Ped-S2-C18 - GNPS, SN

Acute Poststreptococcal
Glomerulonephritis
Pediatric Nephrotic
Syndrome
Acute Poststreptococcal Glomerulonephritis
• Definition
• Acute glomerulonephritis is a disease characterized by
the sudden appearance of edema, hematuria,
proteinuria, and hypertension. It is a representative
disease of acute nephritic syndrome in which
inflammation of the glomerulus is manifested by
proliferation of cellular elements secondary to an
immunologic mechanism.
• It is a pathological process not due to direct infection of
the kidney but one characterized by inflammation and/or
cellular proliferation of the glomerulus.
• Etiology
• APSGN results from an antecedent infection of the skin
(impetigo) or throat (pharyngitis) caused by nephritogenic
strains of group A beta-hemolytic streptococci.
• Nephritogenicity is mainly restricted to certain M protein
serotypes (ie, 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60) that
have shown nephritogenic potential.
• Nontypeable group A streptococci are frequently isolated
from the skin or throat of patients with glomerulonephritis,
representing presumably unclassified nephritogenic
strains.
• Epidemiology
• Sporadic cases
• Epidemic outbursts
• seasonal variation: APSGN following upper respiratory tract
infection, pharyngitis, and tonsillitis is more common in winter
and spring, skin infections are commonly found to precede
APSGN have a peak incidence during summer and autumn.
• more frequent in children aged 2-12 years, with a peak
prevalence in individuals aged approximately 5-6 years.
• Reported age limite: 1 and 90
• 5% are younger than 2 years
• male-to-female ratio, 1.7-2:1
• Pathophysiology
• exact mechanism yet unclear
• mediated by an immunologic process
• Proposed theories:
• (1) glomerular trapping of circulating immune complexes
• (2) in situ immune antigen-antibody complex formation
resulting from antibodies reacting with either
streptococcal components deposited in the glomerulus
or with components of the glomerulus itself, - “molecular
mimicry.”
• Immune complex-mediated mechanism
• Nephritogenic streptococci produce proteins with unique
antigenic determinants. These antigenic determinants
have a particular affinity for sites within the normal
glomerulus. Following release into the circulation, the
antigens bind to these sites within the glomerulus. Once
bound to the glomerulus, they activate complement
directly by interaction with properdin.
• Glomerular-bound streptococcal antibodies also serve as
fixed antigens and bind to circulating antistreptococcal
antibodies, forming immune complexes. Complement
fixation via the classic pathway leads to the generation of
additional inflammatory mediators and recruitment of
inflammatory cells.
• Nonimmune complex-mediated
mechanisms: delayed-type
hypersensitivity, superantigens, and
autoimmune phenomena
• History
• absence of a clear history of a preceding documented
streptococcal infection.
• streptococcal pharyngitis may be followed by a nephritic
syndrome in 1-2 weeks
• Streptococcal pyoderma may be followed by a nephritic
syndrome in 3-6 weeks
• History
• Physicians must consider the possibility of
acute poststreptococcal glomerulonephritis
in children with symptoms that may be
secondary to hypertension or congestive
heart failure, even in the absence of visible
hematuria or a history of a preceding
streptococcal infection!
• Typical presentation:
• General symptoms: malaise, lethargy, anorexia, fever,
abdominal pain, and headache
• Edema- 85% of patients
• Edema usually appears abruptly and first involves the
periorbital area, but it may be generalized.
• The degree of edema deppends on:
• the severity of glomerular involvement,
• the fluid intake,
• the degree of hypoalbuminemia.
• The triad of edema, hematuria, and hypertension is
classic for APSGN!
• Typical presentation:
• Gross hematuria occurs at onset in 30-
50% of children with poststreptococcal
acute glomerulonephritis who require
hospitalization.
• The urine is usually described
as being smoky, cola colored,
tea colored, or rusty
• Oliguria – resolves in a week
• Typical presentation
• hypertension - in 50-90% of children who
are hospitalized
• systolic pressures greater than 200 mm
Hg and diastolic pressures greater than
120 mm Hg are not unusual.
• Hypertension usually resolves in 1-2
weeks and rarely requires long-term
treatment.
• Hypertensive encephalopathy
• Severe hypertension caused by retention
of sodium and water
• headache, vomiting, depressed
sensorium, confusion, visual disturbances,
aphasia, memory loss, coma, and
convulsions.
• Circulatory congestion
• Dyspnea, orthopnea, and cough
• Tachycardia/ bradicardia
• Pulmonary rales
• Cardiac failure is unusual
• Workup
• Cultures from the pharynx or skin may be
positive
• Streptococcal antibodies:
• Antistreptolysin (ASO)
• Antihyaluronidase (AHase)
• Antistreptokinase (ASKase)
• Antinicotinamide-adenine dinucleotidase (anti-
NAD)
• Anti-DNAse B antibodies
• Workup
• C3- briefly low, than normal
• Kidney biopsy- only indicated in atypical cases:
• Failure to document a recent streptococcal infection by a
rise in ASO or streptozyme titer
• Normocomplementemia
• Renal insufficiency, especially if the glomerular filtration
rate remains less than 30 mL/min/1.73 m2 for more than
1 week
• Persistently low complement (C3) levels beyond 6-8
weeks, without resolution of features of acute
glomerulonephritis.
• Recurrent episodes of hematuria, especially frank
hematuria
• Kidney biopsy:
• diffuse hypercellularity of endothelial and mesangial cells
and infiltration of the glomerular tuft with
polymorphonuclear cells.
• epithelial crescents
• Immunofluorescence: discrete granular deposits of IgG
and C3 in a capillary loop and mesangial distribution;
may be absent.
• heavy and sometimes confluent capillary loop deposits
with the total absence of mesangial deposits- described
as starry sky.
• Electron microscopy: subepithelial humps (electron-
dense deposits that may also occur in subendothelial
and intramembranous locations).
Intracapillary and occasional Granular capillary and mesangial staining

