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    Nephrotic Syndrome in Children

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    Alokh Saha Raj
    Nephrotic syndrome in children is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. There are three main types: congenital, primary, and secondary. Primary nephrotic syndrome includes minimal change nephrotic syndrome, mesangial proliferation, and focal segmental glomerulosclerosis. Secondary nephrotic syndrome can be caused by systemic illnesses, infections, allergies, or exposures. Minimal change nephrotic syndrome, the most common type in children, often responds well to steroid treatment but has a high risk of relapse. Treatment involves supportive care, steroids such as prednisone, and managing any complications.

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    Nephrotic Syndrome in Children

    Uploaded by

    Alokh Saha Raj
    53 views27 pages
    Nephrotic syndrome in children is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. There are three main types: congenital, primary, and secondary. Primary nephrotic syndrome includes minimal change nephrotic syndrome, mesangial proliferation, and focal segmental glomerulosclerosis. Secondary nephrotic syndrome can be caused by systemic illnesses, infections, allergies, or exposures. Minimal change nephrotic syndrome, the most common type in children, often responds well to steroid treatment but has a high risk of relapse. Treatment involves supportive care, steroids such as prednisone, and managing any complications.

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    Nephrotic syndrome

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    NEPHROTIC-SYNDROME-1

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    Nephrotic syndrome in children is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. There are three main types: congenital, primary, and secondary. Primary nephrotic syndrome includes minimal change nephrotic syndrome, mesangial proliferation, and focal segmental glomerulosclerosis. Secondary nephrotic syndrome can be caused by systemic illnesses, infections, allergies, or exposures. Minimal change nephrotic syndrome, the most common type in children, often responds well to steroid treatment but has a high risk of relapse. Treatment involves supportive care, steroids such as prednisone, and managing any complications.

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    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    53 views27 pages

    Nephrotic Syndrome in Children

    Uploaded by

    Alokh Saha Raj
    Nephrotic syndrome in children is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. There are three main types: congenital, primary, and secondary. Primary nephrotic syndrome includes minimal change nephrotic syndrome, mesangial proliferation, and focal segmental glomerulosclerosis. Secondary nephrotic syndrome can be caused by systemic illnesses, infections, allergies, or exposures. Minimal change nephrotic syndrome, the most common type in children, often responds well to steroid treatment but has a high risk of relapse. Treatment involves supportive care, steroids such as prednisone, and managing any complications.

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    NEPHROTIC SYNDROME

    In
    Children
    Definition

    • It is a clinical syndrome characterized by the


    following 4 cardinal features:
    – Massive proteinuria (>1 gm/m2 /day)
    – Hypoalbuminaemia ( ≤2.5 gm/dl)
    – Generalized oedema
    – Hyperlipidaemia (>200 mg/day)
    Types

    • CONGENITAL NEPHROTIC SYNDROME


    • PRIMARY NEPHROTIC SYNDROME
    • SECONDARY NEPHROTIC SYNDROME
    PRIMARY NEPHROTIC SYNDROME

    1. Minimal change nephrotic syndrome


    2. Mesangial proliferation
    3. Focal segmental glomerulosclerosis
    SECONDARY NEPHROTIC SYNDROME
    – Systemic Illness
    • SLE, HSP, IDDM, obesity
    – Infections
    • Hep B, C; HIV, malaria, syphilis, schistosomiasis, parvo
    B19
    – Allergy
    • Bee stings, milk
    – Exposures
    • NSAID’s, Penicillamine, gold, ampicillin, heavy metals
    – Malignancy
    Lymphomas, leukaemia
    Minimal Change Nephrotic Syndrome

    • Commonest type in children.


