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    ACUTE GLOMERULONEPHRITIS

    Preceptor :

    dr. Pulung M.Silalahi, Sp.A

    Presentant :

     Fatmawati (07120110091)

    Department of Pediatrics Rumah Sakit Bhayangkara Tk.1 R.S Sukanto-Jakarta

    Facuty of !edicine" Peita#ara an $ni%ersit

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    INTRODUCTION

    • Glomerulonephriti i a term ued !or "idne# dieae with an in$ammation and proli!eration o! glomerular %ell.

    • Glomerulonephriti (G&) i generall# %ategoried into either proli!eratie or non*proli!eratie .

    • +iagnoing the pattern o! G& i important e%aue out%ome - treatment depend on the t#pe.

    • A%ute pot trepto%o%%al glomerulonephriti i the mot %ommon %aue glomerulonephriti in %hildren.

    • A%ute glomerulonephriti uuall# re%ognie aed on

    %lini%al appearan%e u%h a gro hematuria, $uid oerload that mani!eted a edema and h#pertenion, and ome nding o! inu/%ien%# "idne# !un%tion li"e in%reaing o! & and %reatinine.

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    1. ANATOMY

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    Renal artery 

    Segmental Arteries

    Interlobar Arteries

     Arcuata arteries

    Interlobular Arteries

     Afferent arterioles

    Glomerular cappilaries

    Efferent arterioles

    Peritubular capillaries

    Interlobular veins

     Arcuate veins

    Interlobar veins

    Renal vein

    BLOOD SPPL! O" #$E %ID&E! 

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    THE NEPHRON 'onsist of t(o parts ) *+ Renal corpuscle

      , glomerulus

      , glomerular - Bo(man.s/ caps

    0+ Renal tubule

      , pro1imal convulute2 tubule

      , loop of 3enle

      , 2istal convulute2 tubule

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    *. P#,S/0, 

    #3e 4i2ney 2o ma5or (or4 of t3e urinary system+ #3e ot3er parts of t3e system

    mainly passagea(ays an2 storage areas+ "unction of 4i2ney inclu2e )

    •  Regulation of bloo2 ionic composition+

    • Regulation of bloo2 p$+

    • Regulation of bloo2 volume+

    • Regulation of bloo2 pressure+

    • 6aintenence of bloo2 osmolarity+

    • Pro2uction of 3ormones+

    • Regulation of bloo2 glucose level+

    • E1cretion of (astes an2 foreign substances+ By forming urine7 4i2neys 3elp

    e1crete (aste+

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    *+ Glomerular filtration ) (ater an2 most

    solutes in bloo2 plasma move across t3e (all of glomelural capillaries into t3e glomerular

    capsule t3en into renal tubule+

    0. Tubular reabsorbtion )(ater an2 solutes

    return to t3e bloo2 as it flo(s t3roug3

    peritubular capillaries an2 vasa recta+

    3. Tubular secretion+ ) flui2 flo(s along t3e

    renal tubule an2 t3roug3 t3e collecting 2uct7

    t3e tubule an2 2uct cells secrete ot3er materials7

    suc3 as (astes7 2rugs7an2 e1cess ions7 into t3e

    flui2+

    RI&E "OR6A#IO&

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    G3M45A5 F65A63&

    • Glomerular capillaries are relatively

    impermeable to proteins+

    • #3e flui2 t3at enters t3e capsular space is

    calle2 glomerular filtrate+ • 6ore t3an 889 of glomerular filtrate

    return to t3e bloo2 stream via tubular

    reabsorbtion7 so only *,0 liters is e1crete2

    in to urine+

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    •  he glomerular %apilla# wall i the ltration unit and

    %onit o! the !ollowing tru%ture 81. 4ndothelial %ell

    2.Glomerular aement memrane (GM)

    . Podo%#te

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    • 6at3ematically7 t3e G"R e:uals t3e pro2uct of %f an2 t3e net filtration pressure) G"R ; %f < &et filtration pressure

    #3e net filtration pressure representst3e sum of t3e 3y2rostatic an2 colloi2 osmotic forces t3at eit3er favor or oppose filtration across t3e glomerular capillaries+

    • #3e G"R can t3erefore be e1presse2 as G"R ; %f < -PG = PB = pG > pB/

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    Defnition

    • Glomerulonephritis is an inflammatory process affecting primarily the part of kidney that filters blood called

    glomerulus, with infiltration and proliferation of acute

    inflammatory cells.

