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	<id>https://wikem.org/w/index.php?action=history&amp;feed=atom&amp;title=Acute_glomerulonephritis</id>
	<title>Acute glomerulonephritis - Revision history</title>
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	<updated>2026-04-17T18:29:31Z</updated>
	<subtitle>Revision history for this page on the wiki</subtitle>
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	<entry>
		<id>https://wikem.org/w/index.php?title=Acute_glomerulonephritis&amp;diff=376725&amp;oldid=prev</id>
		<title>Cole Ettingoff: Created page with &quot;==Background== Acute glomerulonephritis (AGN) is a syndrome characterized by sudden onset of glomerular inflammation, often due to immune-mediated damage. It may follow infections (e.g., post-streptococcal), be part of systemic diseases (e.g., lupus, vasculitis), or be primary renal pathology (e.g., IgA nephropathy). It can lead to rapid loss of kidney function if not promptly recognized.  ==Clinical Features==  Hematuria (often gross or “tea/cola-colored”)  Proteinu...&quot;</title>
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		<updated>2025-06-07T22:35:27Z</updated>

		<summary type="html">&lt;p&gt;Created page with &amp;quot;==Background== Acute glomerulonephritis (AGN) is a syndrome characterized by sudden onset of glomerular inflammation, often due to immune-mediated damage. It may follow infections (e.g., post-streptococcal), be part of systemic diseases (e.g., lupus, vasculitis), or be primary renal pathology (e.g., IgA nephropathy). It can lead to rapid loss of kidney function if not promptly recognized.  ==Clinical Features==  Hematuria (often gross or “tea/cola-colored”)  Proteinu...&amp;quot;&lt;/p&gt;
&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;==Background==&lt;br /&gt;
Acute glomerulonephritis (AGN) is a syndrome characterized by sudden onset of glomerular inflammation, often due to immune-mediated damage. It may follow infections (e.g., post-streptococcal), be part of systemic diseases (e.g., lupus, vasculitis), or be primary renal pathology (e.g., IgA nephropathy). It can lead to rapid loss of kidney function if not promptly recognized.&lt;br /&gt;
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==Clinical Features==&lt;br /&gt;
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Hematuria (often gross or “tea/cola-colored”)&lt;br /&gt;
&lt;br /&gt;
Proteinuria (may be subnephrotic or nephrotic range)&lt;br /&gt;
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Edema (especially periorbital or dependent)&lt;br /&gt;
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Hypertension&lt;br /&gt;
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Oliguria or anuria&lt;br /&gt;
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Fatigue, malaise&lt;br /&gt;
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In some cases: fever, arthralgia, or rash (if systemic disease)&lt;br /&gt;
&amp;lt;gallery&amp;gt;&lt;br /&gt;
Example.jpg|Caption1&lt;br /&gt;
Example.jpg|Caption2&lt;br /&gt;
&amp;lt;/gallery&amp;gt;&lt;br /&gt;
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==Differential Diagnosis==&lt;br /&gt;
&lt;br /&gt;
Nephrotic syndrome (e.g., minimal change disease)&lt;br /&gt;
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Acute tubular necrosis&lt;br /&gt;
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Interstitial nephritis&lt;br /&gt;
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Hemolytic uremic syndrome (HUS)&lt;br /&gt;
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Thrombotic thrombocytopenic purpura (TTP)&lt;br /&gt;
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Urinary tract infection (for hematuria/proteinuria)&lt;br /&gt;
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Urolithiasis or trauma (for hematuria)&lt;br /&gt;
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==Evaluation==&lt;br /&gt;
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===Workup===&lt;br /&gt;
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Urinalysis: Hematuria, red blood cell casts, proteinuria&lt;br /&gt;
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Blood tests:&lt;br /&gt;
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BUN/Creatinine&lt;br /&gt;
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CBC (anemia, leukocytosis)&lt;br /&gt;
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Complements (C3, C4)&lt;br /&gt;
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Antistreptolysin-O (ASO) titer, anti-DNase B&lt;br /&gt;
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ANA, ANCA, anti-GBM antibodies&lt;br /&gt;
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Renal ultrasound: Evaluate for obstruction or size changes&lt;br /&gt;
&lt;br /&gt;
Kidney biopsy: If unclear diagnosis, severe presentation, or rapid progression&lt;br /&gt;
&lt;br /&gt;
===Diagnosis===&lt;br /&gt;
Diagnosis is clinical, supported by lab findings of kidney injury with hematuria, proteinuria, and often low complement levels. Serologies may point to the underlying cause. Biopsy provides definitive diagnosis when needed.&lt;br /&gt;
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==Management==&lt;br /&gt;
&lt;br /&gt;
Supportive care: Salt and fluid restriction, diuretics for edema, antihypertensives&lt;br /&gt;
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Treat underlying cause:&lt;br /&gt;
&lt;br /&gt;
Post-infectious: usually self-limited; antibiotics if infection active&lt;br /&gt;
&lt;br /&gt;
Lupus nephritis: corticosteroids, immunosuppressants&lt;br /&gt;
&lt;br /&gt;
ANCA vasculitis or anti-GBM disease: steroids, cyclophosphamide, plasmapheresis&lt;br /&gt;
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Nephrology consult for all but mildest cases&lt;br /&gt;
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==Disposition==&lt;br /&gt;
&lt;br /&gt;
Admit if: significant renal impairment, uncontrolled hypertension, volume overload, rapidly progressive features, or systemic disease&lt;br /&gt;
&lt;br /&gt;
Outpatient management may be possible for stable patients with close nephrology follow-up&lt;br /&gt;
&lt;br /&gt;
==See Also==&lt;br /&gt;
&lt;br /&gt;
Nephritic Syndrome&lt;br /&gt;
&lt;br /&gt;
Nephrotic Syndrome&lt;br /&gt;
&lt;br /&gt;
Lupus Nephritis&lt;br /&gt;
&lt;br /&gt;
Rapidly Progressive Glomerulonephritis (RPGN)&lt;/div&gt;</summary>
		<author><name>Cole Ettingoff</name></author>
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