presentasi referat gna
TRANSCRIPT
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ACUTE GLOMERULONEPHRITIS
Preceptor :
dr. Pulung M.Silalahi, Sp.A
Presentant :
Fatmawati (07120110091)
Department of PediatricsRumah Sakit BhayangkaraTk.1 R.S Sukanto-Jakarta
Facuty of !edicine" Peita#ara an $ni%ersit
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INTRODUCTION
• Glomerulonephriti i a term ued !or "idne# dieae withan in$ammation and proli!eration o! glomerular %ell.
• Glomerulonephriti (G&) i generall# %ategoried intoeither proli!eratie or non*proli!eratie .
• +iagnoing the pattern o! G& i important e%aueout%ome - treatment depend on the t#pe.
• A%ute pot trepto%o%%al glomerulonephriti i the mot%ommon %aue glomerulonephriti in %hildren.
• A%ute glomerulonephriti uuall# re%ognie aed on
%lini%al appearan%e u%h a gro hematuria, $uid oerloadthat mani!eted a edema and h#pertenion, and omending o! inu/%ien%# "idne# !un%tion li"e in%reaing o!& and %reatinine.
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1. ANATOMY
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Renal artery
Segmental Arteries
Interlobar Arteries
Arcuata arteries
Interlobular Arteries
Afferent arterioles
Glomerular cappilaries
Efferent arterioles
Peritubular capillaries
Interlobular veins
Arcuate veins
Interlobar veins
Renal vein
BLOOD SPPL! O" #$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 ofglomelural 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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G3M45A5 F65A63&
• 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
%onit o! the !ollowing tru%ture 81. 4ndothelial %ell
2.Glomerular aement memrane (GM)
. Podo%#te
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• 6at3ematically7 t3e G"R e:uals t3epro2uct of %f an2 t3e net filtrationpressure)G"R ; %f < &et filtration pressure
•
#3e net filtration pressure representst3e sum of t3e 3y2rostatic an2 colloi2osmotic forces t3at eit3er favor oroppose filtration across t3eglomerular capillaries+
• #3e G"R can t3erefore be e1presse2as G"R ; %f < -PG = PB = pG > pB/
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Defnition
• Glomerulonephritis is an inflammatory process affectingprimarily the part of kidney that filters blood called
glomerulus, with infiltration and proliferation of acute
inflammatory cells.
• The inflammation happens because of an immunologicprocess that makes pathologic abnormality of glomerulus
• There can be both acute glomerulonephritis and chronicglomerulonephritis
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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 whichtriggers 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 ismore 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'#IOS
Primary renal 2isease
Systemic 2isease
I&"E'#IOS
*+ Ba4teri )
most common )
streptococcal species+
0+ ?irus
@+ "ungal
+ Parasites
*+ 6PG&
0+ IgA nep3ropat3y
@+ 6embranous
nep3ropat3y
+ 6inimal c3ange
2isease
*+ Lupus nep3riti2
0+ Diabetic
nep3ropat3y
@+ $enoc3,Sc3nlein
purpura
+ Goo2pasture
syn2rome
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PATHOLOGY
• Glomerular lesion in acute G&result in glomerular 2epositionof immune comple1es+
• On gross appearance t3e
4i2neys appear symmetricallyenlarge2+
• Immunoflueressencemicroscopy reveals a pattern ofClumpy,bumpy+
• On electron microscopy7
electrone 2ense 2eposurs orC3umps are observe2 onepit3elial si2e of GB6+
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PATHOGENESIS
• Glomerular in:ur# ma# e reult o! 8 geneti%,immunologi% , per!uion, or %oagulation diorder.
• 6mmunologi% in:ur# to the glomerulu reult in
glomerulonephriti .• 4iden%e that glomerulonephriti i %aued #immunologi% in:ur# in%lude morphologi% andimmunopathologi% imilaritie to e;perimental immune*mediated glomerulonephriti< the demontration o!
immune rea%tant (immunogloulin, %omplement) inglomeruli< anormalitie in erum %omplement< and thending o! autoantiodie (anti*GM) in ome o! theedieae .
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PATHOGENESIS
• #(o ma5or mec3anism of immunologic associate2in5ury 3ave been establis3e2 )
*+ in5ury resulting from 2eposition of soluble
circulating antigen,antibo2y comple1es in t3eglomerulus+
0+ In5ury by antibo2ies reacting in situ (it3inglomerulus
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PATHOGENESIS IN PSAGN
-*/ glomerular trapping of circulating immunecomple1es an2
-0/ in situ immune antigen,antibo2y comple1formation 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 F7 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 %lai% de%ription o! tea* or %ola*%olored urine
o%%ur in appro;imatel# 2>?@0 o! patient2. 4dema8 4dema uuall# appear aruptl# and rt inole the
periorital area, ut it ma# e generalied
. =#pertenion 8 =#pertenion o%%ur in appro;imatel# B0?90o! %ae . Cereral %ompli%ation o! h#pertenion in%luding
heada%he, eiure, mental tatu %hange, and iual%hange o%%ur in 0?> o! %hildren
•+ &onpe%i% #mptom u%ha malaie, letharg#, adominalpain, or $an" pain are %ommon.
•. =#pertenion uuall# normalie # D*@ wee" a!ter onet.
