Glomerulonephritis Introduction

Acute glomerulonephritis (AGN) is an alteration in renal function caused by glomerular injury, which is displayed by the classic symptoms of gross hematuria, mild proteinuria, edema (usually periorbital), hypertension, and oliguria. AGN is also classified as either: a primary disease, associated with group A, beta-hemolytic streptococcal infection; or a secondary disease, associated with various systemic diseases (i.e., systemic lupus erythema, sickle cell disease, Henoch's chorea purpura). The most common type of AGN is the primary disease, described as an immune-complex disease (or an antigen-antibody complex formed during the streptococcal infection which becomes entrapped in the glomerular membrane, causing inflammation 8 to 14 days after the onset of this infection). AGN is primarily observed in the early school-age child, with a peak age of onset of 6 to 7 years. The onset of the classic symptoms of AGN is usually abrupt, self-limiting (unpredictable), and prolonged hematuria and proteinuria may occur. AGN results in decreased glomerular filtration rate causing retention of water and sodium (edema); expanded plasma and interstitial fluid volumes that lead to circulatory congestion and edema (hypervolemia); hypertension (cause is unexplained; plasma renin activity is low during the acute phase, hypervolemia is suspected to be the cause).

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