Apalla, Mc Cornellius Furigay, Kreshimaricon

Bundoc, Janine Garlejo, Nikki Anne

Campos, Claire Anne Manuel, Maria Angelica
Caranguian, Marife Rivera, Karessa Marie
IDENTIFYING DATA
Name: MA
Age: 6 y/o
Sex: M
Address: Amulung, Cagayan
Religion: RC
Nationality: Filipino
Date of Birth: Oct 4, 2012
# of admission: 1
Date of Admission: Nov 5, 2018
Source of information: Mother
Reliability: 90 %
 CHIEF COMPLAIN

Tea-colored Urine
HISTORY OF PRESENT ILLNESS
 Facial swelling

No fever
No oliguria
Consulted at a PMD but no medications
given.
Patient was advised to seek consult at
our institution but did not comply
days PTA
HISTORY OF PRESENT ILLNESS

Facial swelling
Bipedal edema
Tea colored urine
Consulted at a PMD
Advised for admission at our
institution but refused
day PTA
HISTORY OF PRESENT ILLNESS
Few hours PTA
 Persistence of above signs and symptoms
 Decreased urine output
Patient was brought to our institution hence
admitted
 D
(+) ATP : Oct 23, 2018
(+) healed pyodermal lesions
(-) asthma
(-) heart disease
(-) diabetes
PAST MEDICAL HISTORY

(-) Previous hospitalization

(-) Previous surgeries
(-) Allergies
 S
BIRTH HISTORY
Prenatal
 LHC 5x
 FeSO4
 (-) Maternal illness
 No exposure to drugs, alcohol
or medications
PAST MEDICAL HISTORY
BIRTH HISTORY
Postnatal
 Term
 Cephalic
 NSD
 CVMC
 G1P1 (1001)
 Good cry and activity
 2600 gms
 no birth complications
PAST MEDICAL HISTORY
NUTRITIONAL HISTORY
 Exclusive breastfeeding for 6 months
 Constitutional feeding at 6 months of age
 Rice, meat and vegetables
GROWTH AND
DEVELOPMENT
✔5m ✔6m

1st word
• Mama, 8 months
✔7m ✔8m ✔10m ✔1y
Toilet-trained
• 3 years
 PAST MEDICAL HISTORY
IMMUNIZATION HISTORY

BCG OPV DPT HEPA B MEASLES

FAMILY HISTORY
(+) hypertension: mother side
(-) heart disease
(-) asthma
(-) diabetes
PERSONAL AND SOCIAL HISTORY
 Only child
 Mother, 23, housewife
 Father, 30, farmer
 Bungalow type house
REVIEW OF SYSTEMS
CONSTITUTIONAL
(-) Fever
(-) Weight loss
HEENT
(-) blurring of vision
(-) otorrhea
(-) nasal congestion
(-) dysphagia
REVIEW OF SYSTEMS

PULMONARY CARDIOVASCULAR
(-) Cough (-) Cyanosis
(-) DOB (-) palpitations
 REVIEW OF SYSTEMS

GASTROINTESTINAL NEUROLOGICAL GENITOURINARY

(-) Headache (-) Dysuria
(-) Abdominal Pain
(-) dizziness
(-) Bloating
REVIEW OF SYSTEMS

MUSCULOSKELETAL
(-) muscular pain
(-) numbness
(-) paresthesia
General Awake, Conscious, Coherent,
NICRD
Vital Signs BP: 160/80
HR: 85
RR: 21
Temp. : 36.8 C
Weight: 18 kg
Ht: 131 cm
Skin No pallor, No cyanosis, No Jaundice
HEENT Anicteric Sclerae, Pink Palpebral Conjunctiva, With
Facial Edema, No TPC, No CLAD

Chest, Lungs Symmetrical Chest Expansion, No Retractions, Clear

Breath Sounds
Heart Adynamic Precordium, Normal Rate, Regular
Rhythm, PMI at 4th ICS LMCL, No murmur

Abdomen Flabby, Distended, NABS, Soft

Genitourinar Grossly Male, Tanner Stage I, No scrotal Edema
y
Extremeties (+) Healed pyodermal lesions, Full Equal Pulses

Neurological GCS 15, Cranial Nerve Exam Unremarkable, No

neurologic deficit noted
 6 y/o
 Male
 Tea-colored urine
 Facial edemaBipedal edema
 Decreased frequency of urination
 (+) history of ATP
 (-) history of medication intake
 (-) history of trauma
 Hypertensive @ 160/100 mmHg (>99th percentile SBP, >95th percentile DBP)
 Abdominal distention
 (-) gross genital abnormality
 (+) healed pyodermal lesions
Presence of at least 5 red blood cells per
microliter of urine

