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    Glomerulonephritis

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    Acute glomerulonephritis (AGN) is an inflammation of the glomeruli most often caused by a streptococcal infection that leads to the formation of immune complexes, with clinical manifestations including edema, hematuria, hypertension, and proteinuria. AGN is typically diagnosed based on clinical history, lab findings like reduced serum C3 and hematuria, and resolved within 1-2 weeks with supportive care like antibiotics, diuretics and antihypertensives. Prognosis is generally good with over 90% recovery but chronic kidney disease may occur in 5-10% of cases.

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    Glomerulonephritis

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    api-19916399
    931 views35 pages
    Acute glomerulonephritis (AGN) is an inflammation of the glomeruli most often caused by a streptococcal infection that leads to the formation of immune complexes, with clinical manifestations including edema, hematuria, hypertension, and proteinuria. AGN is typically diagnosed based on clinical history, lab findings like reduced serum C3 and hematuria, and resolved within 1-2 weeks with supportive care like antibiotics, diuretics and antihypertensives. Prognosis is generally good with over 90% recovery but chronic kidney disease may occur in 5-10% of cases.

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    Acute glomerulonephritis (AGN) is an inflammation of the glomeruli most often caused by a streptococcal infection that leads to the formation of immune complexes, with clinical manifestations including edema, hematuria, hypertension, and proteinuria. AGN is typically diagnosed based on clinical history, lab findings like reduced serum C3 and hematuria, and resolved within 1-2 weeks with supportive care like antibiotics, diuretics and antihypertensives. Prognosis is generally good with over 90% recovery but chronic kidney disease may occur in 5-10% of cases.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    931 views35 pages

    Glomerulonephritis

    Uploaded by

    api-19916399
    Acute glomerulonephritis (AGN) is an inflammation of the glomeruli most often caused by a streptococcal infection that leads to the formation of immune complexes, with clinical manifestations including edema, hematuria, hypertension, and proteinuria. AGN is typically diagnosed based on clinical history, lab findings like reduced serum C3 and hematuria, and resolved within 1-2 weeks with supportive care like antibiotics, diuretics and antihypertensives. Prognosis is generally good with over 90% recovery but chronic kidney disease may occur in 5-10% of cases.

    Copyright:

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    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 35

    Acute glomerulonephritis(AGN)

    Teacher ： Yanli Zhang


    Department ： the Third hospital
    affiliated to ZhengZhou University
    OUTLINE
    Introduction Laboratory
    Etiology and evaluation
    epidemiology Diagnosis
    Pathogenesis Treatment
    Pathology  Prognosis
    Clinical Prevention
    manifestations
    1 Introduction
    The disease is the classic example
    of the acute nephritic syndrome:
    the sudden onset of gross
    hematuria , edema, hypertension,
    and renal insufficiency

    It was the most common cause of


    gross hematueria in children; now
    is IgA nephropathy
    Introduction
    The course of AGN is less than 1 year
    Most AGN belong to acute
    poststreptococcal glomerulonephritis
    (APSGN)
    AGN is 53.7% of urine system diseases
    during same time
    AGN is common during 5~14 years old
    Male: female is equal to 2:1
    2 Etiology and epidemiology

    APSGN follows infection of throat or skin


    During cold weather, APSGN follows
    streptococcal pharyngitis ,whereas
    during warm weather ,APSGN follows
    streptococcal skin infections or
    pyoderma
    The disease is most commonly sporadic
    3.Pathogenesis
    Although morphologic studies and a
    depression in the serum complement
    (C3) level strongly suggest that APSGN
    is mediated by immune complexes, the
    precise mechanisms by which
    nephritogenic streptococci induce
    complex formation remain to be
    determined.
    pathogenesis
    Formation of immune complexes
    including antibodies and streptococcal
    antigens
    Localization (deposition) on
    subepithelial portion of glomerular
    basement membrane
    This leads to localized mesangial and
    endothelial cell proliferation
    Streptococci infection
    complex formation

    C3↓
    AGN

    Mesangial cell
    proliferation Mesangial matrix
    Blood capillary close off
    destroy

    GFR↓ Oliguria or anuira Proteinuria


    hematuria
    Salt and water Edema
    retention hypertension
    4. Pathology
    Most forms of AGN, the kidney appear
    symmetrically enlarged .
    On early phase , classic AGN appear
    endocapillary proliferative
    On light microscopy, AGN appear
    enlarged and relatively bloodless and
    diffuse mesangial cell proliferation with
    an increase in mesangial matrix
    Pathology
    Polymorphonuclear leukocytes and
    neutrophil are common in glomeruli
    during the early stage of the disease.
    Crescents and interstitial inflammation
    may be seen in severe cases.
    On electron microscopy, electron-dense
    deposits, or “humps” are observed on the
    epithelial side of the glomerular basement
    membrances(GBMs)
    In endocapillary proleferative GN,
    “hump” appear outside of basement
    In endocapillary proliferative GN,
    appear enlarged and bloodless
    ,mesangial proliferation and
    5.Clinical manifestations