•. Peritent mi%ro%opi% hematuria %an perit !or 1*2 #ear a!terthe initial reentation
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1. Latent Phase:
#3e interval bet(een e1posure to an
infectious organism an2 t3e clinical
appearance of 2isease+
2. Acute Phase
#3e acute p3ase generally resolves
(it3in H, (ee4+
3. eco!ery Phase
Recovery p3ase occurs after resolution
of flui2 overloa2 (it3 2iuresos,eit3er
spontaneous an2Jor p3armacologically
in2uce2, along (it3 normaliKation of
bloo2 pressure an2 resolution of gross
3ematuria+
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DIAGNOSIS• Anamnesis• P3ysical e1amination
• Laboratory fin2ings
*+ urinalysis ) RB' casts7 proteinuria7 P6& leu4ocytes
0+ G"R is often 2ecrease2 2uring acute p3ase of t3e2isease
@+ Serological mar4ers ) ASO titer an2 2epression of c@level+
• Renal biopsy
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DIFFERENTIAL DIAGNOSIS
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COMPLICATION
• =#pertenie en%ephalopath#.
• Prolonged h#pertenion %an lead tointra%ranial leeding.
• 3ther potential %ompli%ation in%ludeheart !ailure, h#per"alemia,h#perphophatemia, h#po%al%emia,a%idoi,eiure, and uremia.
• A%ute renal !ailure
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PREENTION
• ?accine M
• #3e most effective public 3ealt3 measure in t3e2eveloping (orl2 is to improve 3ygiene an2provi2e better 3ousing con2itions to avoi2overcro(2ing+
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MANAGEMENT AND TREATMENT
• reatment remain argey supporti%e and uuall#addree the mot urgen prolem h#pertenion.
• he importan%e o! upportie therapie in a%uteglomerulonephriti %an not e oer emphaied. ight
lood preure %ontrol, appropriate ue o! diureti%,and %ontrol h#per"alemia, uraemia, and $uid oerload,i! ne%ear# # dial#i, are Euite literall# li!e aing.
• 6n mot %ae o! pot*trepto%o%%al glomerulonephritiwhere in$ammation doe reole pontaneoul#,upportie therapie alone will e u/%ient withimproed renal !un%tion eing een etween !our and1D da# a!ter the initial a%ute !ailure in 9> o! patient.
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*+ Supportive treatment
• Bloo2 pressure control• Dialysis• Antibiotic•
Immunosupression
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*+ Diet an2 Activity
0+ Inpatient 6anagement
@+ Long #erm 6onitoring
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1. Diet an! acti"it#• A low*odium, low*protein diet hould e pre%ried during the
a%ute phae, when edema and h#pertenion are in eiden%e.
• imitation o! $uid and alt inta"e i re%ommended in the %hild who
ha either oliguria or edema.
• Potaium inta"e hould e retri%ted to preent h#per"alemia.
• imited a%tiit# i proal# indi%ated during the earl# phae o! thedieae, parti%ularl# i! h#pertenion i preent. edret ma#
leen the degree and duration o! gro hematuria i! preent.
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$. In Patient Mana%e&ent$ospitaliKation is in2icate2 if t3e c3il2 3as significant 3ypertension or a
combination of oliguria7 generaliKe2 e2ema7 an2 elevation of serum creatinine or
potassium+
• Se!ere "ypertension
Severe 3ypertension7 or t3at associate2 (it3 signs of cerebral 2ysfunction7 2eman2simme2iate attention+ #3ree 2rugs are commonly cite2 as 3aving a 3ig3 benefit,to,
ris4 ratio)
*+ Labetalol -+F,0 mgJ4gJ3 intravenously NI?/7
0+ DiaKo1i2e7 an2
@+ A2nitroprussi2e -+F,0 mcgJ4gJmin I?/
Severe 3ypertension (it3out encep3alopat3y
*+ 3y2ralaKine or nife2ipin
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•#ild$to$moderate hypertension
1. be2rest7 flui2 restriction+
0+ #3e use of loop 2iuretics7 suc3 as furosemi2e -*,@ mgJ4gJ2 oral NPO7
a2ministere2 *,0 times 2aily/7 may 3asten resolution of t3e 3ypertension+
•%dema
*+ Restriction of flui2s
0+ Loop 2iuretics -furosemi2e/+
@+ If congestion is mar4e27 a2minister furosemi2e parenterally -0 mgJ4g/+
• Anuria or oli&uria
Because t3ey may be ototo1ic7 avoi2 large 2oses of furosemi2e in c3il2ren (it3
symptoms of anuria or severe an2 persistent oliguria+ In a22ition7 osmotic 2iuretics7
suc3 as mannitol7 are contrain2icate27 as t3ey mig3t increase vascular volume+
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'. Lon%(Te)& Monito)in%
• Long,term follo(,up for a patient follo(ing acute poststreptococcal
glomerulonep3ritis -APSG&/ primarily consists of bloo2 pressure
measurements an2 urine e1aminations for protein an2 bloo2
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PROGNOSIS• Complete re%oer# o%%ur in 9> o!
%hildren with APSG&.
• 5e%urren%e are e;tremel# rare.
• Mortalit# in the a%ute tage %an eaoided # appropriate management o!
a%ute renal !ailure, %ardia% !ailure, andh#pertenion.
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#$A&%!O