 Pronephros
 Transitory, non-functional structures consisting of a few ducts which
persist
 Mesonephros
 Large elongated organs that function as interim kidneys
 Glomeruli + tubules open into mesonephric ducts
 Metanephros
 Permanent kidneys
 Begin to develop in ~5th week
 Arises caudal to
 mesonephros
Induces a bud
 Ureteric budfrom caudal
divides into calyces of pelvis and collecting tubules and
end ofmedullary pyramids
mesonephric duct
 Develops
(ureter) in anatomic pelvis and migrates to adult position and the new
single definitive artery forms
Physiology
 Physiology - overview
 Regulation of the water and electrolyte content of
the body
 Retention of substances vital to the body such as
protein and glucose
 Maintenance of acid/base balance
 Excretion of waste products, water soluble toxic
substances and drugs
 Endocrine functions
 Water and electrolyte regulation
 Renal blood supply is approx 20% of cardiac
output
 99% to cortex
 1% to medulla
 2 capillary beds,
arranged in series:
 Glomerular
 High pressure for
filtering
 Peritubular
 Low pressure for
absorption
 Water and electrolyte regulation

 Urine formation - 3 phases

 Simple filtration
 Selective and passive
resorption
 Concentration
 Filtration
 Takes place through the semipermeable walls of the glomerular
capillaries
 almost impermeable to proteins and large molecule
 Glomerular filtrate is formed by squeezing fluid through glomerular
capillary bed

Hydrostatic pressure (head of pressure) is controlled by afferent and
efferent arterioles, and provided by arterial pressure

About 20% of renal plasma flow is filtered each minute (125 ml/min).
This is the glomerular filtration rate (GFR).
 Autoregulation
 With a change in arterial blood pressure, there is constriction or dilatation of
the afferent and efferent arterioles, the muscular walled vessels leading to and
from each glomerulus
 Juxtaglomerular apparatus
 Macula densa cells
 Detect chloride concentration
 Juxtaglomerular cells
 Modified smooth muscle cells
 Produce renin
 Converts angiotensin to angiotensin I
 Angiotensin I converted to angiotensin II by
Angiotensin converting enzyme (ACE)
 Causes systemic vasoconstriction and increase
in BP
 6
0
% Tubular reabsorption
o
f

s
o
l
u
t
e

i
s
 Acid-base balance

 Tubular acid secretion

 Ammonia secreted by
tubules (combines with
H+ to form NH4
+
and passed in
urine)
 Hormones
 Renin
Increases production of angiotensin II
 Aldosterone
Stimulates water and sodium ion
resorption
 Atrial in distal
natriuretic tubule (ANP)
hormone
 Produced when atrial pressure increases (eg heart failure)
 Promote Na+, Cl- and water loss
 Antidiuretic hormone
 Increases permability of distal tubule to water, to cinrease water
resorption (therfore increases concentration of urine)
 1,25 dihydroxy vitamin D3
 Promotes calcium absorption from gut
 Erythropoietin (EPO)
 Stimulates marrow to produce red blood cells
ETIOLOGY
Nephrotic syndrome
Idiopathic Nephrotic Syndrome
Secondary Causes of Nephrotic Syndrome
Secondary Causes of Nephrotic Syndrome
Secondary Causes of Nephrotic Syndrome
CLINICAL CONSEQUENCES
Edema
• most common presenting symptom
• Mechanism:
1) Underfill hypothesis
- 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
atrial natriuretic factor, which, along with aldosterone, result in increased sodium and water
retention by the tubules.
Edema
2) Overfill hypothesis
- Associated with primary sodium retention, with subsequent volume expansion
and leakage of excess fluid into the interstitium.
- Epithelial sodium channel in the distal tubule may play a key role in sodium
reabsorption in nephrotic syndrome
- The clinical weaknesses of this hypothesis: an obvious clinical
picture of intravascular volume depletion: low blood pressure, tachycardia,
and elevated hemoconcentration.

