Ada beberapa penyebab glomerulonefritis akut, tetapi yang paling sering ditemukan disebabkan

karena infeksi dari streptokokus, penyebab lain diantaranya:

1. Bakteri : streptokokus grup C, meningococcocus, Sterptoccocus Viridans, Gonococcus,
Leptospira, Mycoplasma Pneumoniae, Staphylococcus albus, Salmonella typhi dll
2. Virus : hepatitis B, varicella, vaccinia, echovirus, parvovirus, influenza, parotitis epidemika
dl
3. Parasit : malaria dan toksoplasma
Bacterial and viral infections

The syndrome of acute glomerulonephritis has been reported following many other bacterial illnesses
(eg,Streptococcus pneumoniae, Staphylococcus aureus and S epidermidis, Rickettsia rickettsiae,
Mycoplasmaspecies, Meningococcus species, Leptospira species). In addition, certain viral illnesses
have preceded the onset of fairly typical acute glomerulonephritis; among the most common are
varicella-zoster virus (VZV), cytomegalovirus (CMV), and the Epstein-Barr virus (EBV).

Most forms of acute poststreptococcal glomerulonephritis (APSGN) are mediated by an immunologic

process. Cellular and humoral immunity is important in the pathogenesis of this disease, and humoral
immunity in APSGN. Nonetheless, the exact mechanism by which APSGN occurs remains to be
determined. The 2 most widely proposed theories include (1) glomerular trapping of circulating
immune complexes and (2) in situ immune antigen-antibody complex formation resulting from
antibodies reacting with either streptococcal components deposited in the glomerulus or with
components of the glomerulus itself, which has been termed molecular mimicry.

Additional evidence has also been presented to support the anti-immunoglobulin activity or glomerular
plasmin-binding activity of streptococcal antigens. The cross-reactivity of streptococci and mammalian
tissue implicating molecular mimicry in acute rheumatic fever led to evidence of a similar mechanism
involved in APSGN. However, the similar cross-reactivity patterns of rheumatogenic and nephritogenic
strains of streptococci argue against molecular mimicry involving M proteins.

Immune complex-mediated mechanisms

An immune complexmediated mechanism is the most widely proposed mechanism leading to the
development of APSGN. Nephritogenic streptococci produce proteins with unique antigenic
determinants. These antigenic determinants have a particular affinity for sites within the normal
glomerulus. Following release into the circulation, the antigens bind to these sites within the
glomerulus. Once bound to the glomerulus, they activate complement directly by interaction with
properdin.

Glomerular-bound streptococcal antibodies also serve as fixed antigens and bind to circulating
antistreptococcal antibodies, forming immune complexes. Complement fixation via the classic
pathway leads to the generation of additional inflammatory mediators and recruitment of inflammatory
cells.

Zymogen (NSAP) and NAPlr

Two major antigens have presently been identified as the potential cause(s) of APSGN: A zymogen
precursor of exotoxin B (SPEB [streptococcal pyrogenic toxin B]) or nephritis strainassociated
protein (NSAP), and nephritis-associated plasmin receptor (NAPlr), a glycolytic enzyme, which has
glyceraldehydes-3-phosphate dehydrogenase (GAPDH) activity[8, 9, 10, 11, 12]

NSAP is a 46- to 47-kd protein that is unique to the extracellular products of nephritogenic
streptococci. NSAP was demonstrated in glomerular deposits of 14 of 21 patients with APSGN, but
none in control biopsy samples from 5 patients with acute kidney injury and 11 with nonstreptococcal
glomerulonephritis. NSAP was also detected in serum from 96% of APSGN patients compared with
15-20% of patients with either acute kidney injury or impetigo. [13] NSAP has antigenic, biochemical, and
structural similarities to streptokinase from group C streptococcal organisms, binds to plasmin, and is
a plasminogen activator. However, streptokinase cannot be demonstrated in glomerular deposits for
patients with APSGN, and serum levels of purified group A streptokinase were similar in patients with
APSGN and those with acute kidney injury. Thus, although NSAP and streptokinase have similarities,
they appear to be 2 distinct proteins.[13]