mesangial neutrophils pattern with segmental areas of
“lumpy-bumpy” staining
• Renal ultrasonography: normal to slightly enlarged

kidneys bilaterally with some evidence of increased
echogenicity
• Chest radiographs commonly demonstrate central
venous congestion in a hilar pattern, enlarged cardiac
shadow.
• Blood tests:
• mild anemia (normocytic, normochromic)
• Normal WBC and thrombocytes or leukocytosis or mild
thrombocytopenia
• Few cases of hypoproteinemia and hyperlipidemia
• concentrations of creatinine and blood urea nitrogen may
be mildly increased
• electrolyte profile is usually normal; hyperkalemia,
hyperphosphatemia and metabolic acidosis are only
present in patients with significant renal functional
impairment
• Total serum calcium, but not ionized calcium levels, may
be low
• Urine tests
• Urine output is most often reduced
• the urine is concentrated and acidic.
• glucosuria occurs occasionally
• proteinuria is commonly present- 3+ by dipstick,
corresponding to fewer than 2 g/m2/d; massive
proteinuria also present.
• Polymorphonuclear leukocytes and renal
epithelial cells
• hyaline and/or cellular casts
• Red blood cell casts
• Complement levels:
• Total complement- low for 6-8 weeks
• C3- low
• C4- normal
• C5- low
• Properdin- low
• Low serum complement level may indicate

the following systemic diseases:
• Systemic lupus erythematosus (SLE)
(focal, 75%; diffuse, 90%)
• Subacute bacterial endocarditis (90%)
• Visceral abscess
• "Shunt" nephritis (90%)
• Cryoglobulinemia (58%)
• Low serum complement level may indicate

the following renal diseases:
• Acute postinfectious glomerulonephritis
(>90%)
• MPGN: Type I (50-80%), type 2 (80-90%)
• A normal serum complement level may

indicate the following systemic diseases:
• Polyarteritis nodosa group
• Hypersensitivity vasculitis
• Wegener granulomatosis
• Henoch-Schönlein purpura
• Goodpasture syndrome
• A normal serum complement level may
indicate the following renal diseases:
• Immunoglobulin (Ig) A (or IgG-IgA)
nephropathy
• Idiopathic rapidly progressive
glomerulonephritis (RPGN)
• Anti-glomerular basement membrane
(GBM) disease
• Negative immunofluorescence findings
• Immune complex disease
• Treatment
• By the time the child with acute poststreptococcal
glomerulonephritis (APSGN) presents with symptoms,
the glomerular injury has already occurred, and the
healing process has begun. Thus, influencing the
ultimate course of the disease by any specific therapy
directed at the cause of the nephritis is not possible.
• Only a small percentage of patients with acute
glomerulonephritis require initial hospitalization, and
most of those are ready for discharge in 2-4 days. As
soon as the blood pressure (BP) is under relatively good
control and diuresis has begun, most children can be
discharged and monitored as outpatients.
• Diet:
• Acute phase: low-sodium, low-protein,
while the edema and hypertension are
present;
• limitation of fluid and salt intake in the child
who has either oliguria or edema
• potassium intake restriction in the oliguric
patient
• Limited activity is indicated during the
early phase
• Severe hypertension treatment:

