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CHAPTER I
INTRODUCTION
1.1. Background
Glomerulonephritis is the major cause of end stage renal failure and high rates of morbidity in
children. Glomerulonephritis terminology used here is to show that the first and major
abnormalities occurred in the glomerulus. Glomerulonephritis is an inflammatory disease of
bilateral kidneys. Inflammation begins in gromelurus and manifests as proteinuria and or
hematuria. Although the primary lesion in gromelurus, but the entire nephron in the end will be
damaged, resulting in kidney failure.1
Indonesia in 2009, reported 260 patients treated in teaching hospitals in 12 months. Most patients
treated in Surabaya (26.5%), followed in succession in Jakarta (24.7%), Bandung (17.6%), and
Palembang (8.2%). Patients of men and women versus 2: 1 and most in children aged between 6-
8 years (40.6%).3
Symptoms of glomerulonephritis can occur in a sudden (acute) or chronic (chronic) are often not
known because it does not cause symptoms. Symptoms may include nausea, anemia, or
hypertension. Common symptoms like swollen eyelids, oliguria, and usually accompanied by
hypertension. The disease is usually (about 80%) healed spontaneously, 10% become chronic,
and 10% resulted fatal.2
1.2. Problems
In this paper, I will discuss about acute glomerulonephritis (AGN). In overview, acute
glomerulonephritis is an immunological reaction in the kidney to specific bacterial or viral which
often occurs is due to streptococcal bacterial infection. Most (75%) of acute post-streptococcal
glomerulonephritis arise after upper respiratory tract infections, caused by the bacteria
Streptococcus group A beta hemolitikus.3
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1.3. Limitation of Problems
- What is the definition of Acute Glomerulonephritis?
- How about the etiology of Acute Glomerulonephritis?
- How about the pathophysiology of Acute Glomerulonephritis?
- What are the symptoms of Acute Glomerulonephritis?
- How can we diagnose it?
- What do we can see in laboratory overview?
- What kind of therapy we can give to the patient?
1.4. Frame of Writing
I. Introduction
1.1Background
1.2Problems
1.3Limitation of Problems
1.4Frame of Writing
II. Kidney Reviews
2.1 Anatomy
2.2 Function
III. Acute Glomerulonephritis
3.1Definiton
3.2Etiology
3.3Pathophysiology
3.4Prevalence
3.5 Clinical Symptoms
3.6 Laboratory Overview
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3.7 Overview Patology
3.8 Diagnose
3.9 Theraphy
IV. Acute Glomerulonephritis and Urinary System
V. Conclusion
VI. References
CHAPTER II
KIDNEY REVIEWS
2.1. Anatomy
Kidney is the bilateral organ that located in the abdominal area, between vertebra retroperitoneal
lumbal 1 and 4. In neonates is sometimes palpable. The kidneys consist of cortex and medulla.
Each kidney consists of pyramid-shaped lobes 8-12. Basic pyramid is located in the cortex and
the peak is called the papilla empties into the calyx minor. In the cortex region propagated
glomeruli, proximal and distal tubules contortus.
The length and weight of kidney average 6 cm
and 24 grams in baby, to 12 cm or more than
150 grams. In the fetal kidney surface uneven,
lobes, then disappears with increasing ages.
Kidney contains 1 million nephrons (glomeruli
and tubules associated with it). In humans,
nephron formation is completed in 35 weeks fetus. No new nephrons formed after birth. Further
development is hypertrophy and hyperplasia of existing structures along with maturation
fungsional. Nephron consists of the glomerulus and Bowman's capsule, proximal tubule, Anse
Henle and distal tubules. Glomeruli with Bowman's capsule premises also called maplphigi
body.4
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2.2. Function
Primary function of kidney is to maintain extracellular fluid volume and composition within
normal limits. Composition and extracellular fluid volume is controlled by glomerular filtration,
reabsorption and secretion tubulus.
The main function of kidney is divided into:
1. The function of excretion
To maintain plasma osmolality by altering water excretion, maintain a plasma pH of about
7.4 to remove excess H + and HCO3 reshape, maintaining levels of each plasmaelectrolytes in normal range, excrete the end products of nitrogen and protein metabolism,
especially urea, uric acid and creatin.
2. Non-excretion function
Produce renin is important to regulate blood pressure, produce erythropoietin is an important
factor in stimulating red blood cell products by the bone marrow, metabolize vitamin D into
its active form, degradation of insulin and produce prostaglandins
The basic function is to cleanse or purify
nephron blood plasma and the substance
is not required when the body's blood
through the kidneys. The most important
substance to be cleaned is the end result
of metabolism such as urea, creatine, uric
acid and others. In addition, sodium ions,
potassium, chloride and hydrogen tend to
accumulate in the body.
