Acute Glomerulonephritis - Causes, Treatment & When to See a Doctor

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What is Acute Glomerulonephritis?

Acute glomerulonephritis (AGN) is a sudden inflammation of the glomeruli, the tiny filtering units inside the kidneys that remove waste and excess fluid from the blood. When the glomeruli become inflamed, they lose their ability to filter properly, leading to the leakage of blood cells and protein into the urine, swelling (edema), hypertension, and a decline in kidney function. AGN can develop over days to weeks and may resolve completely, but in some cases it progresses to chronic kidney disease.

There are two main categories:

• Post‑infectious (post‑streptococcal) glomerulonephritis: follows an infection, most commonly of the throat or skin.
• Immune‑mediated glomerulonephritis: caused by systemic autoimmune diseases (e.g., lupus) or vasculitis.

Because the kidneys are essential for fluid‑balance, electrolyte regulation, and waste removal, early recognition and treatment are crucial to prevent permanent damage.

Common Causes

Acute glomerulonephritis is usually a response to an external trigger that stimulates the immune system. The most frequent causes include:

• Post‑streptococcal infection (pharyngitis or impetigo) – the classic cause in children and adolescents.
• IgA nephropathy (Berger disease) – deposition of immunoglobulin A in the glomeruli, often after a respiratory infection.
• Lupus nephritis – systemic lupus erythematosus causing immune‑complex deposition.
• Rapidly progressive glomerulonephritis (RPGN) – a severe form that can be driven by anti‑glomerular basement membrane antibodies (Goodpasture syndrome) or ANCA‑associated vasculitis.
• Membranoproliferative glomerulonephritis (MPGN) – often linked to chronic infections (e.g., hepatitis C) or complement disorders.
• Henoch‑Schönlein purpura (IgA vasculitis) – a small‑vessel vasculitis that frequently involves the kidneys.
• Infective endocarditis – bacterial infection of heart valves can seed immune complexes to the kidney.
• Hepatitis B or C infection – chronic viral infection can trigger immune‑complex glomerulonephritis.
• Drug‑induced nephritis – certain antibiotics (e.g., penicillins), NSAIDs, or gold compounds.
• Alport syndrome (rarely presents acutely) – a genetic disorder of type IV collagen that can flare with hematuria.

Associated Symptoms

Symptoms arise from impaired filtration, fluid overload, and the inflammatory process itself. Commonly reported signs include:

• Dark, “cola‑colored” urine due to hematuria
• Foamy urine indicating protein loss
• Swelling (edema) most noticeable in the face, eyelids, hands, and ankles
• Decreased urine output (oliguria) or, less commonly, increased frequency
• Painful or tender abdomen (from fluid accumulation)
• High blood pressure (often >140/90 mmHg)
• Fatigue, weakness, and malaise
• Fever or recent history of sore throat/skin infection (especially in post‑streptococcal cases)
• Joint or muscle aches if an underlying systemic disease is present

When to See a Doctor

Because AGN can progress rapidly, prompt medical evaluation is essential. Seek care if you notice any of the following:

• Visible blood in the urine or urine that looks tea‑colored
• Sudden swelling of the face, hands, or feet that doesn’t improve with rest
• New‑onset high blood pressure, especially if accompanied by headaches or visual changes
• Significant decrease in urine volume (<400 mL per day)
• Persistent fever or severe sore throat/skin infection lasting more than 3 days
• Unexplained weight gain (often due to fluid retention)
• Any combination of the above in a child or teenager, as post‑infectious AGN is most common in this age group.

Diagnosis

Diagnosing acute glomerulonephritis involves a combination of clinical assessment, laboratory testing, and imaging. The goals are to confirm kidney inflammation, identify the underlying cause, and gauge severity.

Laboratory Tests

• Urinalysis – looks for red blood cells, red blood cell casts, protein, and leukocytes.
• Serum creatinine & blood urea nitrogen (BUN) – assess kidney function; elevations suggest reduced filtration.
• Estimated glomerular filtration rate (eGFR) – provides a quantitative measure of kidney performance.
• Complement levels (C3, C4) – low C3 may point to post‑streptococcal or membranoproliferative disease.
• Anti‑streptolysin O (ASO) or anti‑DNAse B titers – evidence of recent streptococcal infection.
• Autoimmune panel – ANA, anti‑dsDNA (lupus), anti‑GBM antibodies, ANCA (vasculitis).
• Serologies for hepatitis B, hepatitis C, HIV – rule out infection‑related GN.
• Blood cultures – indicated if endocarditis is suspected.

Imaging

• Renal ultrasound – evaluates kidney size, rule out obstruction, and can detect increased echogenicity typical of inflammation.

