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    Acute Glomerulonephritis

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    MochaLover
    1. Acute glomerulonephritis is an inflammation of the glomeruli that causes sudden onset of edema, hematuria, oliguria, and hypertension. 2. It is commonly caused by a prior streptococcal infection and affects children ages 5 to 12. Antigens from the bacteria deposit in the glomeruli, triggering an immune response that damages the glomerular filtration membrane. 3. Treatment involves strict monitoring, a 10-day course of antibiotics, fluid restriction, diuretics, and controlling hypertension and its complications through blood pressure monitoring and medication if needed. Follow up for at least a year is important to monitor recovery.

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    Acute Glomerulonephritis

    Uploaded by

    MochaLover
    270 views14 pages
    1. Acute glomerulonephritis is an inflammation of the glomeruli that causes sudden onset of edema, hematuria, oliguria, and hypertension. 2. It is commonly caused by a prior streptococcal infection and affects children ages 5 to 12. Antigens from the bacteria deposit in the glomeruli, triggering an immune response that damages the glomerular filtration membrane. 3. Treatment involves strict monitoring, a 10-day course of antibiotics, fluid restriction, diuretics, and controlling hypertension and its complications through blood pressure monitoring and medication if needed. Follow up for at least a year is important to monitor recovery.

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    Acute Nephritic Syndrome Post Strep. Glomerulonephritis

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    1. Acute glomerulonephritis is an inflammation of the glomeruli that causes sudden onset of edema, hematuria, oliguria, and hypertension. 2. It is commonly caused by a prior streptococcal infection and affects children ages 5 to 12. Antigens from the bacteria deposit in the glomeruli, triggering an immune response that damages the glomerular filtration membrane. 3. Treatment involves strict monitoring, a 10-day course of antibiotics, fluid restriction, diuretics, and controlling hypertension and its complications through blood pressure monitoring and medication if needed. Follow up for at least a year is important to monitor recovery.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    270 views14 pages

    Acute Glomerulonephritis

    Uploaded by

    MochaLover
    1. Acute glomerulonephritis is an inflammation of the glomeruli that causes sudden onset of edema, hematuria, oliguria, and hypertension. 2. It is commonly caused by a prior streptococcal infection and affects children ages 5 to 12. Antigens from the bacteria deposit in the glomeruli, triggering an immune response that damages the glomerular filtration membrane. 3. Treatment involves strict monitoring, a 10-day course of antibiotics, fluid restriction, diuretics, and controlling hypertension and its complications through blood pressure monitoring and medication if needed. Follow up for at least a year is important to monitor recovery.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 14

    ACUTE GLOMERULONEPHRITIS AMANINA ZAHRAA ZAINOL

    M121125934
    DEFINITION
    Acute glomerulonephritis (AGN) the inflammation of the glomeruli
    abrupt onset of one or more features of an Acute Nephritic Syndrome:
    1. Oedema e.g. facial puffiness.
    2. Haematuria.
    Microscopic /macroscopic (urine: tea-coloured or smoky)
    3. Oliguria
    4. Hypertension.
    CAUSES OF ACUTE GLOMERULONEPHRITIS
    POST-INFECTIOUS OTHERS (less common)
    Bacterial: Streptococcal commonest, Membranoproliferative
    Staphylococcus aureus, Mycoplasma glomerulonephritis (MPGN)
    pneumonia, Salmonella
    IgA nephropathy
    Virus: EBV, varicella, CMV
    SLE
    Fungi: Candida, aspergillus
    Subacute Bacterial Endocarditis
    Parasites: Toxoplasma, malaria,
    schistosomiasis Henoch-Schoenlein purpura
    POST INFECTIOUS AGN
    Common: Group A beta hemolytic streptococcus
    Assoc. With previous pharyngitis or impetigo
    Predominantly affects children from ages 5 to 12
    Incubation period is 2 to 4 weeks
    PATHOGENESIS
    Increased
    Antigen (group A Deposition of Ag- production of Leukocytes
    beta-hemolytic Antigen-antibody
    Ab Complex in epithelial cells infiltrate the
    streptococcus) product
    glomerulus lining the glomerulus
    glomerulus