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Glomerulus normal capillary
No plasma proteins larger than albumin in the filtrate gromerulus declare the effectiveness of the
glomerular capillary wall as a barrier filtration. Endothelial cells, epithelial basement membrane
and glomerular capillary wall have strong negative ion content. The charge of this anion is resultthan 2 negative charges: proteoglycans (heparan-sulfate) and acid-containing glycoproteins
sialat. Proteins in blood relatively low isoelectric and carry a negative charge is pure. Therefore,
they are rejected by the capillary wall of gromerulus which negative, and limiting the filtration.5
CHAPTER III
ACUTE GLOMERULONEPHRITIS (AGN)
3.1. Definitions
Acute glomerulonephritis (GNA) is an immunological reaction in the kidney to specific bacterial
or viral which often occurs is due to streptococcal bacterial infection. Glomerulonephritis is a
term used to describe various kinds of kidney disease who experience glomerular proliferation
and inflammation caused by an immunological mechanism. While the acute term (acute
glomerulonephritis) reflects the correlation clinics in addition to showing a picture of etiology,
pathogenesis, disease and prognosis.
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Acute glomerulonephritis also called post sterptokokus (GNAPS) is a non-suppurative
inflammatory process that the glomeruli, as a result of bacterial infection of group A
streptococcal beta hemolitikus, type nefritogenik elsewhere.
3.2. Etiology
Most (75%) of acute post-streptococcal glomerulonephritis arise after upper respiratory tract
infections, caused by the bacteria Streptococcus group A beta hemolitikus type 1, 3, 4, 12, 18,
25, 49. Medium Type 2, 49, 55, 56, 57 and 60 cause skin infections 8-14 days after streptococcal
infection, clinical symptoms arise. Hemolitikus beta streptococcal bacterial infection has a risk of
acute post-streptococcal glomerulonephritis ranged 10-15%.
Climatic factors, nutritional status, general condition and allergy also influence after infection
with the germ GNA Streptococcuss. There are several causes of acute glomerulonephritis, but
the most commonly found because of streptococcal infection, other causes include:
1. Bacterial : streptococcal group C, meningococcocus, Sterptoccocus Viridans,
gonococcus, Leptospira, Mycoplasma pneumoniae, Staphylococcus albus,
Salmonella typhi etc.
2. Virus : hepatitis B, varicella, vaccinia, echovirus, parvovirus, influenza, etc.
3. Parasites : malaria and Toxoplasma
Streptococcal
Streptococcus is round-shaped gram-positive bacteria that typically form pairs or chains during
growth. Streptococcus is a heterogeneous group of bacteria. More than 90% of streptococcus
infections in human caused by hemolytic Streptococcus group A. This collection was given the
species name S. pyogenes.5
3.3. Pathophysiology
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Actually not streptococcus causes the damage of the kidneys. Allegedly there is an antibody
directed against an especially antigen which is the element of streptococcus specific plasma
membrane. Antigen-antibody complex formed
in the blood and circulates into the glomerulus
where the complex is mechanically trapped in
the membrane basale then result the lesions and
inflammation that attract polymorphonuclear
leukocytes (PMN) and platelets to the lesion.
Phagocytosis and enzyme release of lysosomes
also damage the glomerular basement
membrane endothel. In response to lesions that occur, proliferation of endothelial cells followed
mesangium cells and subsequent epithelial cells. The increased capillary leak gromerulus causing
protein and red blood cells can get out into the urine that is being formed by the kidneys,
resulting in proteinuria and hematuria. Presumably the antigen-antibody complex is seen as
subepithelial nodules in the electron microscope and as a granular form on immunofluorescence
microscopic; the glomeruli looked swollen light examination and accompanied the invasion
PMN.6
3.4. Prevalence
AGNPS can occur in all age groups, but the commonest in the age group 5-15 years and rarely
occurs in infants. Other references mentioned most often found in children aged 6-10 years. This
disease can occur in men and women, but men are two times more often than women.
