Acute Glomerulonephritis

Author: Malvinder S Parmar, MB, MS; Chief Editor: Vecihi Batuman, MD,
FACP, FASN more...

Overview
Presentation
DDx
Workup
Treatment
Medication

Background

Pathophysiology
Etiology
Epidemiology
Prognosis
Patient Education
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Updated: Jul 17, 2015

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References
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.