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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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REFERENCES

1. Price, Sylvia A, 1995 Patofisiologi :konsep klinis proses-proses penyakit, ed 4, EGC,

Jakarta.

2. Staf Pengajar Ilmu Kesehatan Anak FKUI, 1985, Glomerulonefritis akut, 835-839,

Infomedika, Jakarta.

3. Ilmu Kesehatan Nelson, 2000, vol 3, ed Wahab, A. Samik, Ed 15, Glomerulonefritis akut

pasca streptokokus, 1813-14, EGC, Jakarta.

4. http://www/.5mcc.com/ Assets/ SUMMARY/TP0373.html. Accessed April 8th, 2009.

5. http://www.Findarticles.com/cf0/g2601/0005/2601000596/pi/article.jhtm?term=g

lomerunopritis+salt+dialysis. Accessed April 8th, 2009.

6. markum. M.S, Wiguno .P, Siregar.P,1990, Glomerulonefritis, Ilmu Penyakit Dalam II,

274-281, Balai Penerbit FKUI,Jakarta.

7. Donna J. Lager, M.D.http;//www.vh.org/adult/provider/pathologi/GN/GNHP.html.

Accessed April 8th, 2009.

8. http;//www.enh.org/encyclopedia/ency/article/000475.asp. Accessed April 8th, 2009.

9. http://www.kalbefarma.com/files/cdk/files/08_KlarifikasiHistopatologik.pdf/08_Klarifika

siHistopatologik.html. Accessed April 8th, 2009.

10. http://www.kalbe.co.id/files/cdk/files/11_HematuriPadaAnak.pdf/11_HematuriPadaAnak

.html. Accessed April 8th, 2009.

11. http://pkukmweb.ukm.my/~danial/Streptococcus.html. Accessed April 8th, 2009.

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http://www/http://www.kalbefarma.com/files/cdk/files/08_KlarifikasiHistopatologik.pdf/08_KlarifikasiHistopatologik.htmlhttp://www.kalbefarma.com/files/cdk/files/08_KlarifikasiHistopatologik.pdf/08_KlarifikasiHistopatologik.htmlhttp://www.kalbe.co.id/files/cdk/files/11_HematuriPadaAnak.pdf/11_HematuriPadaAnak.htmlhttp://www.kalbe.co.id/files/cdk/files/11_HematuriPadaAnak.pdf/11_HematuriPadaAnak.htmlhttp://pkukmweb.ukm.my/~danial/Streptococcus.htmlhttp://www.kalbefarma.com/files/cdk/files/08_KlarifikasiHistopatologik.pdf/08_KlarifikasiHistopatologik.htmlhttp://www.kalbefarma.com/files/cdk/files/08_KlarifikasiHistopatologik.pdf/08_KlarifikasiHistopatologik.htmlhttp://www.kalbe.co.id/files/cdk/files/11_HematuriPadaAnak.pdf/11_HematuriPadaAnak.htmlhttp://www.kalbe.co.id/files/cdk/files/11_HematuriPadaAnak.pdf/11_HematuriPadaAnak.htmlhttp://pkukmweb.ukm.my/~danial/Streptococcus.htmlhttp://www/


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12. http://medlinux.blogspot.com/2007/09/glomerulonephritis-akut.html. Accessed April 8th,

2009.

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