Goal of therapy: gradual reduction of edema

- judicious use of diuretics, sodium restriction, and cautious use of
intravenous albumin infusions, if indicated.
Hyperlipidemia
Lipid profile
• increase in cholesterol, triglycerides, low-density lipoprotein, and very-low-
density lipoproteins
• The high density lipoprotein level: unchanged or is low
Mechanism: result of increased synthesis as well as decreased catabolism of
lipids
Increased susceptibility to infections
Infections: cellulitis, spontaneous bacterial peritonitis, and bacteremia.
Mechanism:
• Hypoglobulinemia as a result of the urinary losses of immunoglobulin (Ig)
• Defects in the complement cascade from urinary loss
of complement factors (predominantly C3 and C5)
• Alternative pathway factors B and D, lead to impaired opsonization of
microorganisms.
Increased susceptibility to infections
• Increased risk for infection with encapsulated bacteria and, in particular,
pneumococcal disease
• Spontaneous bacterial peritonitis presents with fever, abdominal pain, and
peritoneal signs.
- Peritoneal leukocyte counts >250
Hypercoagulability
Mechanisms:
• vascular stasis from hemoconcentration and intravascular volume depletion
• increased platelet number and aggregability
• changes in coagulation factor levels.
• increase in hepatic production of fibrinogen along with urinary losses of
antithrombotic factors such as ntithrombin III and protein S.

Deep venous thrombosis may occur in any venous bed, including the cerebral
venous sinus, renal vein, and pulmonary veins.
IDIOPATHIC NEPHROTIC SYNDROME
• Approximately 90% of children with nephrotic syndrome
• Associated with primary glomerular disease without indentifiable causative
disease or drug
• Multiple histologic types:
• Minimal change disease
• Mesangial proliferation
• Focal segmental glomerulosclerosis
• Membranous nephropathy
• Membranoproliferative glomerulonephritis
PATHOLOGY
• Minimal Change Nephrotic Syndrome
• Most common (85%) cause of nephrotic syndrome in children
• Glomeruli appear normal or show minimal increase in mesangial cells and matrix
• Negative findings on immunofluorescence
• Effacement of epithelial cell foot processes on electron microscopy
• >95% respond to corticosteroid therapy
PATHOLOGY
• Mesangial Proliferation
• Diffuse increase in mesangial cells and matrix on light microscopy
• Immunofluorescence might reveal trace to 1+ mesangial IgM and/or IgA staining
• Electron microscopy reveals increased number of mesangial cells and matrix and
effacement of epithelial cell foot processes.
• Approximately 50% respond to corticosteroid therapy
PATHOLOGY
• Focal Segmental Glomerulosclerosis
• Glomeruli show lesions present only in a proportion of glomeruli (focal) and localized to >1
intraglomerular tufts (segmental)
• Mesangial cell proliferation and segmental scarring on light microscopy
• Immunofluorescence positive for IgM and C3 staining in areas of segmental sclerosis
• Electron microscopy segmental scarring of the glomerular tuft with obliteration of glomerular
capillary lumen
• Similar lesions may be seen 2o to HIV infection, vesicoureteral reflux, IV use of heroin and
other drugs of abuse
• Only 20% respond to prednisone
• Disease often pregressive ultimately involving all glomeruli and ESRD in most patients
Diagnosis
• Urinalysis reveals 3+ or 4+ proteinuria, and microscopic hematuria is
present in 20% of children.
• Spot urine protein:creatinine ratio >2.0, and urinary protein excretion >40
mg/m2/hr.
• Serum creatinine value is usually normal, but it may be abnormally elevated
if there is diminished renal perfusion from contraction of the intravascular
volume.
• Serum albumin level is <2.5 g/dL
• Serum cholesterol and triglyceride levels are elevated.
• Serum complement levels are normal. R
• enal biopsy is not routinely performed if the patient fits the standard clinical
picture of MCNS.
TREATMENT of INS
A trial of CORTICOSTEROIDS is the first step prior to kidney biopsy if they
meet ALL of the ff criteria
Age: 1-8 years
Normal kidney function
No macroscopic hematuria
No symptoms of systemic diseases (fever, rash, joint pain, weight loss)
Normal complement levels
Negative ANA
Negative viral screens (HIV, Hep B and C)
No family history of kidney disease
CORTICOSTEROID THERAPY
Phase PREDNISONE dose Period
INDUCTION 60 mg/m2 or 2mg/Kg/d 4-6 weeks BRISK STEROID
OD RESPONSE
Max: 60mg/d -negative proteinuria
-Increased U.O.
-Decreased edema
MAINTENANCE 40 mg/m2 or 1.5mg/Kg/d At least 4 weeks Continued negative
every other day proteinuria
TAPERING Until <10mg/m2 2-5 months
Every other day

