Skip to main content
Onhealthmeup.com - Glomerulonephritis is a kidney disease with an inflammation and glomerular cell proliferation. Inflammation of the kidneys has an effect on immunologic mechanisms associated with bacterial beta-hemolytic streptococcal group A type nephritogenic infections get into the hematogenous phase resulting from inadequate treatment of Pharyngitis, tonsillitis or other dermatitis diseases.

After inadequate treatment causes the bacteria running into the circulation and settle in various organs ranging from the heart, lungs to the kidneys, the biggest effect is on the kidneys and heart where there is a crossing of the body's natural antigenic protein against streptococcus antigens undergoing a cross-reaction so complex the antibody fails to determine and locate where the antigen is originally made by streptococcus. Characteristic of clinical onset of nephrotic syndrome in the form of a collection of syndromes include gross hematuria (bloody urine), edema (puffiness), hypertension and acute renal failure.

Now in Indonesia,  Poststreptococcal Glomerulonephritis (APSGN) acute Glomerulonephritis cases are still high in number and in most cases for acute kidney disorders in children. The age range for APSGN infection is 2-8 years and boys are more dominant to be infected. Where this period of hygiene and healthy living behavior has not been touched or adequately taught. APSGN is also still high due to the lifestyle of Indonesian society towards the treatment of a disease is not completely and comes at a time when chronic infection. Climate also affects APSGN infection where tropical climate is considered fit and suitable for growth of Streptococcus bacteria.

Genetic factors influence the pathogenesis of Streptococcus infection against a human body wherein laboratory tests it is found the role of HLA-D and HLA-DR to show a change in latency with abnormalities in the glomerular basement membrane of immunological processes. It is thought to be an exaggerated response of the host immune system to the antigen stimulus resulting in an antigen-antigen (ab-ag) complex that will cross the basal membrane of the glomerulus. From here there is the activation of a complementary system that releases substances that will attract neutrophils. Lysosome enzymes released by neutrophils will respond more responsively to damage. Another hypothesis theory due to the resulting neuraminidase streptococcus will convert endogenous IgG to autoantigen resulting in the formation of autoantibodies to the altered IgG, resulting in the formation of immune complexes circulating and then settling in the kidneys.

In the case of ailment glomerulonephritis found microscopically mild to a moderate proliferation of mesangial cells and matrix. In severe cases, there will be a proliferation of mesangial cells, diffuse matrix and endothelial cells with polymorphonucleate and monocyte cells as well as capillary lumen blockage. The deposits of immunoglobulins in glomerular capillaries are dominated by IgG and as small amounts of IgM or IgA can be seen through the immunofluorescence microscope. While the electron microscope phase is found the deposit of electron solids or humps lies in a distinctive subepithelial region and will aggregate into Ag-Ab complex.


Clinical Symptoms Of Acute Poststreptococcal Glomerulonephritis


Clinical symptoms of  APSGN as preliminary information to justify the child affected by  APSGN found asymptomatic symptoms of 50%. Where classic cases have previously experienced a respiratory infection or with a sore throat two weeks preceding the onset of swelling.

The latent period after 10-21 is infected with a sore throat and skin infections. And found also as follows:


  • Haematuria can occur with gross hematuria or microscopically, found in 30-50% of hospitalized children.
  • Other variations are not specific such as fever, malaise, pain, decreased appetite, headache or lethargy.
  • On physical examination found hypertension in patients  APSGN  ranging from mild to moderate, with typical characteristics will rise in 3-5 days and will drop slowly 1-2 weeks.
  • Edema can be a swollen face, ranging from the orbital area of the eye and the foot (pretibial).
  • Ascites can be found in 35% of cases of APSGN edema.
  • Clinically circulating dams can be evident with takipne and dyspnea.
  • Symptoms can also be accompanied by oliguria to anuria due to decreased Glomerular Filtration Rate (GFR).
  • APSGN Support Checkup
  • In laboratory examination can be found as follows:

