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Acute Glomerulonephritis
Author: Malvinder S Parmar, MB, MS; Chief Editor: Vecihi Batuman, MD, FACP,
FASN more...
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Updated: Jul 17, 2015

Background

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Background
Acute glomerulonephritis (GN) comprises a specific set of renal diseases in which
an immunologic mechanism triggers inflammation and proliferation of glomerular
tissue that can result in damage to the basement membrane, mesangium, or
capillary endothelium. Acute poststreptococcal glomerulonephritis (PSGN) is the
archetype of acute GN. Acute nephritic syndrome is the most serious and potentially
devastating form of the various renal syndromes.
Hippocrates originally described the natural history of acute GN, writing of back pain
and hematuria followed by oliguria or anuria. Richard Bright described acute GN
clinically in 1827, which led to the eponymic designation Bright disease. With the

development of the microscope, Langhans was later able to describe these


pathophysiologic glomerular changes.
Acute GN is defined as the sudden onset of hematuria, proteinuria, and red blood
cell (RBC) casts. This clinical picture is often accompanied by hypertension,
edema, azotemia (ie, decreased glomerular filtration rate [GFR]), and renal salt and
water retention. Acute GN can be due to a primary renal disease or to a systemic
disease. Most original research focuses on acute PSGN.
Treatment of PSGN is mainly supportive, because there is no specific therapy for
renal disease. When acute GN is associated with chronic infections, the underlying
infections must be treated. This article addresses the aspects of GN that are
relevant to its acute management.
Go to Emergent Management of Acute Gldmerulonephritis and Acute
Poststreptococcal Glomerulonephritis for complete information on these topics.
Next Section: Pathophysiology
READ MORE ABOUT ACUTE GLOMERULONEPHRITIS ON MEDSCAPE
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