Glomerulonephritis (nephritic syndrome) is a disorder oI glomeruli (clusters oI microscopic

blood vessels in the kidneys with small pores through which blood is Iiltered). It is characterized
by body tissue swelling (edema), high blood pressure, and the presence oI red blood cells in the
urine.
O Glomerulonephritis can be caused by various disorders, such as inIections, an inherited
genetic disorder, or autoimmune disorders.
O !eople may have tissue swelling, headaches, visual disturbances, and seizures.
O iagnosis is based on tests oI blood and urine and sometimes imaging tests, a biopsy oI
the kidneys, or both.
O !eople need to restrict salt and protein intake and take diuretics or antibiotics until kidney
Iunction improves.
Glomerulonephritis can develop over a short time period (acute glomerulonephritis) or develop
and progress slowly (chronic glomerulonephritis). In 1 oI children and 10 oI adults who have
acute glomerulonephritis, it evolves into rapidly progressive glomerulonephritis, in which most
oI the glomeruli are destroyed, resulting in kidney Iailure.
Causes
Glomerulonephritis can be primary, aIIecting only the kidneys, or secondary, caused by a vast
array oI disorders that aIIect other parts oI the body.
Acute Glomerulonephritis: Acute glomerulonephritis most oIten occurs as a complication oI
throat or skin inIection by streptococcus, a type oI bacteria. Acute glomerulonephritis that occurs
aIter a streptococcal inIection (post-streptococcal glomerulonephritis) typically develops in
children between the ages oI 2 and 10 Iollowing recovery Irom the inIection. InIections with
other types oI bacteria, such as staphylococcus and pneumococcus, viral inIections, such as
chickenpox, and parasitic inIections, such as malaria, can also result in acute glomerulonephritis.
Acute glomerulonephritis that results Irom any oI these inIections is called postinIectious
glomerulonephritis. NoninIectious causes oI acute glomerulonephritis include
membranoproliIerative glomerulonephritis, immunoglobulin A (IgA) nephropathy, thin
basement membrane disease, Henoch-Schnlein purpura, systemic lupus erythematosus (lupus),
cryoglobulinemia, Goodpasture's syndrome, and Wegener's granulomatosis. Acute
glomerulonephritis that develops into rapidly progressive glomerulonephritis most oIten results
Irom conditions that involve an abnormal immune reaction.
Chronic Glomerulonephritis: OIten, chronic glomerulonephritis seems to result Irom one oI the
same conditions that cause acute glomerulonephritis, such as IgA nephropathy or
membranoproliIerative glomerulonephritis. Sometimes, acute glomerulonephritis does not
resolve and instead becomes chronic. Occasionally, chronic glomerulonephritis is caused by
hereditary nephritis, an inherited genetic disorder. In many people, the cause oI chronic
glomerulonephritis cannot be identiIied.








Secondary Causes oI Glomerulonephritis
O Infections
4 acterial inIections
(streptococcus,
staphylococcus,
pneumococcus)
4 ungal inIections
4 !arasitic inIections (malaria)
4 'iral inIections (hepatitis
and C, HI')
O ',sculitis
4 Churg-Strauss syndrome
4 Cryoglobulinemia
4 icroscopic polyangiitis
4 Wegener's granulomatosis
O Immune disorders
4 Goodpasture's syndrome
4 Serum sickness
4 Systemic lupus
erythematosus
O eredit,ry disorders
4 Hereditary nephritis
4 Nail-patella syndrome
O rugs
4 Gold
4 !amidronate
4 !enicillamine
4 !ropylthioracil

Symptoms
About halI oI the people with ,cute glomerulonephritis have no symptoms. II symptoms do
occur, the Iirst to appear are tissue swelling (edema) due to Iluid retention, low urine volume,
and production oI urine that is dark because it contains blood. Edema may Iirst appear as
puIIiness oI the Iace and eyelids but later is prominent in the legs. lood pressure increases as
kidney Iunction becomes impaired. In turn, high blood pressure and swelling oI the brain may
produce headaches, visual disturbances, and more serious disturbances oI brain Iunction (Ior
example, seizures or coma). In older people, nonspeciIic symptoms, such as nausea and a general
Ieeling oI illness (malaise), are more common.
When r,pidly progressive glomerulonephritis develops, weakness, Iatigue, and Iever are the
most Irequent early symptoms. Loss oI appetite, nausea, vomiting, abdominal pain, and joint
pain are also common. About 50 oI people have a Ilu-like illness in the month beIore kidney
Iailure develops. These people have edema and usually produce very little urine. High blood
pressure is uncommon and rarely severe when it does occur.
ecause chronic glomerulonephritis usually causes only very mild or subtle symptoms, it goes
undetected Ior a long time in most people. Edema may occur. High blood pressure is common.