• labetalol (0.5-2 mg/kg/h i.v),
• Diazoxide
• nitroprusside (0.5-2 mcg/kg/min iv)
• nicardipine 5 mg/h iv, maximum dose 15
mg/h
• furosemide at doses of 2 mg/kg iv
• hydralazine
• nifedipine
• Mild to moderate hypertension:

• Oral furosemide- 1-3 mg/kg/d
• hydralazine or nifedipine
• In anuria or oliguria avoid large doses of

furosemide; osmotic diuretics, such as
mannitol, are contraindicated, as they
might increase vascular volume
• Steroid therapy is indicated in:

• severe crescentic glomerulonephritis
• rapidly progressive glomerulonephritis
• Henoch-Schönlein purpura (HSP) nephritis
• membranoproliferative glomerulonephritis
• antibiotics (penicillin or erythromycin) for

10 days to ensure eradication of the
streptococcus may be recommended
• Differential diagnosis:
• Glomerulonephritis associated with other infections: Streptococcus
pneumoniae, Staphylococcus aureus and S epidermidis, Rickettsia
rickettsiae,Mycoplasma species, Meningococcus species,
Leptospira species
• Crescentic glomerulonephritis
• Diffuse proliferative glomerulonephritis
• Endocarditis-associated glomerulonephritis
• Hematuria
• IgA nephropathy
• Membranoproloferative glomerulonephritis
• Shunt nephritis
• Prognosis
• almost always favorable in children, but not so
with nonstreptococcal forms of the condition
• Edema usually resolves within 5-10 days, and
the blood pressure usually returns to normal
after 2-3-6 weeks.
• Proteinuria may disappear within the first 2-3
months or may slowly decrease over 6 months.
Intermittent or postural proteinuria has been
noted for 1-2 years after onset.
• Prognosis
• Gross hematuria usually disappears within 1-3 weeks
but may be exacerbated by physical activity.
• C3 concentration returns to normal in more than 95% of
patients by the end of 8-10 weeks.
• Microscopic hematuria usually disappears after 6
months, but its presence for as long as 1 year should not
cause undue concern, and even more prolonged
hematuria (1-3 y) has been observed in some patients
who ultimately have demonstrated complete resolution of
their renal disease.
• Strongly consider the possibility of chronic renal disease
when both hematuria and proteinuria persist longer than
12 months.
• Complications
• hypertension with or without central
nervous system manifestations
• anemia- autoimmune hemolytic,
diminished erithropoiesis
• pulmonary edema
• congestive heart failure, miocarditis
• acute kidney injury
Pediatric Nephrotic Syndrome
• Definition
• Nephrotic syndrome, or nephrosis, is defined by
the presence of nephrotic-range proteinuria,
edema, hyperlipidemia, and hypoalbuminemia.
While nephrotic-range proteinuria in adults is
characterized by protein excretion of 3.5 g or
more per day, in children it is defined as protein
excretion of more than 40 mg/m2/h or a first-
morning urine protein/creatinine of 2-3 mg/mg
creatinine or greater. 24 hour urine or first
morning urine may be used for analysis.
• Background
• Nephrotic syndrome is not a disease itself, but
the manifestation of many different glomerular
diseases.
• The glomerular diseases that cause nephrotic
syndrome generally can be divided into primary
and secondary etiologies. Primary (idiopathic)
nephrotic syndrome is associated with
glomerular diseases intrinsic to the kidney and
not related to systemic causes.
• Background
• Primary nephrotic syndrome may be caused by:
• minimal change nephrotic syndrome
• focal segmental glomerulosclerosis,
• membranous nephropathy,
• membranoproliferative glomerulonephritis,
• C3 glomerulonephritis,
• IgA nephropathy,
• diffuse mesangial proliferation
• It can be sensitive or resistant to corticosteroid
treatment.
Secondary nephrotic syndrome refers to an etiology extrinsic to