Prevalence: 0.5-2% among school-age

children

Significant hematuria: >50 RBCs/uL

 Red Urine

Medication
Upper Tract Lower Tract
intake

Rhabdomyol Glomerulus Pelvis

ysis

Myoglobin vessels Ureter

Hemolysis tubules bladder

Glomerular Non Glomerular
Acute Postinfectious GN Fever
Membranoproliferative GN Strenuous Exercise
IgA Nephropathy Mechanical trauma
Alport Syndrome Menstruation
Benign Familial hematuria Foreign Bodies
Hemolytic Uremic Syndrome Urinary Tract Infection
Lupus Nephritis Hypercalciuria/Urolithiasis
Henoch-Schonlein Purpura Sickle Cell Disease/trait
Coagulopathy
Tumors
Drugs/Toxins
Anatomic abnormalities
Erythrocyte deformity
Idiopathic
 MC chronic glomerular
disease in children
 common in older children
(10-35 y/o)

 higher predilection to male

than female 2:1

 acute onset of fever and

hematuria; follows viral
syndrome

 30 - 50% of cases can have

Hypertension and Edema of
the hands and feet.
Rule In Rule Out
 History of ATP  Short latency period (1-2 days) from
onset of upper respiratory/GI infection

 Common in males

 Recurrent episodes of gross hematuria

 Hematuria

 Edema

 Hypertension CANNOT TOTALLY RULE OUT

 Most common small
vessel vasculitis in
childhood.

 Characterized by
purpuric rash, arthritis
and abdominal pain.
Rule In Rule Out

 History of ATP  Purpuric rashes

 Hematuria  Arthritis

 Edema

 Hypertension
 Occur in 1% of boys & 1-3
% of girls
 M>F during 1st year of life
 3 basic Forms:
 Pyelonephritis
 Cystitis
 Asymptomatic Becteuria
Rule in Rule Out
 Hematuria  Fever
 Dysuria/Frequency/Urgency
 Strong smelling urine
 Abdominal/flank pain
 Classic example of the acute
nephritic syndrome

 Sudden onset of gross hematuria,

edema, hypertension, and renal
insufficiency

 One of the most common

glomerular causes of gross
hematuria in children
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
Rule IN Rule OUT