Yoshizawa et all isolated a 43-kd protein called preabsorbing antigen (PA-Ag) that is putatively
identical to endostreptosin.[14, 15] PA-Ag has the ability to preabsorb the antibody in convalescent sera
from patients with APSGN and thus prevent its deposition in glomeruli. PA-Ag activates the alternative
pathway.[15] This 43-kd protein was later identified by Yamakami et al as NAPlr. [16] These researchers
noted that NAPlr was present in 100% of the early biopsy samples from in glomeruli of patients with
APSGN.[17] The glomerular distribution of NAPlr deposition and plasmin activity determined by in situ
zymography are identical.

The fact that NAPlr did not co-localize with C3 in glomerular deposits suggests that (1) complement
was activated by NAPlr in the circulation rather than in situ, and (2) NAPlr induced APSGN
independently of complement activation by binding to the glomerular basement membrane (GBM) and
mesangial matrix via its adhesive character, subsequently trapping and activating plasmin and
causing in situ glomerular damage by degrading the GBM or activating latent matrix metalloproteases.
[17, 18]

A proposed mechanism for acute poststreptococcal glomerulonephritis is that soluble, released NAPlr
binds to glomeruli and provide a mechanism to capture plasmin activated by streptokinase. The
activated plasmin bound to NAPlr associates with the GBM and mesangium. Both NAPlr and NSAP
are capable of inducing chemotactic (monocyte chemoattractant protein 1) and interleukin (IL)6
moieties in mesangial cells, promoting enhanced expression of adhesion molecules. Peripheral blood
leukocytes also release other cytokines such as tumor necrosis factor-alpha, IL-8, and transforming
growth factor-beta, which react with NSAP. These findings highlight the inflammatory potential of
these nephritogenic antigens.[19, 20, 21, 22]

Bound plasmin can cause tissue destruction by direct action on the glomerular basement membrane
or by indirect activation of procollagenases and other matrix metalloproteinases (MMPs). NAPlr can
also activate the alternate complement pathway, leading to accumulation of polymorphonuclear cells
and macrophages and local inflammation. In addition, the in situformed and circulating immune
complexes can readily pass through the altered glomerular basement membrane and accumulate on
the subepithelial space as humps.

Complement activation from both serum profiles and immunofluorescence patterns for glomerular
deposits indicates that C3 activation in APSGN is predominantly via the alternative pathway. [23, 24, 25] The
immune deposits consist of immunoglobulin G (IgG), C3, properdin, and C5. [25] These deposits rarely
contain C1q or C4, both components of the classic complement pathway. A recent study also showed
evidence for activation of the lectin-binding pathway from deposition of membrane-bound lipoprotein
in some patients with APSGN.[26]

During the early phase of the diseases (first 2 wk), evidence of classical pathway activation is seen,
as demonstrated by transient depression of serum C1q, C2, and/or C4 concentrations. [27, 28, 29] and the
presence of circulating C1-inhibitor-C1r-C1s complexes or C4d fragments. It is proposed that the
circulating immune complexes in the acute stage of the disease due to classic complement pathway
activation is distinct from that seen in the glomerular immune deposits. APSGN with typical findings on
histopathology may occur in patients with no evidence of complement activation, as manifested by
depression of serum C3 concentrations.[30, 31]

Hypocomplementemic patients differ from normocomplementemic patients by virtue of the presence

of factor B in the glomerular deposits and the absence of factor H, which is a regulatory protein of the
alternative pathway.[25] These findings suggest that the glomerular immune deposits of C3bBb
convertase may be due to ongoing complement activation in situ rather than systemic activation.
Crescentic APSGN may have an increased association with normocomplementemia. The reason for
this possible association of normocomplementemia with crescent formation in APSGN is not clear.