the kidney.
• Causes:
• (1) autoimmune and vasculitic diseases, such as Henoch-
Schonlein purpura, systemic lupus erythematosus and
antineutrophil cytoplasmic antibody (ANCA)–associated
vasculitis;
• (2) infectious diseases, such as congenital syphilis, malaria,
human immunodeficiency virus and hepatitis B and C;
• (3) malignancy;
• (4) environmental and drug exposure, such
as heroin and mercury;
• (5) systemic diseases such as diabetes mellitus
• Other types of nephrotic syndrome:
• Infantile NS (presenting before age 3 mo) and congenital NS
(presenting at age 4-12 mo) have been associated with defects
in the nephrin gene (NPHS1), phospholipase C epsilon 1 gene
(PLCE1), and the Wilms tumor suppressor gene (WT1).
• Familial, autosomal-recessive form of focal segmental
glomerulosclerosis is caused by mutations in the podocin gene
(NPHS2)
• autosomal-dominant forms of familial focal segmental
glomerulosclerosis is caused by Mutations in the α-actinin-4
gene (ACTN4) and the gene TRPC6.
• Nephrotic syndrome associated with other genetic syndroms:
Nail-patella syndrome, Pierson syndrome, Schimke immuno-
osseous dysplasia
• Etiology
• Causes of INS include the following:
• Minimal change nephrotic syndrome
• Focal segmental glomerulosclerosis
• Memebranoproliferative glomerulonephritis
• Membranous glomerulonephritis (MGN)
• C3 glomerulonephritis
• IgA nephropathy
• Idiopathic crescentic glomerulonephritis
• Etiology
• Causes of genetic or congenital nephrotic syndrome include the
following:
• Finnish-type congenital nephrotic syndrome (NPHS1, nephrin)
• Denys-Drash syndrome (WT1)
• Frasier syndrome (WT1)
• Diffuse mesangial sclerosis (WT1, PLCE1)
• Autosomal recessive, familial FSGS (NPHS2, podocin)
• Autosomal dominant, familial FSGS (ACTN4, α-actinin-4; TRPC6)
• Nail-patella syndrome (LMX1B)
• Pierson syndrome (LAMB2)
• Schimke immuno-osseous dysplasia (SMARCAL1)
• Galloway-Mowat syndrome
• Oculocerebrorenal (Lowe) syndrome
• Etiology
• Infections that can cause secondary
nephrotic syndrome include the following:
• Congenital syphilis, toxoplasmosis,
cytomegalovirus, rubella
• Hepatitis B and C
• HIV/acquired immunodeficiency syndrome
(AIDS)
• Malaria
• Etiology
• Drugs that can cause secondary nephrotic
syndrome include the following:
• Penicillamine
• Gold
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Interferon
• Mercury
• Heroin
• Pamidronate
• Lithium
• Etiology
• Systemic diseases :
• Systemic lupus erythematosus
• Malignancy - Lymphoma, leukemia
• Vasculitis- Wegener granulomatosis (granulomatosis
with polyangiitis), Churg-Strauss syndrome
(eosinophilic granulomatosis with polyangiitis),
polyarteritis nodosa, microscopic polyangiitis, Henoch-
Schönlein purpura (HSP)
• Immune-complex–mediated - Poststreptococcal
(postinfectious) glomerulonephritis
• Presentation
• Edema- initially edema is intermittent and
insidious, then generalised- anasarca.
• Periorbital, labial and scrotal
• Pitting
• More noticeable in the face in the morning
and predominantly in lower extremities
later in the day.
• Presentation
• A history of a respiratory tract infection
immediately preceding the onset of
nephrotic syndrome is frequent; upper
respiratory infections and otitis media are
often associated with relapses of
idiopathic nephrotic syndrome.
• Gross hematuria- more frequent in
membranoproliferative glomerulonephritis;
renal vein thrombosis must also be
considered.
• Presentation
• anorexia,
• irritability,
• fatigue,
• abdominal discomfort
• Diarrhea
• Respiratory distress- due to massive
ascites and thoracic compression or frank
pulmonary edema, effusions
• Clinical examination
• Edema- described above
• Tachypnea, respiratory distress
• Hypertension may be present
• Abdominal tenderness might indicate peritonitis.
• Hypotension and signs of shock can be present in
children presenting with sepsis.
• Thrombosis can cause various findings: tachypnea and
respiratory distress (pulmonary thrombosis/embolism),
hematuria (renal vein thrombosis), and seizure (cerebral
thrombosis).
• Workup
• To establish the presence of nephrotic syndrome :
• Urinalysis
• Urine protein quantification
(by first-morning urine
Confirms:
protein/creatinine or (1)nephrotic-range proteinuria,
24-hour urine protein) (2) hypoalbuminemia, and
• Serum albumin (3) hyperlipidemia
• Lipid panel
• Workup
• Complete blood count (CBC)
• Metabolic panel (Serum electrolytes, BUN and
creatinine, calcium, phosphorus, and ionized calcium
levels)
• Testing for HIV, hepatitis B and C
• Complement studies (C3, C4)
• Antinuclear antibody (ANA), anti–double-stranded DNA
antibody (in selected patients)
• 25-OH-vitamin D; 1,25-di(OH)-vitamin D;
• free T4; and thyroid-stimulating hormone
• Workup
• Genetic studies
• Kidney ultrasonography
• Chest radiography
• Mantoux test
• Kidney biopsy
• Workup- for children younger than 1:
• Congenital infection (syphilis, rubella,
toxoplasmosis, cytomegalovirus, HIV)
• Kidney biopsy
• Genetic tests for NPHS1, NPHS2, WT1, and
PLCE1 as guided by biopsy findings and clinical
presentation; presence of extrarenal syndromic
findings might indicate other genetic testing,
such as LAMB2 (Pierson
syndrome), LMX1B (nail-patella syndrome),
and SMARCAL1 ( Schimke immunoosseous
dysplasia)
• Workup- urine studies:
• RBC casts, if present, are suggestive of acute
glomerulonephritis, such as postinfectious nephritis,
or a nephritic presentation of chronic
glomerulonephritis, such as membranoproliferative
glomerulonephritis (MPGN).
• Granular casts may be present and are non-specific
to etiology
• First morning urine protein/creatinine
• 24 hour urine protein/creatinine
• 24-hour urine protein level more than 40 mg/m 2/h
• Workup- blood studies