2012 KDIGO
RELAPSE
Many children with nephrotic syndrome experience at least 1 relapse (uPCR
>2000mg/g or >3+ on dipstick for 3 consecutive days

60 mg/m2 or 40 mg/m2 or
INFREQUENT RELAPSE 2mg/Kg/d OD until 1.5mg/Kg/d every
3 days complete other day for at
remission least 4 weeks

60 mg/m2 or
2mg/Kg/d OD Lowest dose on Daily prednisone
FREQUENT until 3 days 1. Alternate days during URTI and
RELAPSE complete other infection
2. OD
remission

Complete remission – uPCR <200mg/g pr <1+ dipstick

STEROID-SPARING AGENTS
• For
• STEROID-DEPENDENT
• FREQUENT RELAPSERS
• STEROID-RESISTANT
• SEVERE CORTICOSTEROID TOXICITY (cushingoid appearance, hypertension, cataracts,
and/or growth failure
STEROID-SPARING AGENTS
STEROID-SPARING AGENTS
COMPLICATION
• INFECTION
• Bacterial peritonitis
• Streptococcus pneumoniae
• Escherichia coli
• Sepsis
• Pneumonia
• Cellulitis
• Urinary tract infection
• Thromboembolic events
• increased prothrombotic factors (fibrinogen, throm- bocytosis, hemoconcentration, relative
immobilization)

• decreased fibrinolytic factors (urinary losses of antithrombin III, proteins C and S).

• Diuretics to minimize such occurences

 PROGNOSIS
• Steroid-responsive
• Repeated relapse, which decreases as the child grows older

• Steroid-resistant
• Poorer prognosis
progressive renal insufficiency, ultimately leading to end-stage renal disease
requiring dialysis or kidney transplantation
JOURNAL REVIEW
CLINICAL QUESTION
• What is the frequency of First-Year Relapse in Children with Nephrotic
Syndrome?
OBJECTIVE
• The purpose of this study was to identify factors at initial presentation that
could predict the relapse pattern in the first year after diagnosis without taking
into consideration the histopathology found on renal biopsy.
Study Design
• This study analyzed the medical records of children who were seen before
March 1997 and followed for at least 1 year.
Study Variables
• Age
• Sex
• Race
• Presence or absence of hematuria
• Days to remission
Inclusion Criteria
• Population: Children diagnosed with steroid-sensitive nephrotic syndrome
• Intervention: Initial steroid therapy 60 mg/m2 for at least 4 weeks followed by equal number of
weeks of alternate day therapy in the dose of 40 mg/m2
• Comparator: The number of treatment days until the patient’s urine became protein free
• Outcome: Of all the presenting features, the rapidity of initial response to hematuria could
predict future relapse
• Method: Retrospective chart review
Exclusion Criteria
• Patients with incomplete data from initial presentation
• Patients who were followed up for less than 12 months
• Steroid-resistant patients
Methodology
• The study was conducted as a retrospective chart review of all
pediatric patients with NS referred to and followed by the pediatric
nephrologists at Robert Wood Johnson Medical School.
Results
Conclusion
• In conclusion, of all the presenting features, the rapidity of response to steroid
therapy combined with the presence of hematuria, could predict future
relapses and should be well documented.
Thank you!