Serum IgG levels are elevated in about 44% of patients with APSGN. [32] Less than 50% of patients with
elevated serum IgG levels, however, have glomerular deposits of IgG. Elevated IgG levels were more
likely to be found in patients with antistreptolysin O titers of greater than or equal to 833 Todd units
(P < .001). However, elevated serum IgG concentrations do not correlate with severity of disease, age
of the patient, or serum albumin or C3 levels. It would appear that failure to form antibody to a
glomerular-bound protein produced by nephritogenicStreptococcus, is thought to be the origin of the
IgG in glomerular deposits, is in some way significantly associated with elevated serum levels of IgG
and antibody to streptolysin O.[32]

A mechanism for acute poststreptococcal glomerulonephritis proposed by Yoshizawa et al is shown in

the image below.

A schematic representation of the proposed mechanism for acute

poststreptococcal glomerulonephritis (APSGN). C = Activated complement; Pl = Plasmin; NAPlr = Nephritis-associated
plasmin receptor; SK = Streptokinase; CIC = Circulating immune complex.
There is considerable evidence both for and against most putative nephritogenic antigens. Genomic
sequencing of nephritogenic strains of streptococci may lead to the discovery of new nephritogenic
antigen candidates in conserved and differing regions of the streptococcal genome. This will lead to
improved understanding of the pathogenetic mechanism(s) leading to the development of APSGN.

Nonimmune complex-mediated mechanisms

Other nonimmune complex mediated mechanisms have been proposed for the development of
APSGN, such as delayed-type hypersensitivity, superantigens, and autoimmune phenomena.

A role for delayed-type hypersensitivity has been implicated in the pathogenesis of this disease. Early
in the course of APSGN, resident endothelial and mesangial cells are predominantly proliferated, and
this is accompanied by infiltration with polymorphonuclear leukocytes and monocytes. Macrophages
are effector cells that cause resident cellular proliferation. The infiltration of macrophages in the
glomeruli is mediated by complement-induced chemotaxis and, most likely, by an antigen-specific
event related to delayed-type hypersensitivity mediated by helper/inducer T cells.

Streptococcal M proteins and pyrogenic exotoxins can act as superantigens. These cause a marked
expansion of T cells expressing specific T-cell receptor B-chain variable gene segments. Massive T-
cell activation occurs, with release of T-cellderived lymphokines such as IL-1 and IL-6.

Autologous IgG in APSGN becomes antigenic and elicits an anti-IgG rheumatoid factor response,
leading to formation of cryoglobulins. Cryoglobulins, rheumatoid factors, and other autoimmune
phenomena occur in APSGN and are thought to play a role in the pathogenesis of the disease
together with streptococcal superantigens.

prognosis

Clearly and specifically explain the nature of the disease, its course, and the eventual prognosis of the
condition to the child (if old enough to understand) and the parents and/or caregivers. They need to
understand that, although complete resolution is expected, a small possibility exists for persistent
disease, and that an even smaller possibility exists for progression. This information is necessary for
some patients to ensure that compliance with the follow-up program occurs.

Clearly outline a follow-up plan and discuss the plan with the family. Blood pressure measurements
and urine examinations for protein and blood constitute the basis of the follow-up plan. Perform
examinations at 4- to 6-week intervals for the first 6 months and at 3- to 6-month intervals thereafter,
until both hematuria and proteinuria have been absent and the blood pressure has been normal for 1
year. Documenting that the low C3 has returned to normal after 8-10 weeks may be usefu

Medikasi
Medication Summary
The need for medicines in acute poststreptococcal glomerulonephritis (ASPGN) is usually limited in
scope and in length. Administer antibiotics (penicillin or erythromycin) for 10 days to ensure
eradication of the streptococcus if the disease is believed to be acute poststreptococcal
glomerulonephritis and if risk of contamination is present. Some clinicians use this treatment only
when evidence suggests an active infection.

Antihypertensives are usually not necessary after the child leaves the hospital, although mild
hypertension may persist for as many as 6 weeks. The medications that can be used span the entire
range of antihypertensives, such as vasodilators (eg, hydralazine), calcium channel-blocking agents
(eg, long-acting nifedipine, amlodipine), or angiotensin-converting enzyme (ACE) inhibitors (eg,
enalapril).

Carefully monitor blood pressure (BP) for at least 1 week after the drug is discontinued to ensure that
rebound hypertension does not occur.