 History of ATP
 Hematuria
 Edema
 Hypertension
 Decreased Urine
Frequency
 S O A P
(+) tea- Awake, conscious, coherent, not in ACUTE Low salt, low fat diet
colored urine cardiorespiratory distress GLOMERULONE Limit fluid intake 133 cc/hr
(+) decreased Vital signs: PHRITIS Insert heplock
frequency in BP: 160/100 Wt: 18 kg Diagnostics:
urination CR: 85 Ht: 131 cm CBC with pc
RR: 20 BSA: 0.8 m2 Urinalysis with RBC
T: 36.8 morphology
No pallor, no jaundice BUN, Crea
(+) Facial edema, anicteric sclerae, C3, ASO Titer
pink palpebral conjunctivae, (-) CLAD Na, K, Cl
Symmetrical chest expansion, (-) Chest xray-PA/Lat
retractions, clear breath sounds Therapeutics:
Adynamic precordium, normal rate, Furosemide 20 mg/IV now
regular rhythm, PMI at 4th ICS LMCL, (-)  BP: 130/90  Another
murmur Furosemide 20 mg/IV 
Flabby, normoactive bowel sounds, soft 120/70  Furosemide 20
Grossly male, (-) scrotal edema mg/IV q6
(+) Healed pyodermal lesions, (+) (200T) Pen G
Bipedal edema, full and equal pulses (10) Paracetamol
GCS 15 Amlodipine 2.5 mg/tab OD
CBC URINALYSIS
 Color Amber
 Hgb 97 L
 Transparency Turbid
 Hct 0.30 L
 pH 6.5
 RBC 4.21 L
 SG 1.025
 Plt 444 H
 Protein +++
 MCV 70 L
 Glucose Negative
 MCH 23 L
 Ketone Negative
 MCHC 329
 Blood +++
 WBC 11.6 H
 Neutro 50.4  Bilirubin Negative
 Lymph 33.8  Urobilinogen NORMAL
 Mono 5.9
 Eos 9.5 H  Nitrite Negative
 Baso 0.4  Leukocytes Negative
 WBC 143
 RBC 93
 Epith cells 16
 Hyaline cast 42
 Bacteria 22
RBC Morphology  Creatinine 52.1 L
 BUN 3.4
 60% Normal RBCs
 Na 148.5
 40% Dysmorphic RBCs
K 4.45
 Cl 109.8
 C3 0.246 L
 ASO Titer 6400 IU/ml H
 S O A P
(+) tea- Awake, conscious, coherent, not in ACUTE Low salt, low fat diet
colored cardiorespiratory distress GLOMERULONEPHR Limit fluid intake 133 cc/hr
urine Vital signs: ITIS Maintain heplock
BP: 110/70 Diagnostics:
CR: 92 TPAG
RR: 20 Lipid profile
T: 37.1 Therapeutics:
No pallor, no jaundice Furosemide 20 mg/IV q6
(+) Facial edema, anicteric sclerae, pink (200T) Pen G
palpebral conjunctivae, (-) CLAD (10) Paracetamol
Symmetrical chest expansion, (-) Amlodipine 2.5 mg/tab OD
retractions, clear breath sounds
Adynamic precordium, normal rate,
regular rhythm, PMI at 4th ICS LMCL, (-)
murmur
Flabby, normoactive bowel sounds, soft
Grossly male, (-) scrotal edema
(+) Healed pyodermal lesions, (+)
Bipedal edema, full and equal pulses
GCS 15
UO: 1.9cc/kg/hr
 S O A P
(-) tea- Awake, conscious, coherent, not in ACUTE Low salt, low fat diet
colored cardiorespiratory distress GLOMERULONEPHR Limit fluid intake 260 cc/hr
urine Vital signs: ITIS Maintain heplock
BP: 100/70
CR: 89 Therapeutics:
RR: 20 Furosemide 20 mg/IV q8
T: 36.8 (200T) Pen G
No pallor, no jaundice (10) Paracetamol
Anicteric sclerae, pink palpebral Amlodipine 2.5 mg/tab OD
conjunctivae, (-) CLAD
Symmetrical chest expansion, (-)
retractions, clear breath sounds
Adynamic precordium, normal rate,
regular rhythm, PMI at 4th ICS LMCL, (-)
murmur
Flabby, normoactive bowel sounds, soft
Grossly male, (-) scrotal edema
(+) Healed pyodermal lesions, (+)
Bipedal edema, full and equal pulses
GCS 15
UO:1.5cc/kg/hr
TPAG
 Total protein 74.47
 Albumin 30.62 L
 Globulin 43.85 H
 A/G Ratio 0.69 L
 S O A P
(-) tea- Awake, conscious, coherent, not in ACUTE MGH
colored cardiorespiratory distress GLOMERULONEPHR
urine Vital signs: ITIS Home meds:
BP: 90/60 1. Amoxicillin 250mg/5ml,
CR: 90 4 ml TID x 7 days
RR: 20 2. Amlodipine 2.5 mg/tab
T: 36.7 OD x 5 days
No pallor, no jaundice
Anicteric sclerae, pink palpebral Low salt, low fat diet
conjunctivae, (-) CLAD Follow up on Nov. 12,2018
Symmetrical chest expansion, (-)
retractions, clear breath sounds
Adynamic precordium, normal rate,
regular rhythm, PMI at 4th ICS LMCL, (-)
murmur
Flabby, normoactive bowel sounds, soft
Grossly male, (-) scrotal edema
(+) Healed pyodermal lesions, (-)
Bipedal edema, full and equal pulses
GCS 15
UO:1.5cc/kg/hr
 The kidneys preserve homeostasis through:
 maintain fluid and electrolyte balance
 excrete metabolic waste products through glomerular filtration and
tubular secretion
 generate energy (gluconeogenesis)
 Produce important endocrine hormones (renin, vitamin D
metabolites, erythropoietin
 Fetal urine production contributes to amniotic fluid volume,
lung maturation, and somatic development.
 Congenital renal disorders may be associated with
reduced (oligohydramnios) or increased amniotic fluid
volume (polyhydramnios).
 Pulmonaryhypoplasia and fetal maldevelopment of the face
and extremities may result from insufficient amniotic fluid.
 Risk factors for renal disease can be detected by a
careful history.
 A detailed family history may identify hereditary
renal conditions. Poor growth and/or feeding,
abnormal fluid intake and/or output may indicate
underlying renal dysfunction.
 Laboratory Result
Examination
Urinalysis with RBC May demonstrate RBCs, RBC casts, Proteinuria, PMNs, or dysmorphic
morphology RBCs particularly acanthocytes
Proteinuria normalizes 4-6 wks after onset
Microscopic hematuria may persists for 1-2 yrs after initial
presentation
CBC Mild normochromic anemia may be present from hemodilution and
low grade hemolysis
Serum C3 Reduced in acute phase and returns to normal 6 to 8 wks after onset
ASO Titer Increased after pharyngeal infection rarely increases in strep skin
infection
Anti-Dnase B Documents Recent Strep Skin infection
Serum Electrolytes To correct any electrolyte abnormalities
BUN and Creatinine Renal function tests
Chest X-ray Pulmonary Edema
Renal Biopsy Persistent microscopic hematuria
Children with recurrent gross hematuria with dec. renal function,
proteinuria or HTN.
Genetic disorder- mutation
Immunologic disorder- histopathologic
Perfusion disorder
coagulation disorders.
Proliferation
Sclerosis
Tubulointerstitial fibrosis
Criteria INS APSGN
Age 1-10 y/o 3-15 y/o
Sex M> F M=F
Edema Generalized Localized
Gross Hematuria (-) +++
Oliguria ++ +++
Preceding Infection +/- +
Phases - +
Criteria INS APSGN