Comparison between men and women is 2:1. Allegedly there is a risk factor associated with age
and gender. Tribe or race is not related to the prevalence of this disease, but the possibility of
increased prevalence in people with low socioeconomic, so the neighborhood does not health.3
3.5. Clinical Symptoms
Clinical features show the variability. Sometimes mild symptoms but not infrequently a child
comes with severe symptoms. Damage to the capillary of gromelurus resulted in haematuria and
albuminuria, as has been stated previously. Urine may appear reddish or like coffee sometimes
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accompanied by mild edema around the eyes or restricted throughout the body. Generally there
is severe edema in oliguria and if there is heart failure. Edema that occurs associated with
decreased glomerular filtration rate (GFR), resulting in excretion of water, sodium, nitrogen
substances may be reduced, resulting in edema and azotemia. Increased aldosterone may also
play a role in water and sodium retention. Morning edema often occurs on the face especially
periorbita edema, although edema is most evident under section member body when mid-
morning. The degree of edema usually depends on the weight of glomerulus inflammation,
whether accompanied with congestive heart trouble.7
Hypertension is present in 60-70% of children with the GNA on the first day, then at the end of
the first week to be normal again. If there is damage to kidney tissue, the blood pressure will
remain high for several weeks and become permanent if the condition becomes chronic illness.Not some high body temperature, but can be very high on the first day. Sometime symptoms of
fever persist is existed, even though no symptoms of other infections that preceded it.
Gastrointestinal symptoms such as vomiting, no appetite, constipation and diarrhea are not
uncommon GNA. Hypertension always occurred despite an increase in blood pressure may be
only moderate. Hypertension occurs due to expansion of extracellular fluid volume.
3.6. Laboratory Overview
Urinalysis showed proteinuria (+1 to +4), macroscopic hematuria was found almost in 50% of
patients, abnormalities of urine sediment with erythrocytes disformik, leukosituria and granular,
erythrocyte albumin (++), (+), leukocyte cylinders (+) and others. Sometimes the levels of serum
urea and creatin increased with signs of kidney failure such as hypercalemia, acidosis, and
hypocalcaemia, hiperphospatemia. Sometimes it appears the massive proteinuria with nephrotic
syndrome symptoms. C3 is very noticeable decline in patients with acute glomerulonephritis
pascastreptokokus with levels between 20-40 mg / dl (normal 50-140 mg/dl). The decline is not
related C3 with severity of illness and healing.8
Streptococcus infection should be sought by the throat and skin cultures. Cultures may be
negative if it had been given antimicrobial. Several serological tests against antigens
sterptokokus can be used to prove the existence of infection, among others antisterptozim, Asto,
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antihialuronidase, and anti-Dnase B screening antisterptozim quite useful by being able to
measure antibodies against several antigens sterptokokus. Titer of anti sterptolisin O may
increase in 75-80% of patients with GNAPS with pharyngitis, although some do not produce
sterptolisin.
3.7. Overview pathology
Macroscopic kidney looked a little enlarged, pale and there is bleeding spots on the cortex.
Microscopic look almost all glomeruli affected, so that could be called glomerulonephritis
difuse. Proliferation of glomerular endothelial cell seems harsh resulting in capillary lumen and
Bowman closed the hoop space. In addition there is also a capsule epithelial cell infiltration,
infiltration polimorfonucleus cells and monocytes. On electron microscope examination will
appear irregularly thickened basal membrane. There are lumps humps in subepitelium which
may be formed by gamma-globulin, complement and antigen of Streptococcus.
Histopathology of glomerulonefritis by 20 magnification of
light microscope. Caption: Images taken using a light
microscope (hematosylin and eosin with a magnification 25 ).
Figure shows that make glomerular urinary space enlargement
and hypercelluler. Hypercelluler happened by proliferation ofendogenous cells and PMN leukocyte infiltration.
Histopathology of glomerulonephritis by light microscopy 40
magnification
Histopathology of glomerulonephritis by electron
microscope.
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Caption: Images taken using an electron microscope. Figure shows proliferation of endothel
cells and mesangial cells also infiltrating leucocytes which joined with deposit electrons in
subephitelia.9
3.8. Diagnosis
Diagnosis of acute glomerulonephritis pascastreptococcus need to be suspected in patients with
clinical symptom such as a real hematuria arising suddenly, swollen and acute renal failure after
streptococcal infection. Distinctive mark on urinalysis glomerulonephritis, evidence of
streptococcal infection in laboratory and low levels of complement C3 supports evidence for a
diagnosis. But some other circumstances may resemble acute glomerulonephritis
pascastreptokok in early disease like IgA nephropathy and chronic glomerulonephritis. Children
with IgA nephropathy, hematuria often show real symptoms suddenly soon after upper
respiratory tract infections such as acute glomerulonephritis pascastreptokok, but macroscopic
hematuria in IgA nephropathy, occur simultaneously during faringitas (synpharyngetic
hematuria), while in acute glomerulonephritis arise pascastreptokok hematuria 10 days after
faringitas , while hypertension and swollen rarely seen in nephropathy-IgA.