Diuretic agents (eg, furosemide) are rarely necessary after the first 2 days; hypertension persisting
beyond the first week may suggest a diagnosis other than acute glomerulonephritis.

Patofisiologi
GNA PS timbul setelah infeksi tertentu, terutama strain tertentuyaitu grup A streptokokus.
Daerah infeksi biasanya saluran napas atas,termasuk telinga tengah, atau kulit.
Glomerulonefritis pascastreptokokusdapat terjadi setelah radang tenggorok dan jarang
dilaporkan bersamaandengan demam rematik akut.
1,2
GNA PS berawal apabila host rentan yang terpapar kumanStreptokokus grup A strain
nefritogenik bereaksi untuk membentuk antibodi terhadap antigen yang menyerang. GNA PS
merupakan kelainankompleks imun, namun mekanisme interaksi antara antigen dan
antiboditidak diketahui. Kompleks imun yang mengandung antigen streptokokusini
mengendap pada glomerulus. Ukuran komplek streptokokus-imunoglobulin adalah 15 nm
(streptokokus 10 nm dan imunoglobulin 5nm). Sedangkan ukuran
pore
membrana basalis pada anak dan dewasaadalah 2-3 nm dan 4-4,5 nm. Oleh karena itu GNA PS
banyak terjadi padaanak-anak daripada dewasa.
1,3
Kompleks antigen-antibodi terbentuk dalam aliran darah danterkumpul dalam glomerulus.
Akibat hal ini akan terjadi inflamasi padaglomerulus dan akan mengaktifkan sistem
komplemen.
4

17GNA PS adalah suatu penyakit imunologik akibat reaksi antigen-antbodi yang terjadi
dalam sirkulasi atau
in situ
dalam glomerulus. Prosesinflamasi yang mengakibatkan terjadinya jejas renal dipicu oleh
3
:a.
Aktivitas plasminogen menjadi plasmin oleh streptokinaseyang kemudian diikuti
oleh aktivasi kaskade komplemen.b.

Deposisi kompleks Ag-Ab yang telah terbentuk sebelumnya kedalam glomerulus.c.

Ab antistreptokokus yang telah terbentuk sebelumnya berikatandengan molekul tiruan (

molecule mimicy
) dari protein renalyang menyerupai Ag Streptokokus (jaringan glomerulus yangnormal yang
bersifat autoantigen bereaksi dengan Ab dalamsirkulasi yang terbentuk sebelumnya untuk
melawan AgStreptokokus)Sistem imun humoral dan kaskade komplemen akan aktif
bekerjaapabila terdapat deposit subepitel C3 dan IgG dalam membran basalglomerulus.
Kadar C3 dan C5 yang rendah dan kadar komplemen jalurklasik (C1q, C2 dan C4) yang
normal menunjukkan bahwa aktivasikomplemen melalui jalur alternatif. Deposisi IgG terjadi
pada faseberikutnya yang diduga oleh karena Ab bebas berikatan dengankomponen kapiler
glomerulus, membran bassal atau terhadap AgStreptokokus yang terperangkap dalam
glomerulus. Aktivasi C3glomerulus memici aktivasi monosit dan netrofil. Infiltrat
inflamasitersebut secara histologik terlihat sebagai glomerulonefritis eksudatif.Psoduksi
sitokin oleh sel inflamasi memperparah jejas glomerulus.Hiperselularitas mesangium dipacu
oleh proliferasi sel glomerulus akibatinduks oleh mitogen lokal.
3
Gejala GNA PS biasanya berlangsung singkat. Dengan berkhirnyaserangan Ag Streptokokus,
maka reaksi inflamasi akan mereda danstruktur glomerulus kembali normal.
3
Semua bentuk GNA PS dimediasi oleh proses imunologis. Baik imunitas humoral maupun
imunitas seluler. Imunitas seluler GNA PSdimediasi oleh pembentukan kompleks antigen-
antibodi streptkokus yang

