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Nephrotic Syndrome (NS)

Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. The majority of cases are idiopathic, with minimal change nephrotic syndrome being the most common type. Edema develops due to a loss of negative charges in the glomerular capillary wall that increases permeability to proteins and causes a drop in colloid osmotic pressure. Treatment involves corticosteroids, diuretics, antibiotics for infection prevention, and hospitalization for complications such as dehydration. The prognosis is generally good, with mortality risks from infection and relapses decreasing over time.

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Nur Suci Amanah
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64 views16 pages

Nephrotic Syndrome (NS)

Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. The majority of cases are idiopathic, with minimal change nephrotic syndrome being the most common type. Edema develops due to a loss of negative charges in the glomerular capillary wall that increases permeability to proteins and causes a drop in colloid osmotic pressure. Treatment involves corticosteroids, diuretics, antibiotics for infection prevention, and hospitalization for complications such as dehydration. The prognosis is generally good, with mortality risks from infection and relapses decreasing over time.

Uploaded by

Nur Suci Amanah
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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NEPHROTIC SYNDROME (NS)

Definition
The syndrome nephrotic is characterized by

• Proteinuria (> 40mg/m2/hour),


• Hypoalbuminemia (albumin<2,5 g%),
• Edema, and
• Hyperlipidemia
Etiologi

90 % idiopathic nephrotic syndrome

75 % minimal change nephrotic syndrome (MCNS)


10 % focal segmental glomerulosclerosis (FSGS)
< 5 % membranous nephropathi

10 % Membrano proliferative glomerulonephritis


(MPGN)
Classification
1. Primary nephrotic syndrome
The term applied to disease limited to the kidney
• Minimal change, lipoid disease, nil disease
• Focal segmental schlerosis
• Membranous nephropathy
• Proliferative nephritis (mesangial, focal, diffuse)
2. Secondary nephrotic syndrome
• Lupus nephritis
• Henoch-Schonlein purpura
• Heriditery nephritis
• Drugs,toxins,infections
Pathophysiology

The underlying pathogenetic


abnormality of NS is proteinuria
due to an increase in glomerular
capillary wall permeability.
1. The capillary wall loss the negative charge
glycoprotein barries
2. Increase glomerular permeability to proteins
In principle edema may develop
by two mechanism :
A. The capillary hydraulic pressure
increases as a result of constant
elevation of plasma volume : “overflow”
concep (nehpritic edema)
B. The colloid osmotic pressure in plasma
drops : “underfilling “ theory (nephrotic
edema
Nephritic edema Nephrotic edema
Renal salt and water Alteration of Starling forces
retention (Capillary colloid osmotic pressure )
Expansion of
circulatory volume Edema formation

Alteration of Starling forces Volume contraction


(Capillary hydraulic pressure )

Edema formation Renal salt and water retention

Proposed scheme of edema formation in


patiens with glomerular disease
Proteinuria

Hypoalbuminemia

Plasma oncotic pressure

Transudation of fluid from intravascular


compartment to the interstitial space (= edema)

Exacerbating Release Decreasing edema


antidiuretic intravascular volume
hormone
Reabsorbed Na & H2O are
Renal perfusion lost in the interstitial space

Activating the Renin-Angiotensin-


Aldosteron system

Na distal tubular reabsorption

H2O Reabsorption in the collecting duct

Mechanism of edema formation in “Circulation underfilled” Theory


Clinical manifestation
Idiopathic nephrotic syndrome
• Prevalency male : female = 2 : 1
• Most commonly between the age of 2 and 6 years
• Edema, initially noted around the eyes, and in the lower
extremities is “ pitting”. It becomes generalized

Diagnosis
 Proteinuria on the dipstick +2 (approximately 100 mg/dl).
 Serum cholesterol and triglycerides levels are elevated
 Serum albumin levels is generally less than 2,5 gram/dl
 Renal function may be normal or reduced
Laboratory Test in N S

To confirm NS
Serum (albumin, globulin, cholesterol)
Urine protein : qualitative (dipstick : albumin)
quantitative (24-hr collection)
To distinguish primary from secondary NS
Urinalysis
Screening test for sickle cell anemia
Serum C3 complement
Serum antinuclear antibody
Hepatitis B surface antigen
Management test
Complete Blood Counts , serum
electrolytes,serum creatinine, BUN
Management

A. General Principles
• No sistematic dietary advice is necessary
in simple cases of SRNS
• Antibiotic is indicated in cellulitis, peritonitis, septicemia,etc.
• Diuretic: Edematous child in the absence of hypovolemia
diuretic : furosemide (1-2 mg /kgBW/day)
• Albumin infusions : Expensive & can hazardous but may be life
saving, its indications include :
• Hypovolemia (abdominal pain, hypotension, oliguria)
• Renal insufficiency

Complication :
Infections : S.pneumoniae, chickenpox and measles
Thrombocytosis : Hypercoagulable state.
B.Corticosteroid

• Prednisolon an active metabolit of


prednison.
• Both have been widely used but remains
unclear whether their mode of action is -
anti-inflamatory,
- immunosupressive,
- or both
Initial Treatment

a. Introduction of remission
Prednisolon 60 mg/m2/day or 2 mg/kgBW/ day
at least 4 weeks daily being required

b. Withdrawal : There are two alternative :


- Modified ISKDC regimen :
40 mg/m2 BSA on alternate days for 4 weeks
- Withdraw prednisolon gradually :
over 6-8 weeks or longer
2. Relapse
A characteristic feature of SRNS is to relapse
(recurrence of proteinuria often triggered by
infection or allergic events)
Relapse are usually as responsive as the initial
episode. Up to 25 % of the relapses
spontaneously remit
Prompt treatment is necessary in children who
have a history of severe relapses, especially if
complicated by hypovolemia.
Prednisolon 60 mg/m2/day until remission is
sufficient.
Acute complication of nephrotic syndrome

Without steroid therapy


Bacterial infection
Hypovolemia
Hypercoagulability (thromboembolic phenomena)
Respiratory embarrassment

With steroid therapy


Bacterial infection
Hypovolemia
Hypercoagulability
Respiratory embarrassment
Hypertension
Altered behavior
Steroid withdrawal (benign intracranial hypertension)
Indications for hospital
admission or patient with
nephrotic syndrome

• Newly diagnosed patiens


• Severe dehydrations (poor intake, persistent
vomiting)
• Unexplained fever (suspected bacterial infection)
• Refractory edema (respiratory distress)
• Peritonitis
• Renal insufficiency (elevated serum creatinine)
Outcome

Mortality
The mortality rate for SSNS is 1 to 2,5 %
usually from sepsis, hypovolemia, and
thrombocytosis.

Relapses
In most cases the relapses eventually cease
The earlier the onset of SRNS, the more likely
that the disease will be protracted

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