Kidney Biopsy

When the cause remains unclear or the disease appears aggressive (rapidly rising creatinine, heavy proteinuria, or suspicion of RPGN), a percutaneous kidney biopsy is performed. Histologic patterns help determine the specific type of GN and guide targeted therapy.

Treatment Options

Treatment is tailored to the underlying cause, severity of kidney involvement, and the patient’s overall health.

General Measures

• Fluid and salt restriction – limit sodium to < 2 g/day and fluid intake to 1.5‑2 L/day to reduce edema and hypertension.
• Blood pressure control – ACE inhibitors or ARBs are first‑line; they also reduce proteinuria.
• Diuretics (e.g., furosemide) for symptomatic edema.
• Dietary protein moderation – 0.8‑1.0 g/kg/day to lessen the kidney’s workload while preserving nutrition.
• Vaccinations – especially influenza and pneumococcal vaccines, as chronic kidney disease increases infection risk.

Specific Therapies

• Post‑streptococcal GN – primarily supportive; antibiotics (penicillin or cephalosporin) are given to eradicate residual streptococcal organisms, and NSAIDs are avoided because of nephrotoxicity.
• IgA nephropathy – ACE‑I/ARB for blood pressure and proteinuria; steroids or immunosuppressants (e.g., cyclophosphamide) only in rapidly progressive cases.
• Lupus nephritis – high‑dose corticosteroids plus mycophenolate mofetil or cyclophosphamide; maintenance therapy often includes azathioprine.
• ANCA‑associated vasculitis / Goodpasture syndrome – combination of high‑dose intravenous methylprednisolone, oral prednisone taper, and either cyclophosphamide or rituximab; plasma exchange is considered for severe pulmonary‑renal involvement.
• Hepatitis‑related GN – antiviral therapy (e.g., direct‑acting antivirals for HCV) alongside immunosuppression if needed.
• Drug‑induced GN – immediate cessation of the offending agent; supportive care; steroids may be used if inflammation persists.

Hospital‑Based Interventions

• Intravenous antihypertensives (nicardipine, labetalol) for severe hypertension.
• Dialysis (hemodialysis or peritoneal dialysis) when there is refractory fluid overload, hyperkalemia, or uremic symptoms.
• Plasmapheresis for anti‑GBM disease or severe ANCA vasculitis.

Follow‑up Care

After acute management, patients need regular monitoring of kidney function, blood pressure, and urine protein. Frequency depends on disease severity but typically includes visits every 3–6 months for the first year.

Prevention Tips

Because many triggers are infectious or immune‑mediated, prevention focuses on reducing exposure and managing underlying conditions.

• Prompt treatment of streptococcal throat or skin infections; complete the full course of antibiotics.
• Good hand hygiene and avoiding close contact with individuals who have active bacterial infections.
• Vaccination against hepatitis B and hepatitis C screening for at‑risk populations.
• Control of systemic diseases such as diabetes, lupus, and hypertension to lower the risk of secondary GN.
• Avoid unnecessary use of nephrotoxic medications (high‑dose NSAIDs, certain antibiotics) without physician oversight.
• Maintain a healthy lifestyle—balanced diet, regular exercise, adequate hydration—to support overall kidney health.
• Regular medical check‑ups for people with a family history of kidney disease or known autoimmune disorders.

Emergency Warning Signs

If any of the following develop, seek emergency medical care immediately (call 911 or go to the nearest emergency department):

• Sudden, severe swelling of the face, lips, or tongue (possible anaphylaxis related to immune‑complex disease)
• Rapidly worsening shortness of breath or chest pain (may signal fluid overload or pulmonary edema)
• Blood pressure spikes above 180/120 mmHg with headache, visual changes, or confusion
• Sudden decrease in urine output to almost none (anuria)
• Persistent vomiting or nausea with inability to keep fluids down
• High fever (>39 °C / 102 °F) with chills, especially after a recent infection
• Severe abdominal or flank pain accompanied by blood in the urine

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**References**

1. Mayo Clinic. “Acute glomerulonephritis.” https://www.mayoclinic.org. Accessed May 2024.
2. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). “Glomerulonephritis.” https://www.niddk.nih.gov. Accessed May 2024.
3. American College of Rheumatology. “ANCA‑Associated Vasculitis Treatment Guidelines.” 2023.
4. Cleveland Clinic. “Post‑streptococcal glomerulonephritis.” https://my.clevelandclinic.org. Accessed May 2024.
5. World Health Organization. “Guidelines for the Management of Hepatitis C.” 2022.
6. UpToDate. “Management of acute glomerulonephritis in adults.” 2023 (subscription required).

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