Acute glomerulonephritis |
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Authors: | R N Srivastava |
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Institution: | (1) Apollo Indraprastha Hospital, 110 044 New Delhi |
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Abstract: | Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal
function. The commonest form of AGN in developing countries is that following a beta hemolytic streptococcal infection where
the glomerular injury is mediated by deposition of immune complexes. In the usual patient with moderately severe poststreptococcal
AGN (PSAGN) the above-mentioned features are present However, gross or microscopic hematuria may be the only abnormality.
A similar picture may occasionally be produced by a variety of infections (when GN is referred to as post-infectious and the
mechanism of glomerular damage and the renal histology are similar to that in PSAGN), primary renal glomerular disorders (eg.
membranoproliferative GN, IgA nephropathy), collagen vascular diseases (systemic lupus erythematosus), systemic vasculitis
(Henoch Schonlein purpura) and hereditary nephritis and some nonglomerular conditions. PSAGN may also present with one or
more of its complications such as profound volume expansion with heart failure and hypertensive encephalopathy. PSAGN resolves
rapidly and has an excellent prognosis. Patients with severe renal involvement and life threatening complications need expert
supportive management. AGN with associated systemic features or very pronounced azotemia, nonstreptococcal AGN and unresolving
GN need prompt, appropriate evaluation that often includes a renal biopsy. If extensive crescentic changes are found (crescentic
GN), aggressive immunosuppression will be necessary. |
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Keywords: | Acute glomerulonephritis Poststreptococcal glomerulonephritis Hematuria |
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