18bersifat nefritogenik dan imun kompleks yang bersirkulasi. Prosesterjadinya adalah

stretokokus yang bersifat nefritogenik memprodksiprotein dengan antigen determinan khas.
Antigen deteriminan inimemiliki afinitas spesifik terhadap glomerulus normal.
5
Antigen ini kemudian akan berikatan pada glomerulus. Sekaliberikatan antigen ini akan
mengaktifkan komplemen secara lansungmelalui interaksi dengan properdin. Komplemen
yang telah teraktivasi iniakan menyebabkan timbul mediator inflamasi dan kemudian
timbulinflamasi.
5
Antigen nefritogenik lainnya adalah zymogen (
nephritic strain-associated protein NSAP
) dan
nephritis plasmin binding protein
(NAP1r).NSAP ini ditemukan pada biosi ginjal pasien dengan GNA PS dan tidak ditemukan
pada bentuk lain GNA maupun demam rematik. NAP1r jugaditemukan pada biopsi renal awal pasien
GNA PS. Setelah NAP1r iniberikatan dengan glomerulus dan menyebabkan pembentuk
plasmin yangdiaktivasi oleh streptokinase yang kemudian beikatan dengan NAP1r.Akibat
ikatan ini membran basal glomerular menjadi rusak secaralangsung. NAP1r juga akan
mengaktivasi komponen melalui jaluralternatif dan menyebabkan terkumpulnya sel PMN dan
makrofag danterjadi inflamasi setempat.
5
Mekanisme lainnya adalah kompleks nonimun, yang pertamaadalah hipersensitifitas tipe
lambat. Pertama, terjadi proliferasi padaendotel, hal ini akibat infiltrasi leukosit PMN dan
monosit dan makrofagmerupakan sel efektornya. Infiltrasi makrofag ini dimediasi
olehkomplemen dan sel T helper.
5
Kedua, adanya protein stretokokus M dan eksotoksin pirogenik yang bersifat superantigen.
Hal ini menyebabkan aktivasi sel Tmasif danpelepasan limfokin seperti IL1 dan IL6.
5
Ketiga, IgG autologus akan bersifat antigenic dan menyebabkanpementukan
cryoglobulin
. Cryoglobulin,factor rematik akan menjadisuperantigen

Manifestasi Klinis
AnamnesisAdanya riwayat infeksi streptokokus sebelumnya seperti faringitis,tonsilitis, atau
pioderma.Berikut merupakan beberapa keadaan yang didapatkan dari anamnese
1
:1.

Periode latena.

Terdapat periode laten antara infeksi streptokokus dengan onsetpertama kali muncul gejala.b.

Pada umumnya, periode laten selama 1-2 minggu setelah infeksitenggorok dan 3-6 minggu
setelah infeksi kulitc.

Onset gejala dan tanda yang timbul bersamaan dengan faringitisbiasanya merupakan
imunoglobulin A (IgA) nefropati daripadaGNA PS.2.

Urin berwarna gelapa.

Merupakan gejala klinis pertama yang timbulb.

Urin gelap disebabkan hemolisis eritrosit yang telah masuk kemembran basalis glomerular
dan telah masuk ke sistem tubular.3.

Edema periorbitala.

Onset munculnya sembab pada wajah atau mata tiba-tiba. Biasanyatampak jelas saat psaat
bangun tidur dan bila pasien aktif akantampak pada sore hari.b.

Pada beberapa kasus edema generalisata dan kongesti sirkulasiseperti dispneu dapat timbul.c.
Edema merupakan akibat dari tereksresinya garam dan air.d.

Tingkat keparahan edema berhubungan dengan tingkat kerusakanginjal.4.

Gejala nonspesifik a.

Yaitu gejala secara umum penyakit seperti malaise, lemah, dananoreksia, muncul pada 50%
pasien.

21b.

15 % pasien akan mengeluhkan mual dan muntah.c.

Gejala lain demam, nyeri perut, sakit kepala.