Edema Anasarca Localized

Hypertension +/- +++

Congestion +/- +

Pleural effusion + -
 Small amounts of protein are found in the urine of
healthy children (<4 mg/m2/hour or UPr/Cr <0.2).

 Nephrotic proteinuria in children is defined as

protein greater than 40 mg/m2/hour or U Pr/Cr
>2.0.
 Proteinuria may be transient /persistent, asymptomatic/
symptomatic, and orthostatic/ fixed
 Proteinuria may be glomerular (disruptions of the normal
glomerular barrier to protein filtration) or tubular
(increased filtration, impaired reabsorption, or secretion of
proteins)
 protenuria
 hypoalbuminemia
 hyperlipidemia
 Nephrotic syndrome
 Persistent heavy proteinuria (mainly albuminuria) (>2 g/m2/24 h)
 hypoproteinemia (serum albumin <3.0 g/dL)
 Hypercholesterolemia (>250 mg/dL)
 Edema
 Certain HLA types (HLA-DR7, HLA-B8, and HLA-B12) are associated
with an increased incidence of NS
 Minimal change nephrotic syndrome (MCNS)
 most common histologic form of primary NS in children.
 More than 80% of children less than 7 years of age with
NS have MCNS.
 Children 7 to 16 years old with NS have a 50% chance of
having MCNS.
 Males are affected more frequently than females (2:1).
 Focal segmental glomerulosclerosis (FSGS)
 10% to 20% of children with primary NS
 less impressive proteinuria
 A circulating factor that increases glomerular
permeability is found in some patients
 More than 35% of children with FSGS progress to renal
failure
 Membranoproliferative glomerulonephritis
 hypocomplementemia with signs of glomerular renal
disease
 typically persistent, and has a high likelihood of
progression to renal failure over time.
 Membranous nephropathy
 less than 5% of children with primary NS
 seen most commonly in adolescents and children with
systemic infections, such as hepatitis B, syphilis, malaria,
and toxoplasmosis, or on specific medications (gold,
penicillamine).
Congenital NS
 during the first 2 months of life
 Prenatal onset is supported by elevated levels of
maternal alpha-fetoprotein
 Hematuria may originate from glomerular disease, tubulointerstitial processes, and
lower urinary tract disorders
 Microscopic hematuria- more than 3 to 5 red blood cells (RBCs) per high-power
on freshly voided and centrifuged urine
 is often benign.

 Isolated asymptomatic microscopic hematuria is found in up to 4% of healthy

children. In most cases this is a transient
 finding.
 Patients with hematuria can present with a number of
symptoms suggesting specific disorders.
 Tea- or cola-colored urine, facial or body edema,
hypertension, and oliguria are classic symptoms of
glomerulonephritis.
 Immune-mediated inflammation is the mechanism of
glomerulonephritis (GN).
 Hematuria
 Hypertension
 Oliguria
 Edema
 Postinfectious glomerulonephritis
 Immunoglobulin A (IgA) nephropathy
 Membranoproliferative glomerulonephritis,
 Henoch-Schönlein purpura (HSP) nephritis
 Systemic lupus erythematosus (SLE) nephritis