    Restrict Scarring & loss of Thickening of


    glomerular blood glomerular glomerular
    Oliguria flow filtration filtration Haematuria
    (Reduce GFR) membrane membrane

    Hydrostatic
    Water retention HPT pressure Edema
    increases
    CLINICAL FEATURES
    Acute Nephritic Syndrome
    Edema, haematuria, oliguria, hypertension

    Hypertensive encephalopathy
    blurred vision, severe headaches, altered mental status, or new seizures.

    Pulmonary edema
    Tachypnoea, orthopnoea, and cough

    Nonspecific symptoms
    malaise, lethargy, abdominal pain, or flank pain are common.
    DIAGNOSIS: INVESTIGATION
    Urinalysis
    Haematuria, RBC cast: pathognomonic in AGN, Proteinuria: +

    Antistreptolysin O (ASO) Titer: >200IU/ml or high anti-DNAase B (serological marker for skin infection)
    Renal profile
    FBC: leukocutosis
    Complement level : C3 low at the onset of symptoms normalized by 6 weeks but C4 normal
    USS KUB : Not necessary if patient has clear cut acute nephritic syndrome.
    CXR: if suspected fluid overload
    Renal biopsy: only if
    Severe ARF requiring dialysis
    Absence of post-streptococcal infection
    Haematuria and proteinuria, diminished renal function, and/or a low C3 level persist more than 2 months after onset.
    MANAGEMENT
    Strict monitoring - fluid intake, urine output, daily weight, BP
    Penicillin V for 10 days to eliminate - haemolytic streptococcal infection or erythromycin
    Oral penicillin V 500 000 U for 10 days

    Fluid restriction
    Day 1 : up to 400 mls/m/day. Do not administer intravenous or oral fluids if child has pulmonary oedema.
    Day 2 : till patient diureses 400 mls/m/day (as long as patient remains in circulatory overload)
    When child is in diuresis free fluid is allowed

    Diuretic (e.g. Frusemide) -pulmonary oedema and hypertension.


    Diet no added salt to diet.
    Look out for complications :
    Hypertensive encephalopathy usually presenting with seizures
    Pulmonary oedema (acute left ventricular failure)
    Acute renal failure
    MANAGEMENT: HPT
    Asymptomatic 1. Bed rest & BP monitoring hourly
    2. BP high: Oral Nifedipine 0.25 0.5mg/kg & repeated 4 hourly if needed
    OR t.d.s
    3. Recheck BP hour later
    4. May add Frusemide: 1mg/kg/dose
    5. May add other anti-HPT: if BP still high
    Captopril 0.1-0.5 mg/kg 8 hourly
    Metoprolol 1-4 mg/kg 12 hourly
    6. BP monitoring hourly for 4 hours then 4 hourly if stable
    Symptomatic/severe Emergency management: reduce BP sufficiently to avoid HPT complications
    but maintain it at a level sufficient for vital organs.
    Symptom & signs: Target:
    Headache, vomiting, loss of 1. Reduce BP to <90th centile of BP for age, gender or height
    vision, convulsions, 2. Total BP to be reduced = observed mean BP desired mean BP
    papilloedema. 3. Reduced by 25% of target BP over 3-12 hours
    4. Next 75% is achieved over 48 hours
    MANAGEMENT: PULMONARY EDEMA
    1. Prop up patient
    2. Oxygen therapy: 2L/min, maintain SPo2 >95% OR Ventilator support
    3. IV Frusemide: 2mg/kg/dose stat, double the dose 4 hours later if poor response
    4. Fluid restriction: withhold fluid for 24 hours if possible
    5. Consider dialysis if no response to diuretics.
    FOLLOW UP
    at least 1 year
    Monitor BP
    Urinalysis and Renal Profile to evaluate recovery
    Repeat C3 level: 6 weeks later if not already normalised by the time of discharge.

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