Pemeriksaan Fisik
Adanya gross hematuri (urin yang berwarna seperti teh), denganatau tanpa edema (paling
mudah terlihat edema periorbital atau matatampak sembab), pada kasus yang agak berat dapat timbul
gangguanfungsi ginjal biasanya berupa retensi natrium dan urin. Gejala lain yangmuncul tidak
spesifik. Bila disertai dengan hipertensi, dapat timbul nyerikepala. Demam tidak selalu ada.
Pada kasus berat (GN destruktif) dapattimbul proteinuria masif (sindrom nefrotik), edema
anasarka atau asites,dan berbagai gangguan fungsi ginjal yang berat.
4
1.

Sindrom Nefritis Akuta.

Gejala yang timbul adalah edema, hematuria, dan hipertensidengan atau tanpa klinis GNA
PS.b.

95% kasus klinis memiliki 2 manifestasi, dan 40% memiliki semuamanifestasi akut nefritik
sindrom2.

Edemaa.

Edema tampak pada 80-90% kasus dan 60% menjadi keluhan saatke dokter.b.

Terjadi penurunan aliran darah yang bermanifestasi sedikit eksresinatrium dan urin menjadi
terkonsentrasi. Adanya retensi natriumdan air ini menyebabkan terjadinya edema.3.

Hipertensia.

Hipertensi muncul dalam 60-80% kasus dan biasanya pada orangyang lebih besar.b.

Pada 50% kasus, hipertensi bisa menjadi berat.c.

Jika ada hipertensi menetap, hal tersebut merupakan petunjuk progresifitas ke arah lebih
kronis atau bukan merupakan GNA PS.d.

Hipertensi disebabkan oleh retensi natrium dan air yang eksesif.e.

Meskipun terdapat retensi natrium, kadar natriuretic peptida dalamplasma meningkat.f.

Aktivitas renin dalam plasma rendah.

22g.

Ensefalopati hipertensi ada pada 5-10% pasien,biasanya tanpadefisit neurologis.4.

Oliguriaa.

Tampak pada 10-50% kasus, pada 15% output urin <200ml.b.

Oliguria mengindikasikan bentuk

cresentic
yang berat.c.

Biasanya transien, dengan diuresis 1-2 minggu.5.

Hematuriaa.

Muncul secara umum pada semua pasien.b.

30% gross hematuria.6.

Disfungsi ventrikel kiria.

Disfungsi ventrikel kiri dengan atau tanpa hipertensi atau efusiperikardium dapat timbul pada
kongestif akut dan fasekonvalesen.b.

Pada kasus yang jarang, GNA PS dapat menunjukkan gejalaperdarahan pulmonal

Penatalaksanaan
GNA-PS tipikal tidak memerlukan penatalaksanaan spesifik.Terapi antibiotik yang sesuai
merupakan indikasi bila infeksi tetap ada.Gangguan pada fungsi ginjal yang mengakibatkan
hipertensi memerlukanpenanganan yang lebih spesifik, pengurangan konsumsi natrium,pengobatan
dengan diuretik atau obat antihipertensi. Pada kasus beratyang telah terjadi kegagalan ginjal,
dapat dilakukan hemodialisa atauperitoneal dialisa. Kortikosteroid juga dapat diberikan untuk
mengurangiperjalanan infeksi.
4
Terapi Medis :Terapi simtomatis untuk mengontrol edema dan tekanan darah
5
1.

Pada fase akut batasi garam dan air, jika hipertensi dapat diberikandiuretik. Loop diuretik
meningkatkan output urin.2.

Untuk hipertensi yang tidak dapat dikontrol dengan diuretik. Biasanyacalsium channel
blocker. Pada hipertensi maligna pemberiannitroprusid atau parenteral agen.

263.

Antibiotik golongan penisilin jika infeksi primer masih berlangsung.4.

Indikasi untuk dialisis pada hiperkalemia dan manifestasi klinisuremia.5.

Pembatasan aktivitas fisik diperlukan pada beberapa hari pertama sakit6.

Steroid, obat-obat imunosupresan dan plasmaferesis masih dalamperdebatan.

13.