 Granulomatosis w/polyangiitis(Wegener granulomatosis)

 microscopic polyarteritis nodosa
 Goodpasture syndrome
 hemolytic-uremic syndrome
 is the most common form of acute GN
 most frequently in children 2 to 12 years of age and is more
common in boys
 can occur following infections with other bacterial and viral
Pathogens
 Can develop regardless of whether the child was treated with
antibiotics at the time of infection.
 Monitor blood pressure because hypertension may be severe
enough to lead to complications such as heart failure, seizures, and
encephalopathy.
 most common chronic GN
 asymptomatic microscopic hematuria, or recurrent gross
hematuria concurrent with an upper respiratory infection
as opposed to several days later, as with PSGN
 presents with typical features of acute GN, but the renal insufficiency
progresses more quickly and severely.
 Renal biopsy shows glomerular epithelial cell proliferation with
crescents.
 may be idiopathic or secondary to any of the known types of GN.
 Early recognition of RPGN is crucial to prevent the progression to
end-stage renal disease
 (ESRD) that occurs without prompt treatment
 caused by X-chromosome mutations in type IV
collagen leading to an abnormal glomerular
basement membrane (GBM) and may present with
either asymptomatic microscopic or gross
hematuria.
 Acute glomerulonephritis comprises a specific set
of renal diseases in which an immunlogic
mechanism triggers inflammation and proliferation
of glomerular tissue that can result in damage to the
basement membrane, mesangium or capillary
endothelium.
 Sudden onset of hematuria, protenuria and red
blood cell casts in the urine.
 Hypertension
 Edema
 Azotemia
 Salt and water retention
 PSAGN is due to prior infection with the nephritogenic strains of Group A beta-
hemolytic streptococci.
 The most consistent strains reported or demonstrated in earlier studies are:
 M-type 12 for pharyngitis related
 M-type 49 for pyoderma-related attacks.
 immune-complex mediated disease - immunoglobulin G (IgG) and complement
C3 fluorescent material in the same GBM areas
 Increased titer of streptococcal enzymes; Decreased serum complement titer
 Clearance of immune complexes is related to clinical recovery patients.

 The streptococcal antigenic component, whether or not it is in the cell wall or

cytoplasm of the organisms, remains to be elucidated.
prominent: non specific
 oliguria: UO < 400
symptoms:
ml/day  fever
 nausea
 Rust/ tea/cola
colored urine or  Headache
hematuria  Shortness of breath
or dyspnea
 Swelling/ edema:
 flank pain
 Eyes
 Abdominal pain
 face
 Anorexia
 feet, ankles, hands
 Skin pallor
 abdomen
 malaise
 hypertension: usually
mild to moderate
 antecedent
GABHS
infection: skin

Endostreptosin Ag
Lipoteichoic acid & previously planted in
polysaccharide Ag in glomeruli
the circulation

Immune IC Induce Ab
Granular
response: production:
Ag Ab – Ag
deposition Ab – Ag
pattern
excess complex in circ. in immunofluor
complex in
ence
glomeruli glomeruli
microscopy
AG IC deposition in

EXCESS glomeruli

Proliferation and
C3 convertase
swelling of parietal
Few days to enzyme
epithelial,
weeks: additional formation: C3
endothelial &
Ab enter cleavage
mesangial cells
circulation

Ag ultimately C3
removed from fragmentation,
Decrease
circulation Complement
activation C3

Glomerulonephri Chemotaxis:
tis subsides leukocytic Injury to
infiltration and capillary walls
degranulation
 INJURY TO
CAPILLARY WALLS

Escape of Albumin/Protein
RBC Inc permeability leakage

Albuminuria/protein
uria
hematuria Dec oncotic
pressure

Accumulation of
Tea colored
fluid in interstitial
urine spaces

edema
Proliferation and INCREASE
swelling of parietal GLOMERULAR Stretched renal
epithelial, endothelial SIZE capsule
& mesangial cells
Narrowing of
glomerular
capillary lumen Flank pain

oliguria Dec GFR

Reciprocal Enhanced Na
Fluid retention reabsorption

hypertensi
Hypervolemi Na
on
a retention
Oliguric Phase
- acute salt and water overload and
related and complications as
hypertensive encephalopathy, renal
failure and CHF.
Diuretic Phase
 spontaneous voiding or sudden volume
increments with diuretic agents.
 unrecognized hypovolemia that ensues can
cause serious electrolyte disturbances or even
shock.
 BP normalizes and the child starts feeling better.
 Immediate convalescent periods.
 most hospitalized children are ready for discharge.
 Except perhaps for residual gross or significant
microscopic hematuria, all alarming indices seen in
the oliguric period are gone,
 Serial urinalyses will still show proteinuria, micro-
hematuria and casts, findings which may persist for
a few months to even a year notwithstanding
excellent clinical recovery
acute phase
resolves w/in 6–8 wks
urinary protein excretion & HPN
usually normalize by 4–6 wks
after onset
persistent microscopic hematuria
1–2 yr after initial presentation
 MANAGEMENT