    General manifestations
    Antecedent infection
    Typical manifestations
    Severe manifestations
     Atypical manifestations
    5.1 General manifestations
    Many people with glomerulonephritis
    have no symptoms
     When symptoms occur, they are often
    flu-like, such as general fatigue, nausea,
    vomiting, loss of appetite, fever, and
    abdominal and joint pain.
    These types of general symptoms can
    continue for up to one month before
    symptoms of kidney failure appear.
    5.2 Antecedent infection
    90% patients have an
    antecedent
    streptococcal infection
    Respiratory and skin
    infections are chief
    Typical manifestation is
    6~12 days after
    pharyngitis or 14~28
    days after skin infection
    5.3 Typical manifestations
    ①Edema : 70% show
    edema; unsunken;
    face and eyelid upper
    are generally involved
    ②Hemuturia:
    50%~70% show gross
    hematosis ,after
    1~2wk, change into
    microscopic
    hematosis
    Typical manifestations
    ③Proteinuria: in general, <3g/d
    ④Hypertension:30%~80% show
    hypertension, during preschool
    age >120/80mmHg, school age
    >130/90mmHg
    Urine volume: decrease
    Resolution should occur within 2
    weeks , if not , consider other causes
    5.4 Severe manifestations
    Severe cycle bloodshot

    Hypertensive encephalopathy

    Acute renal failure


    ①Severe cycle bloodshot
    Cause: salt and water retention
    cause blood volume increase
    Alerting when AGN children show
    tachypnea or moist crackles
    Severe show dyspnea, gallop
    rhythm, edema worsen, even die
    ②Hypertensive encephalopathy
    Cause: vessel plasma
    Hypertension suddenly ascend
    >150~160/100~110mmHg
    Symptoms: headache, vomiting,
    diplopia, even convulsion, coma
    After hypertension controlled,
    these symptoms disappear
    ③Acute renal failure
    Causes: mesangial cell
    proliferation, blood capillary close
    off, GFR↓
    Symptoms: Oliguria or anuira,
    electrolyte disturbances,
    metabolic acidosis
    5.5 Atypical manifestations
    AGN has no symptoms: only
    microscopic hematouria, no other
    clinical manifestations
    AGN has symptoms out of kidney: has
    streptococcal history, serum C3 level is
    reduced, edema, hypertension is
    notable, but urine routine is normal
    AGN show nephritic syndrome: edema,
    proteinuria is notable, but pathology
    change is typical
    6. Laboratory evaluation
    1. Urine routine ： proteinuria 1+~3+ ，
    including RBC and cast
    2. ASO↑
    3. C3↓
    4. ESR ↑
    (erythrocyte sedimentation rate )
    Laboratory evaluation
    5. A 24 hour urine collection allows
    measurement of the excretion of
    proteins and creatinine.
    6. Creatinine clearance from the
    bloodstream by the kidneys is
    considered an index of the
    glomerular filtration rate
    kidney biopsy
    Kidney biopsy is essential to
    establish a diagnosis of atypical
    or prolonged AGN, determine the
    cause, and create an effective
    treatment plan and know its
    prognosis
    7. Diagnosis
    ①For about 1~3wk before AGN has
    streptococcal infection
    ②Clinical manifestations: edema,
    hypertension, hematuria, proteinuria
    ③Urinalysis finding protein, RBC, cast
    ④Serum C3 level reduce and/or ASO↑
    8. Treatment
    Goals of treatment

    Principles of treatment
    Goals of treatment
    Stop the ongoing inflammation and
    lessen the degree of scarring that
    ensues.
    Decrease the damage to the glomeruli
    Decrease the metabolic demands on
    the kidneys
    Improve kidney function.
    Principle of Management
    • [No special therapy]
    • 1. Bed Rest
    Reduce activities according to the progress
    of disease
    2.Diet
    Restrict fluid and daily salt intake
    azotemia—restrict protein intake
    Principle of Management
    • 3.Antibiotic therapy—Penicillin7~10d
    • 4.Symptomatic therapy
    Edema---Diuretics
    (furosemide, spironolactone)
    Hypertention---Antihypertensive drugs
    (nifepine)
    Hypertensive Encephalopathy---sodium
    nitroprusside
    Principle of Management
    Kidney failure--- dialysis
    Once kidney failure has occurred, waste
    products must be removed from the bloodstream
    for the kidneys through a process called dialysis.

    A kidney transplant may also be an option.


    9. Prognosis

    Recovery is >90%

     with <1% mortality in past

     chronic disease in 5-10%


    10. Prevention
    Avoiding upper respiratory infections,
    as well as other acute and chronic
    infections, especially those of a
    streptococcal origin.

    Cultures of the infection site, usually


    the throat, should be obtained and
    antibiotic sensibility of the offending
    organism determined.
    Prevention
    Prompt medical assessment for
    necessary antibiotic therapy should
    be sought when infection is
    suspected.
     The use of prophylactic
    immunizations is recommended as
    appropriate.

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