The disease may progress to kidney Iailure, which can cause itchiness, Iatigue, decreased
appetite, nausea, vomiting, and diIIiculty breathing.
iagnosis
octors investigate the possibility oI acute glomerulonephritis in people whose laboratory test
results indicate kidney dysIunction or blood in the urine and in people who develop symptoms oI
the disorder, particularly those who have had strep throat or other inIections. Laboratory tests
show variable amounts oI protein and blood cells in the urine and oIten kidney dysIunction, as
shown by a high concentration oI urea and creatinine (waste products) in the blood.
In people with rapidly progressive glomerulonephritis, casts (clumps oI red blood cells or white
blood cells) are almost always visible in a urine sample that is examined under a microscope.
lood tests detect anemia and oIten an abnormally high number oI white blood cells. When
doctors suspect glomerulonephritis, a biopsy oI the kidney is usually done to conIirm the
diagnosis, help determine the cause, and determine the amount oI scarring and potential Ior
reversibility. Kidney biopsy is done by inserting a needle in one oI the kidneys under ultrasound
or computed tomography (CT) guidance to obtain a small amount oI kidney tissue. Although
kidney biopsy is an invasive procedure and occasionally can become complicated, it is usually
saIe.
Additional tests are sometimes helpIul Ior identiIying the cause. or example, a throat culture
may provide evidence oI streptococcal inIection. lood levels oI antibodies against streptococci
may be higher than normal or progressively increase over several weeks. Acute
glomerulonephritis that Iollows an inIection other than strep throat is usually easier to diagnose,
because its symptoms oIten begin while the inIection is still obvious. Cultures and blood tests
that help identiIy the organisms that cause these other types oI inIections are sometimes needed
to conIirm the diagnosis.
Chronic glomerulonephritis develops gradually, and thereIore, a doctor may not be able to tell
exactly when it began. It may be discovered when a urine test, done as part oI a medical
examination, reveals the presence oI protein and blood cells in a person who is Ieeling well, has
normal kidney Iunction, and has no symptoms. octors usually do an imaging test oI the
kidneys, such as an ultrasound, CT scan, or magnetic resonance imaging (#I) scan. A kidney
biopsy is the most reliable way to distinguish chronic glomerulonephritis Irom other kidney
diseases. A biopsy, however, is rarely done in advanced stages. In these cases, the kidneys are
shrunken and scarred, and the chance oI obtaining speciIic inIormation about the cause is small.
octors suspect that the kidneys are shrunken and scarred iI kidney Iunction has been poor Ior a
long time and the kidneys appear abnormally small on an imaging test.
!rognosis
Acute poststreptococcal glomerulonephritis resolves completely in most cases, especially in
children. About 0.1 oI children and 25 oI adults develop chronic kidney Iailure.
The prognosis Ior people with rapidly progressive glomerulonephritis depends on the severity oI
glomerular scarring and whether the underlying disease, such as inIection, can be cured. In about
75 oI the people who are treated early (within weeks to a Iew months), kidney Iunction is
preserved and dialysis is not needed. However, because the early symptoms can be subtle and
vague, many people who have rapidly progressive glomerulonephritis are not aware oI the
underlying disease and do not seek medical care until kidney Iailure develops. II treatment
occurs late, the person is more likely to develop chronic kidney Iailure. The prognosis also
depends on the cause, the person's age, and any other diseases the person might have. When the
cause is unknown or the person is older, the prognosis is worse.
In some children and adults who do not recover completely Irom acute glomerulonephritis, other
types oI kidney disorders develop, such as asymptomatic proteinuria and hematuria syndrome or
nephrotic syndrome. Other people with acute glomerulonephritis, especially older adults, oIten
develop chronic glomerulonephritis.