• Serum albumin- less than 2.5 g/dL
• Elevated total cholesterol, low-density
lipoprotein (LDL)-cholesterol
• Elevated triglycerides with severe
hypoalbuminemia
• High-density lipoprotein (HDL)-cholesterol
(normal or low)
• Workup
• Hyponatremia
• Low total calcium, normal ionized calcium
• increased hemoglobin and hematocrit -
hemoconcentration
• platelet count often increased
• In acute kidney failure: elevated BUN and
creatinine levels
• Workup
• liver enzymes
• HIV infection, hepatitis B, and hepatitis C
• Low complement levels (C3, C4) are found in
postinfectious nephritis, MPGN, and lupus
nephritis.
• ANA and anti–double-stranded DNA antibody
assays are used to screen for collagen-vascular
disease in patients with systemic symptoms
(fever, rash, weight loss, joint pain)
• Workup- genetic tests:

• Mutations: NPHS1 and WT1, NPHS2, PLCE1,
LAMB2, SMARCAL1, NPHS2, ACTN4, TRPC6.
• Renal ultrasound
• Enlarged kidneys, normal echogenicity
• Chest X-ray: pleural effusion, pulmonary edema, TB
• Mantoux test
• Kidney biopsy- indications:
• Children younger than 1
• Symptoms of systemic disease (e.g., fever, rash,
joint pain)
• Laboratory findings indicative of secondary
nephrotic syndrome (e.g., positive ANA findings,
positive anti–double-stranded DNA antibody
findings, low complement levels)
• Elevated creatinine levels unresponsive to
correction of intravascular volume depletion
• A relevant family history of kidney disease
• Histologic findings
• Minimal change nephrotic syndrome
• Diffuse mesangial proliferation
• Focal glomerulosclerosis
• Membranoproliferative glomerulonephritis
• Membranous nephropathy
• A trial of corticosteroids is the first step in treatment of
idiopathic nephrotic syndrome (INS) in which kidney
biopsy is not initially indicated.
• Patients may be considered for steroid treatment prior to
kidney biopsy if they meet all of the following criteria:
• Age 1-8 years
• Normal kidney function
• No macroscopic (gross) hematuria
• No symptoms of systemic disease (fever, rash, joint pain,
weight loss)
• Normal complement levels
• Negative antinuclear antibody (ANA) assay
• Negative viral screens (ie, HIV, hepatitis B and C)
• No family history of kidney disease
• Kidney biopsy should be performed prior
to any immunosuppressive treatment,
including steroids, in patients who meet
one or more of the following criteria:
• Age younger than 1 year or older than 8
years
• Presence of recurrent gross hematuria
• Relevant family history of kidney disease
• Symptoms of systemic disease
• Positive viral screens
• Secondary nephrotic syndrome or INS other

