Presentasi Referat Gna

8/19/2019 Presentasi Referat Gna

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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

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