!rimary Glomerular isorders That Can Cause Glomerulonephritis
isorder escription !rognosis
ibrillary
glomerulonephritis
A rare disease in which
abnormal proteins are
deposited around the
glomerulus; it may also
cause nephrotic syndrome
The prognosis is poor; end-
stage kidney Iailure occurs
in halI oI people within 4
years. It is not clear how
much treatment (with
corticosteroids and
immunosuppressants) helps
!rimary rapidly
progressive
glomerulonephritis
A group oI disorders that
cause microscopic damage
to the glomeruli and
progress rapidly; sometimes
they are caused by an
inIection or other treatable
disorder
The prognosis is poor; at
least 80 oI people develop
end-stage kidney Iailure
within 6 months without
treatment. The prognosis is
better Ior people younger
than 60 years or iI an
underlying disorder causing
the glomerulonephritis
responds to treatment
Immunoglobulin A
(IgA) nephropathy
The most common Iorm oI
glomerulonephritis in the
world; caused by immune
complexes (combinations oI
antigens and antibodies)
deposited in the kidney
Usually the disorder
progresses slowly; end-stage
kidney Iailure develops in
about 20 to 40 oI people
aIter 5 to 25 years;
progresses more slowly in
children
Thin basement
membrane disease
(benign Iamilial
hematuria)
A hereditary disorder caused
by thinning oI a part oI the
glomerulus called the
basement membrane
The prognosis is excellent;
most people do not develop
end-stage kidney Iailure
embranoproliIerative An uncommon type oI II caused by immune
glomerulonephritis glomerulonephritis
primarily occurring between
the ages oI 8 and 30;
sometimes the cause is
unknown, or the disorder
may be caused by immune
complexes (combinations oI
antigens and antibodies)
attaching to the kidney
complex disease, a partial
remission may occur; the
outcome is not as good in
people in whom the cause
remains unknown. About
halI oI untreated people will
progress to end-stage kidney
Iailure within 10 to 15 years,
while in most others the
kidney Iunction stabilizes or
improves
Treatment
No speciIic treatment is available in most cases oI acute glomerulonephritis. ollowing a diet
that is low in protein and sodium may be necessary until kidney Iunction recovers. iuretics may
be prescribed to help the kidneys excrete excess sodium and water. High blood pressure needs to
be treated.
When a bacterial inIection is suspected as the cause oI acute glomerulonephritis, antibiotics are
usually ineIIective because the nephritis begins 1 to 6 weeks (average, 2 weeks) aIter the
inIection, which has, by then, usually resolved. However, iI a bacterial inIection is still present
when acute glomerulonephritis is discovered, antibiotic therapy is started. Antimalarial drugs
may be beneIicial iI the cause oI the syndrome is malaria.
or rapidly progressive glomerulonephritis, drugs to suppress the immune system are started
promptly. High doses oI corticosteroids are usually given intravenously Ior about a week,
Iollowed by a variable period oI time when they are taken by mouth. Cyclophosphamide

, an immunosuppressant, may also be given. In addition, plasmapheresis is sometimes used to
remove antibodies Irom the blood. The sooner treatment occurs, the less likely are kidney Iailure
and the need Ior dialysis. Kidney transplantation is sometimes considered Ior people who
develop chronic kidney Iailure, but rapidly progressive glomerulonephritis may recur in the
transplanted kidney.
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (A#s)
either alone or in combination oIten slow progression oI chronic glomerulonephritis. Taking
drugs to reduce high blood pressure and reducing sodium intake are considered beneIicial.
#estricting the amount oI protein in the diet is modestly helpIul in reducing the rate oI kidney
deterioration. End-stage kidney Iailure can be treated with dialysis or a kidney transplant.
Asymptomatic !roteinuria and Hematuria Syndrome
Asymptomatic proteinuria and hematuria is the result oI diseases oI glomeruli (clusters oI
microscopic blood vessels in the kidneys that have small pores through which blood is Iiltered)
characterized by steady or intermittent loss oI small amounts oI protein and blood in the urine.
Small amounts oI protein excreted in the urine (proteinuria) or blood excreted in the urine
(hematuria) are sometimes discovered in people without symptoms, when urine tests are done Ior
some routine purpose. The presence oI casts (clumps oI red blood cells) or abnormally shaped
red blood cells is a clue Ior doctors that the blood in the urine came Irom glomeruli. Casts and
proteinuria may be present because the person is recovering Irom a recent undiagnosed episode
oI nephritis. II this situation seems likely, a doctor needs only to recheck the person over the next
weeks or months to make sure that the abnormalities resolve. II casts and proteinuria persist, the
cause is usually one oI three disorders. One is immunoglobulin A (IgA) nephropathy, a type oI
nephritis caused by deposition oI immune complexes (combinations oI antibodies and antigens)
in the kidney that can be very mild and nonprogressive or become a severe disease leading to
kidney Iailure. Another is hereditary nephritis (Alport's syndrome), a progressive disorder that
can be severe and lead to kidney Iailure. The third disorder is thin basement membrane disease
(benign Iamilial hematuria). Thin basement membrane disease is a hereditary disorder caused by
thinning oI a part oI the glomerulus called the basement membrane. It Iollows a mild and
nonprogressive course. The diagnosis can usually be made with a kidney biopsy. However, a
kidney biopsy is rarely done because the likelihood oI Iinding a treatable disease is very low.
octors usually recommend that people with asymptomatic proteinuria and hematuria have a
physical examination and undergo urine testing once or twice a year. Additional tests are done iI
the amount oI protein or blood increases much, or iI symptoms occur that suggest the
development oI a speciIic disease. ost people with asymptomatic proteinuria and hematuria
syndrome do not worsen, and the condition may persist indeIinitely.