than minimal change nephrotic syndrome are
indicated by:
• Sustained elevation in serum creatinine levels
• Low C3/C4 levels
• Positive ANA findings
• Positive anti–double-stranded DNA antibody
assay
• In these cases, histology guides treatment, and
steroids may or may not be indicated.
• In selected preadolescent patients older

than 8 years (≤12 y), empirical steroid
treatment can be considered.
• Children older than 12 years require a
kidney biopsy.
• Initial treatment: Oral prednisone, starting

as a daily dose of 60 mg/m2/day or 2
mg/kg/day (maximum, 60 mg/day) for 4–6
weeks. After 4–6 weeks, switch to 40
mg/m2 or 1.5 mg/kg (maximum, 40 mg) on
alternate days for 2–5 months with
tapering, with a minimum total duration of
treatment of 12 weeks
• Treatment of infrequent relapse (1 relapse in 6 months or

1-3 relapses in 12 months): Administer initial treatment
dose (60 mg/m2/day or 2 mg/kg/day) until urinary protein
is negative for 3 days; after urine is negative for protein
for 3 days, change prednisone to 40 mg/m2 or 1.5 mg/kg
(maximum, 40 mg) on alternate days for 4 weeks, then
stop or taper dose
• Treatment of frequent relapse (2 relapses in 6 months or
≥4 relapses in 12 months): Continue infrequent relapse
treatment for 3 months at lowest dose to maintain
remission or use corticosteroid-sparing agents, including
alkylating agents, levamisole, calcineurin inhibitors,
mycophenolate mofetil
• Hyperlipidemia treatment:
• Statins (simvastatin, lovastatin)
• Fibrates (gemfibrozil)
• Bile-acid binding resins (cholestyramine)
• Probucol- increases QT
• Gemfibrozil
• Thromboembolism
• anticoagulants (such as heparin) and/or
• fibrinolytic agents (ie, tissue plasminogen
activator, streptokinase, urokinase)
• secondary prevention, warfarin for 6
months
• Diuretic therapy
• furosemide (starting at 1-2 mg/kg/d)
• albumin at a dose of 1 g/kg for diuretic-
resistant edema
• Persisting hypertension
• Diuretics, angiotensin-converting enzyme
inhibitors or angiotensin II receptor
blockers, calcium channel blockers and
beta-blockers
• Frequently Relapsing and Steroid-Dependent Disease
• Alkylating agents: cyclophosphamide, chlorambucil, nitrogen
mustard
• Calcineurin inhibitors: cyclosporin A, tacrolimus
• Levamisole
• Mycophenolate mofetil
• Investigational treatment:
• Rituximab
• Rituximab
• Plasmapheresis
• Galactose
• Zinc
• Diet: sodium-restricted diet should be

maintained while a patient is edematous
and until proteinuria remits;
• protein restriction is not indicated, except
in cases of acute or chronic kidney failure
when severe azotemia
• Pneumococcal vaccination, yearly
influenza vaccination
• Prognosis: INS is usually a chronic,

relapsing disease and most patients
experience some degree of morbidity.
• The prognosis varies, depending on
whether the nephrotic syndrome is steroid
responsive or steroid resistant.

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Acute Poststreptococcal

Intracapillary and occasional Granular capillary and mesangial staining

• Renal ultrasonography: normal to slightly enlarged

• Low serum complement level may indicate

• Low serum complement level may indicate

• A normal serum complement level may

• Severe hypertension treatment:

• Mild to moderate hypertension:

• In anuria or oliguria avoid large doses of

• Steroid therapy is indicated in:

• antibiotics (penicillin or erythromycin) for

Secondary nephrotic syndrome refers to an etiology extrinsic to

• Workup- blood studies

• Workup- genetic tests:

• Secondary nephrotic syndrome or INS other

• In selected preadolescent patients older

• Initial treatment: Oral prednisone, starting

• Treatment of infrequent relapse (1 relapse in 6 months or

• Diet: sodium-restricted diet should be

• Prognosis: INS is usually a chronic,

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