    • Prompt response to steroid
    • High tendency to relapase
    • Not associated with hypertension, haematuria
    and azotaemia
    Pathogenesis (MCNS)

    • Glomerular membrane looses its capacity to


    withhold albumin
    • Albumin passes to glomerular filtrate
    • Leads to proteinuria
    • Hypoalbuminaemia
    • Loss of plasma oncotic pressure
    • Shifting of fluid from plasma to interstitial space
    • Development of oedema, ascites, pleural effusion
    Microscopic Examination

    • Light microscopy:
    No detectable glomerular pathology is noted.
    • Electron microscope:
    Fusion of foot process of podocytes in
    glomerular membrane.
    Clinical Manifestations

    • Age: 2-6 years


    • Facial puffiness, massive peri-orbital swelling
    • Generalized oedema( Ascites ,Scrotal swelling)
    • Scanty urination
    • BP normal
    • Colour of urine normal
    • BSUA: ++++
    Features of Complication
    • Cough & respiratory distress (pleural effusion)
    • Abdominal pain (ischemia, RVT, peritonitis)
    • Pain, redness & tenderness of skin( cellulitis)
    • Fever & dysuria (UTI)
    • Haematuria
    • Diarrhoea
    • Neurodeficit like hemiplegia
    • Features of steroid toxicity
    Investigation
    1. Urine R/M/E: protein +++, RBC usually absent
    2. 24 hours urinary total protein:
    (> 1gm/m2/day) or (3.5 gm/day)
    3. Spot urinary protein creatinine ratio: >2
    4. Serum total protein : low
    5. Serum albumin: low
    6. Serum cholesterol: high
    7. Serum C3 : Normal in MCNS
    8. Serum electrolyte: Normal
    Investigation Cont’d…
    • For aetiology and complication:
    • CBC: usually normal
    • Urine C/S: for UTI
    • X-ray chest: (pleural effusion, TB)
    • USG of Abdomen: (RVT, ascites)
    • Renal biopsy
    Treatment
    A. Supportive:
    • Diet: Normal ( protein rich)
    • Fluid: usually liberal intake.
    Restriction in severe oedema
    • Mx of oedema:
    Diuretics usually avoided except in severe cases.
    • Antibiotics
    • Scrotal support by coconut bandage
    Rx Cont’d…
    B. Specific: Prednisolone

    a. 60mg/m2/day or 2mg/kg/day (maximum 60 mg) in


    single morning dose for 4- 6 weeks .

    b. Followed by 40mg/m2/day in single morning dose every


    alternate day for 8 weeks to 5 months, with tapering the
    dose.

    .
    C. Treatment of Complication
    • Spontaneous bacterial peritonitis
    • UTI
    • Renal vein thrombosis
    • Gut ischaemia
    • Thrombo-embolic manifestation
    • Prompt Rx of infection
    • Dyslipidaemia
    Some Definitions
    • Response: attainment of remission within the initial 4
    weeks of corticosteroid therapy.
    • Remission: Consists of urinary protein: creatinine ratio
    of <0.2 or <1+ protein on urine for 3 consecutive days.
    • Relapse NS: Defined as of urinary protein: creatinine
    ratio of >2 or ≥3+ protein on urine for 3 consecutive
    days.
    • Steroid resistance: Failure to achieve remission after 8
    weeks of steroid therapy.
    Treatment of Relapse Case
    Prednisolone :

    a. 60mg/m2/day in single morning dose until


    protein free urine for 3 consecutive days.
    b. Followed by 40mg/m2/day in single morning
    dose every alternate day .
    c. Duration of Rx depends on frequency of
    relapse of the individual child.
    Indications for Biopsy
    • Pretreatment
    • Onset age < 6 months
    • Macroscopic hematuria
    • Microscopic hematuria and
    HTN • Post treatment
    • Low C3 – Steroid resistance
    • Renal failure – Frequent relapsers
    • Onset between <1 year or > – Before starting
    12 years cyclophosphamide
    • Persistent HTN or hematuria or cyclosporine
    Steroid Toxicity
    • Cushingoid habitus • Peptic ulceration
    • Obesity • Pancreatitis
    • Striae • Posterior lens opacities
    • Hirsutism • Myopathy
    • Acne • Increased ICP
    • Growth failure • Susceptibility to
    • Avascular necrosis infection
    • Osteoporosis
    Follow Up
    • Maintaining nephrotic chart
    ( pulse, BP, weight, oedema, BSUA, abdominal
    girth, intake-output chart)
    • 2 weekly follow-up
    • Advice caregiver for heat coagulation
    • Signs of steroid toxicity.
    THANK YOU

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