Other chronic glomerulonephritis also showed a clinical picture of acute macroscopic hematuria,
swollen, hypertension and kidney failure. Some who showed symptoms of chronic
glomerulonephritis was membranoproliferatif glomerulonephritis, lupus nephritis, and
proliferative glomerulonephritis kresentik.
Differences with acute glomerulonephritis pascastreptokok difficult to know at the beginning
infected. In acute glomerulonephritis pascastreptokok history of the disease rapidly improved
(hypertension, swollen and will quickly recover renal failure), proteinuria, nephrotic syndrome
and still more rarely seen in acute glomerulonephritis pascastreptokok than in chronic
glomerulonephritis. The pattern of serum C3 complement levels during follow-up is a sign
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(marker) that is important to distinguish acute glomerulonephritis chronic glomerulonephritis
pascastreptokok with another.9
3.9. Theurapy
There are no specific treatments that affect healing in glomerular abnormalities.
- Absolute rest for 3-4 weeks. Previously recommended rest for 6-8 weeks to allow the kidneys
to heal. But the latest investigation shows that the mobilization of patients after 3-4 weeks of the
first occurrence of no adverse effects on disease course of their illness.
- Giving penicillin in the acute phase. Antibiotics do not affect the severity of
glomerulonephritis, but reduce the spread of streptococcal infections that may still exist. Giving
penicillin is recommended only for 10 days, while providing a long prophylaxis after nefritisnya
recovers against germs that cause is not recommended because there is a permanent immunity.Theoretically, a child may become infected again with germs nefritogen other, but this
possibility is very small. Giving penicillin can be combined with amoksislin 50 mg / kg divided
into 3 doses for 10 days. If the group is allergic to penicillin, erythromycin was replaced with 30
mg / kg / day divided into 3 doses.10
-Food. In the acute phase are given low-protein diet (1 g / kg / day) and low salt (1 g / day). Soft
food given to the patients for high temperatures and ordinary food when the temperature was
normal again. In patients without complications of fluid administration are adjusted to the needs,
while if there are complications such as heart failure, edema, hypertension and oliguria, the
amount of fluid given should be limited.
- Treatment of hypertension. Giving fluids is reduced, giving sedativa to calm patients so that
they can simply relax. In hypertension with cerebral symptoms given reserpin and hidralazin.
Parenteral magnesium sulfate is not recommended anymore because of toxic effects.
- When anuria last long (5-7 days), then urea must be removed from the blood in several ways
such as peritoneum dialysis, hemodialysis, rinses the stomach and intestines (this action is less
effective, exchange transfusion). If the above procedure cannot be done because of technical
difficulties, then the expenditure venous blood can be done and sometimes help as well. 11
CHAPTER IV
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ACUTE GLOMERULONEPHRITIS AND URINARY SYSTEM
Acute glomerulonephritis certainly make things worse our urinary system. The most fatal
relationship is if someone with acute glomerulonephritis and acute renal insufficiency resulting
in kidney failure and even it happened because oliguria to anuria which can last 2-3 days. Occur
as a result of reduced glomerular filtration. Although oliguria or anuria the old rare in children.12
CHAPTER V
CONCLUSION
Glomerunefritis kidney disease is bilateral trade. Acute glomerulonephritis most commonly
occurs in children 3 to 7 years, although young adults and teenagers can also be attacked, a
comparison of this disease in men and women 2:1. GNA is an immunological reaction in the
kidney to specific bacterial or viral. Common symptoms associated with the onset of the disease
are fatigue, anorexia and sometimes fever, headache, nausea, vomiting. Overview of the most
frequently found were: hematuria, oliguria, edema, and hypertension. The main objective in the
management of glomerulonephritis is to minimize damage to the glomerulus, minimizing the
metabolism of the kidney, improve kidney function. There are no specific treatments that affect
healing glomerular abnormalities. We can give penicilin to heal all residual infections, bed rest
during the acute stage, diet if there is edema or symptoms of heart failure and the
antihypertensive if necessary, while corticosteroids had no effect on acute post-infection
glomerulofritis strepkokus. Prognosis diseases in children both while the prognosis in adults is
not so good.
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Infomedika, Jakarta.
3. Ilmu Kesehatan Nelson, 2000, vol 3, ed Wahab, A. Samik, Ed 15, Glomerulonefritis akut
pasca streptokokus, 1813-14, EGC, Jakarta.
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lomerunopritis+salt+dialysis. Accessed April 8th, 2009.
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274-281, Balai Penerbit FKUI,Jakarta.
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Accessed April 8th, 2009.
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.html. Accessed April 8th, 2009.
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