Prognosis
Hanya sedikit pasien dengan GNA yang memerlukan perawatan dirumah sakit. Dan sebagian
besar akan pulang dalam waktu 2-4 hari.Semakin ce[at tekanan darah berada dalam nilai
normal dan diuresis telahkembali, sebagian besar anak dapat dirawat jalan.
5
Sebagian besar pasien akan sembuh, tetapi 5% di antaranyamengalami perjalanan penyakit
yang memburuk dengan cepat denganpembentukan kresen pada epitel glomerulus. Diuresis
akan menjadinormal kembali pada hari ke 7-10 setelah awal penyakit, denganmenghilangnya
senbab dan secara bertahap tekanan darah menjadi normalkembali. Fungsi ginjal membaik
dalam 1 minggu dan menjadi normaldalam waktu 3-4 minggu. Komplemen serum menjadi
normal dalamwaktu 6-8 minggu. Tetapi kelainan sedimen urin akan tetap terlihat
selamberbulan-bulan bahkan bertahun-tahun pada sebagian besar pasien.
2

28
DAFTAR PUSTAKA
1.

Geetha D.Poststreptococcal Glomerulonephritis.[Internet].Available

fromURL:http://emedicine.medscape.com/article/240337-overview.Accessedon 22 April
2010.2.

Noer MS. 2002.Glomerulonefritis.Dalam: Alatas H, Tambunan T, TrihonoPP,Pardede SO.

Buku Ajar Nefrologi Anak.Edisi 2. Jakarta : BalaiPenerbit FKUI.p 345-3523.

Noer MS.2006.Glomerulonefritis Akut Pasca Streptokokus.Dalam:Kumpulan Makalah

Simposium dan Workshop Sehari: Kegawatan padaPenyakit Ginjal Anak.Makasar:UKK
Nefrologi IDAI.p56-674.
Lum GM.2005.Glomerulonephritis.In:Hematuria&GlomerularDisease.In:Kidney&Urinary tr
act.In:Hay WW,LevinMJ,etc.editors.Current Pediatric Diagnosis and
Treatment.NewYork:McGraw-Hill.p.7135.

Bhimmma R.Acute PoststreptococcalGlomerulonephritis.

[Internet]Available fromURL:http://emedicine.medscape.om/article/980685-
overview.Accessed on23 April 2010. 6. Parmar MS.Acute Glomerulonefritis.
[Internet].Available fromURL:http://emedicine.medscape.com/article/239278-
overview.Accessedon 23 April 2010.7.

Noer MS,Soemyarso N.Hipertensi.Bagian Ilmu Kesehatan Anak UNAIRSurabaya.

[Internet].Diunduh dariURL:http://www.pediatrik.com/isi03.php?
page=html&hkategori=pdt&direktori=pdt&filepdf=0&pdf=&html=07110-hrji262.htm.

28
DAFTAR PUSTAKA
1.

Geetha D.Poststreptococcal Glomerulonephritis.[Internet].Available

fromURL:http://emedicine.medscape.com/article/240337-overview.Accessedon 22 April
2010.2.

Noer MS. 2002.Glomerulonefritis.Dalam: Alatas H, Tambunan T, TrihonoPP,Pardede SO.

Buku Ajar Nefrologi Anak.Edisi 2. Jakarta : BalaiPenerbit FKUI.p 345-3523.

Noer MS.2006.Glomerulonefritis Akut Pasca Streptokokus.Dalam:Kumpulan Makalah

Simposium dan Workshop Sehari: Kegawatan padaPenyakit Ginjal Anak.Makasar:UKK
Nefrologi IDAI.p56-674.

Lum GM.2005.Glomerulonephritis.In:Hematuria&GlomerularDisease.In:Kidney&Urinary tr
act.In:Hay WW,LevinMJ,etc.editors.Current Pediatric Diagnosis and
Treatment.NewYork:McGraw-Hill.p.7135.

Bhimmma R.Acute PoststreptococcalGlomerulonephritis.

[Internet]Available fromURL:http://emedicine.medscape.om/article/980685-
overview.Accessed on23 April 2010. 6. Parmar MS.Acute Glomerulonefritis.
[Internet].Available fromURL:http://emedicine.medscape.com/article/239278-
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