    • The inflammation happens because of an immunologic process that makes pathologic abnormality of glomerulus

    • There can be both acute glomerulonephritis and chronic glomerulonephritis

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     Acute Glomerulnephritis • Acute glomerulonephritis is a disease

    characterized by sudden appearance of :

    1. Edema

    2. ematuria

    !. ypertension

    ". #liguria

    • This due to the immunologic response which triggers inflammation and proliferation of

    glomerular tissue that result in damage to the

    glomerular layer.

    Nephritic Syndrome

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    EPIDEMIOLOGY 

    • $%A&' can happened either sproradically or epidemically

    • Epidemic outbreaks ha(e taken place in communities with

    densely populated dwellings that ha(e poor hygienic conditions.

    • %poradic A$%&' following upper respiratory tract infection is more common in winter and spring in temperate areas, whereas

    skin infections are commonly found to precede A$%&' in the

    more tropical and subtropical areas.

    • )n de(eloping countries A$%&', usually occurs in children, predominately males, most cases occur in patients aged *+1*

    years.

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    &O& I&"E'#IOS

    Primary renal 2isease

    Systemic 2isease

    I&"E'#IOS

    *+ Ba4teri )

    most common )

    streptococcal species+

    0+ ?irus

    @+ "ungal

    + Parasites

    *+ 6PG&

    0+ IgA nep3ropat3y 

    @+ 6embranous

    nep3ropat3y 

    + 6inimal c3ange

    2isease

    *+ Lupus nep3riti2

    0+ Diabetic

    nep3ropat3y 

    @+ $enoc3,Sc3nlein

    purpura

    + Goo2pasture

    syn2rome

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    PATHOLOGY

    • Glomerular lesion in acute G& result in glomerular 2eposition of immune comple1es+

    • On gross appearance t3e

    4i2neys appear symmetrically enlarge2+

    • Immunoflueressence microscopy reveals a pattern of Clumpy,bumpy+

    • On electron microscopy7

    electrone 2ense 2eposurs or C3umps are observe2 on epit3elial si2e of GB6+

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    PATHOGENESIS

    • Glomerular in:ur# ma# e reult o! 8 geneti%, immunologi% , per!uion, or %oagulation diorder.

    • 6mmunologi% in:ur# to the glomerulu reult in

    glomerulonephriti .• 4iden%e that glomerulonephriti i %aued # immunologi% in:ur# in%lude morphologi% and immunopathologi% imilaritie to e;perimental immune* mediated glomerulonephriti< the demontration o!

    immune rea%tant (immunogloulin, %omplement) in glomeruli< anormalitie in erum %omplement< and the nding o! autoantiodie (anti*GM) in ome o! thee dieae .

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    PATHOGENESIS

    • #(o ma5or mec3anism of immunologic associate2 in5ury 3ave been establis3e2 )

    *+ in5ury resulting from 2eposition of soluble

    circulating antigen,antibo2y comple1es in t3eglomerulus+

    0+ In5ury by antibo2ies reacting in situ (it3in glomerulus

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    PATHOGENESIS IN PSAGN

    -*/ glomerular trapping of circulating immune comple1es an2

    -0/ in situ immune antigen,antibo2y comple1 formation resulting from antibo2ies reacting  (it3 eit3er streptococcal  components 2eposite2

    in t3e glomerulus or (it3 components of t3eglomerulus itself+

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    • $ost factor

    • Streptococcus factor , &ep3ritogenic strains of group A

     beta,3emolytic streptococci+

    , 6 Protein in bacterial (all -6

    protein serotypes ie7 *7 07 7 *07 *7

    0F7 87 FF7 F7 an2 H/

    , &ep3ritogenic antigen ) &ep3ritis

    associate2 streptococcal plasmin

    receptor -&APLr/ an2 pyogenic

    e1oto1in - SPEB/

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    Clinical Manifestation

    #ypical presentations Atypical presentation

    1. =ematuria8 the %lai% de%ription o! tea* or %ola*%olored urine

    o%%ur in appro;imatel# 2>?@0 o