MARIFE CARANGUIAN, POST GRADUATE INTERN

ACUTE POSTSTREPTOCOCCAL GLUMERULONEPHRITIS (APSGN)
-Treatment is directed in treating the acute effect of renal insufficiency and
hypertension.
-Treatment of hypertrnsion:
> soduim restriction
> diuresis
> calcuim channel antagonist vasodilator
> ACE inhibitors
- early systemic antibiotic therapy for streptococcal throat and skin infection does not
eliminate the risk.
-the use of 10 days coarse if systemic antibiotic plus Pen G limit the spread of
nephrotogenic organism.
IDIOPATHIC NEPHROTIC SYNDROME
- First episode of nephrotic syndrome and mild to moderate . edema may
managed as outpatient.
- treatment of initial episode of nephrotic sybdrome: prednisone or prednisolone
should administered as single daily dose of 60mg/m2/day ir 2mg/kg/day to max of
60mg daily for 4-6 weeks followed by alternate day prednisone for 8 weeks-5
months
- Children with uncomplicated nephrotic syndrome ages 1-8 years old are likely to be
steroid responsive. Steroid may initiate without renal biopsy.
- Children with features that of MCNS less likely renal biopsy should consider before
treatment.
EDEMA: Sodium restriction (1500mg daily)
Water restriction
Furosemide
If with evidence of hemoconcentration, hypotension, tachycardia give 25%
albumin IV Plus slow infusion of furosemide

DYSLIPIDEMIA: Low fat diet

Cholesterol intake should be <300mg/day
OBESITY: glucocorticoid increase BMI, Anticipatory diet counseling. Is
recommended.

RELAPSE OF NEPHROTIC SYNDROME:

- protein: creatinine ratio of >2 or >_3+ protein in urine dipstick testing for 3
consecutive days.
Treatment is same with initial episode of nephrotic syndrome except that daily
prednisone course are shortened.
Daily high dose prednisone is given until child achieved remission and regime is
switched to alternate day therapy.
CRITERIA INS APSGN

Fluid restriction +/- +++

Salt restriction +/- +

Ambulation + -

Prednisone +++ -

Diuretics +/- ++

Albumin + -

Anti hypentensive +/-

drug
 increased incidence of serious infections
 bacteremia and peritonitis ( Streptococcus pneumoniae, Escherichia coli, or Klebsiella), is
due to urinary loss of immunoglobulins and complement
 Hypovolemia
 may result from diarrhea or diuretic use.
 The loss of coagulation factors, antithrombin, and plasminogen
 may lead to a hypercoagulable state with a risk of thromboembolism (TE).

 Hyperlipidemia
 promotes increased atherosclerotic vascular disease
 Most children with NS eventually go into remission.
 80% of children with MCNS experience NS relapse(heavy proteinuria that persists
for 3 or more consecutive days)
 Transient (up to 3 days) proteinuria may occur with intercurrent infection in
children with MCNS and is not considered a relapse.
 effective for true relapse.
 Steroid-responsive patients have little risk of chronic renal failure.
 Patients with FSGS may initially respond to steroids but later develop resistance.
Many children with FSGS
 progress to end-stage kidney failure
 Recurrence of FSGS occurs in 30% of children who undergo renal transplantation.
 In typical cases, the gross hematuria, proteinuria, and edema decline quickly (in 5
to 10 days).
 Microscopic hematuria may persist for months or even years; over 95% of children
recover completely with no longterm sequelae.
 Children with IgA nephropathy and other forms of chronic GN have a greater risk
of progression to ESRD.
 The prognosis for renal recovery in chronic GN and in RPGN is variable and
related to the underlying disorder and disease severity.
 The presence of persistent, heavy proteinuria, hypertension, decreased kidney
function, and severe glomerular lesions on
 biopsy is associated with poor outcomes.
 idiopathic isolated asymptomatic microscopic hematuria or suspected thin
basement membrane disease typically have an excellent renal prognosis.
 Long-term follow-up, including yearly urinalysis (to rule out proteinuria) and blood
pressure, is required to exclude progressive forms of renal disease