Acute Poststreptococcal Glomerolunephritis
Glumerolunephritis is the inflammation of the glumeruli of the kidney. Acute glumerolunephritis (AGN) is a disease described as the abrupt appearance of edema, hematuria, proteinuria and hypertension. The inflammation of the glomerulus is manifested by the spread of cellular elements as a result of an immune response.
Acute Poststreptococcal Glomerolunephritis (APSGN) occurs as an immune complex disease after an infection with nephritogenic streptococci (most commonly subtypes of Group A beta-hemolytic streptococci). As a result of the antigen-antibody reaction, aggregates of molecules are formed and circulate throughout the body. The glomeruli, the filtering portion of the kidney, trap some of this circulating molecules resulting to the inflammation of glomeruli.
- Occurs more commonly in males.
- Most common in children between 5-10 years (peak prevalence at about 5-6 years).
- Occurs more often during winter and spring.
Acute poststreptococcal glomerulonephritis is an immune reaction of the body to nephritogenic streptococci infection. It usually follows an infection caused by the group A beta hemolytic streptococci such as:
- Strep throat
- Otitis media
- Recent respiratory infection
- Scarlet fever
In Acute poststreptococcal glomerulonephritis (APSGN), the streptococcal product acts as the antigen that stimulates the circulating antibodies which results to deposit of molecules in the glomeruli leading to injury of the kidney. The IgG, major immunoglobulin found in the human blood, can be detected in the bloodstream and the glomerular capillary walls. This results to antigen-antibody reaction which is characterized by the formation and circulation of the complexes (molecules) in the body. A complement, cascade of proteins activated by antigen-antibody reactions which plugs or obstructs the glomerul, is formed. Complement fixation reaction of the glomeruli results to tissue damage.
As endothelial cells on the linings of the glomerulus are increased as a response to the inflammatory process, it can result to the infiltration of the leukocytes in the glomeruli. Intravascular coagulation may occur in small renal tubules. The thickening of the glomerular filtration membrane results to the scarring and loss of the filtering surfaces. Thus, unusual large particles (such as protein) can be excreted in the urine due to the increased glomerular permeability related to ischemic damage. Decreased glomerular filtration rate (GFR) would result to the accumulation of sodium and water in the bloodstream.
- History of recent group A streptococcal infection (2-3 weeks)
- Sudden onset of hematuria
- Urine: tea-colored, reddish-brown or smoky
- Abdominal pain
- Low-grade fever
- Edema (mild)
- Decreased urine output
- Cardiac involvement: orthopnea, cardiac enlargement, pulmonary edema, galloping heart rhythm
- Anti-streptolysin O (ASO) titer elevated
- BUN and serum creatinine elevated
- Anti-Dnase B titer elevated
- 1+ to 4+ protein in urine
- Increased specific gravity of the urine
The course of acute glomerulonephritis is 1-2 weeks. Antibiotics are ineffective in treating the disease because APSGN is caused by an antigen-antibody inflammatory response to a previous infection. Unless residual streptococcal infection is suspected, penicillin may be given.
- If heart failure occurs, place the child in a semi-fowler’s position, digitalis therapy and oxygen administration.
- Calcium channel blocker – for diastolic BP of more than 90 mmHg.
- Normal diet for age
- Weighing the child every day and monitoring intake and output.
- Children can attend school and engage in normal activities after 1 week but competitive activity is limited.