Urine examination found volume decreased with dark or brownish color like fresh meat wash water.
Erythrocytes 60-85% of cases in the presence of bleeding signs on the glomerulus and also found hematuria on macros and micros.
Proteinuria in urine is proportional to haematuria as long as it does not exceed the 2gr / m2 limit.
LFG decreases with water and salt excretion capacity leading to extracellular fluid volume expansion.
Anemia will disappear if the spleen (edema) is also lost and correlates to fluid and urine volume and some studies suggest that the erythrocyte lifespan is reduced due to serum protein changes and hormone regulation.
Culture and culture test became standard gold, supported by a serologic test of immune response to Streptococcus antigen. Increased antibody titer against streptolysin-O (ASTO) occurs after 10-14 days.
The decrease in serum complement C3 levels was present in 80-90% of cases within the first 2 weeks, while the properdin level decreased by 50%, for IgG often increased by 1600mg / 100ml. at the beginning of the disease, there are cryogenic cyclobulins containing IgG, IgM and complement C3.
Nearly a third of patients have a pulmonary dam with radiological features of 84.5% cardiomegaly, 68.2% pulmonary circulatory dam, and 63.5% pulmonary edema.


Treatments for Acute Poststreptococcal Glomerulonephritis


APSGN Treatment of patients is supportive and symptomatic. Treatment is required when there is a moderate to severe renal dysfunction (creatinine clearance 50 mg, children with signs and symptoms of uremia, vomiting, lethargy, hypertensive encephalopathy, anuria or oliguria persist.


  • Hypertensive patients may be given diuretics or anti-hypertension. When mild hypertension (systolic blood pressure 130 mmHg and diastolic 90 mmHg) is generally observed without therapy. Moderate hypertension (systolic blood pressure> 140 -150 mmHg and diastolic> 100 mmHg) is treated with oral or intramuscular hydralazine (IM), oral or sublingual nifedipine. In practice it is better to treat the patient's hypertension 1-2 days rather than giving anti-hypertension a long time. In severe hypertension, hydralazine is given 0.15-0.30 mg / kbBB intravenously, can be repeated every 2-4 hours or 0.03-0.10 mg / kgBB (1-3 mg / m2) iv, or sodium nitroprussid 1 -8 m / kgBB / min. In hypertensive crisis (systolic> 180 mmHg or diastolic> 120 mmHg) given diazoxide 2-5 mg / kgBW iv rapidly with furosemide 2 mg / kgBW iv. Alternatively, clonidine drip 0.002 mg / kgBB / times, repeated every 4-6 hours or given sublingual nifedipine 0.25-0.5 mg / kgBb and may be repeated every 6 hours if necessary.
  • Fluid retention is treated with fluid and sodium restriction. Liquid intake is proportional to invensible water loss (400-500 ml / m2 body surface area/day) plus half or less of urine coming out. When weight is not reduced diuretics such as furosemide 2mg / kgBB, 1-2 times / day.
  • Use of antibiotics does not affect the course of the disease. However, patients with a positive culture should be given antibiotics for eradication of the organism and prevent spread to other individuals. Given an antimicrobial injection of benzathine penicillin 50.000 U / kg IM or oral erythromycin 40 mg/kg body weight/day for 10 days if the patient is penicillin allergy. The restriction of food depends on the severity of edema, renal failure, and hypertension.
  • Proteins need not be limited if the 61 urea content is less than 75 mg / dL or 100 mg / dL.
  • When azotemia occurs the protein intake is limited to 0.5 g / kg/day.
  • In heavy edem and circulation dams can be given NaCl 300 mg/day whereas if minimal edem and mild hypertension are given 1-2 g / m2 / day. When accompanied by oliguria, potassium should be limited. Anuria and oliguria persist, occurring in 5-10% of children.
  • Treatment is similar to ARF with various causes and rarely cause 

You Might Also Like:

Comment Policy: Comments are welcomed and encouraged on this site, but there are some instances where comments will be edited or deleted.
Open To Comment