Hereditary Nephritis (Alport's Syndrome)
Hereditary nephritis (Alport's syndrome) is a genetic disorder in which kidney Iunction is poor,
blood is present in the urine, and deaIness and eye abnormalities sometimes occur.
Hereditary nephritis is usually caused by a deIective gene on the X chromosome, but it
sometimes results Irom an abnormal gene on a nonsex (autosomal) chromosome. Other Iactors
inIluence how severe the disorder is in a person who has the gene. emales with the deIective
gene on one oI their two X chromosomes usually do not have symptoms, although their kidneys
may Iunction somewhat less eIIiciently than normal. ost oI these Iemales have some blood in
the urine. ales with the deIective gene develop more severe problems because males do not
have a second X chromosome to compensate Ior the deIect. ales usually develop kidney Iailure
between the ages oI 20 and 30. any people with the deIective gene on only one autosomal
chromosome have no symptoms other than blood in the urine, but the urine may also contain
varying amounts oI protein, white blood cells, and casts (small clumps oI cells) that are visible
under a microscope. Kidney Iunction in people who have the deIective gene on two autosomal
chromosomes slowly worsens, and kidney Iailure usually occurs.
Hereditary nephritis can aIIect other organs. Hearing problems, usually an inability to hear
sounds in the higher Irequencies, are common. Cataracts can also occur, although less oIten than
hearing loss. Abnormalities oI the cornea, lens, or retina sometimes cause blindness. Other
problems include a low number oI platelets in the blood (thrombocytopenia) and abnormalities
that aIIect several nerves (polyneuropathy).
!eople who develop kidney Iailure need to undergo dialysis or receive a kidney transplant.
Genetic testing is usually oIIered to people who want to have children.
Nail-!atella Syndrome
The nail-patella syndrome (also called osteo-onychodysplasia, arthro-onychodysplasia, and
onycho-osteodysplasia) is a rare hereditary disorder that results in abnormalities oI the kidneys,
bones, joints, and Iingernails.
The gene that causes nail-patella syndrome is dominant. Commonly, people who have this
syndrome have one or both kneecaps (patellas) missing, one oI the arm bones (the radius)
dislocated at the elbow, and the pelvic bone abnormally shaped. They have either no Iingernails
or poorly developed ones, with pitting and ridges. About 30 to 40 oI people with this
syndrome have blood or protein in their urine, which may prompt the doctor to order kidney
Iunction tests. Kidney Iailure eventually develops in about 30 oI the people with aIIected
kidneys by the time they are 50 or 60. The diagnosis is conIirmed by bone x-rays and a biopsy oI
kidney tissue.
There is no eIIective treatment Ior this syndrome. Controlling blood pressure may slow the rate
oI deterioration oI kidney Iunction. Those who develop kidney Iailure need dialysis or a kidney
transplant. Genetic testing is usually oIIered to people who want to have children.
Last Iull review/revision arch 2007 by Seyed-Ali Sadjadi,

,s,r kel,in,n : #eaksi autoimun yang mengakibatkan pengendapan IgG, C3, subepitel pada
membrana basalis glomerulus selanjutnya menyebabkan peradangan, koagulasi glomeruli,
membrane glomeruli menjadi porous sehingga molekul-molekul protein melewatinya
membentuk silinder hialin
I.IAGNOSIS
asa inkubasi : 2-3 minggu postinIeksi dengan streptokokus grup A ? hemolitikus
A.Keluhan pokok
O Edema mendadak mulai pada muka/kelopak mata, lalu pada kaki dan pada kemaluan
O Oliguri/anuri
O Hematuri
.1anda penting
O Edema anasarka
.Pemeriksaan laboratorium
O !roteinuri/albuminuri
O Sedimen urine mengandung :
4 Lekosit
4 Eritrosit (#C)
4 Silinder #C/granuler
.Pemeriksaan khusus
ImunoIluoresens :
O !engendapan IgG, C3
ikroskop electron :
O humps(pengendapan subepitelial)
II.KOMPLIKASI
1.Gagal ginjal akut (GNA)
2.Gagal ginjal kronik (GNK)
3.Hipertensi
4.Edema pulmonal
5.EnseIalopati
6.!ayah jantung
7.!erdarahan otak
III.PENATALAKSANAAN
A.1erapi umum
1. Istirahat
O Harus dirawat inap
2.iet
O #endah garam
3.edikamentosa
Obat pertama :
O Tidak ada yang spesiIik
O Terapi inIeksi pencetus
Obat alternative :
O Antihipertensi
O iuretikum
.1erapi komplikasi -
I'.PROGNOSIS
O Sekitar 95 sembuh setelah 2 bulan
O Sisanya 5 menjadi persisten