Acute poststreptococcal glomerulonephritis
OVERVIEW
What is acute post-streptococcal glomerulonephritis?
Acute post-streptococcal glomerulonephritis (APSGN) is the most common type of acute glomerulonephritis, primarily caused by β-hemolytic streptococcal infection.
Clinically, it manifests as a rapidly developing glomerular disease characterized by hematuria, proteinuria, edema, hypertension, and decreased glomerular filtration rate. APSGN is more common in children, as well as in adult patients with alcoholism or drug addiction. Elderly patients often experience more severe symptoms. With advancements in medicine, the prevalence of this disease has significantly declined, but it remains high in economically underdeveloped regions.
Is acute post-streptococcal glomerulonephritis common?
Statistics show that over 470,000 cases of APSGN occur worldwide annually, with 97% in developing countries, and approximately 5,000 resulting in death. The disease is more prevalent in children, with males affected twice as often as females (2:1 ratio). It is most common in children aged 5–12 years and rare in those under 2 years old.
What are the main pathogenic bacteria of acute post-streptococcal glomerulonephritis?
APSGN is typically caused by β-hemolytic streptococcal "nephritogenic strains" (commonly Group A types 12 and 49) and rarely occurs secondary to other infections.
Is acute post-streptococcal glomerulonephritis contagious or hereditary?
APSGN is a clinical syndrome following infection and is generally neither contagious nor hereditary.
SYMPTOMS
What are the common symptoms of acute poststreptococcal glomerulonephritis?
Acute poststreptococcal glomerulonephritis often occurs after streptococcal infections such as upper respiratory tract infections, skin infections, or scarlet fever. The specific manifestations are as follows:
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Hematuria: Almost all cases present with hematuria, with 40% showing gross hematuria. The urine appears pink or tea-colored, typically without blood clots, lasting 1–2 weeks. Microscopic hematuria may persist for 1–6 months, and in rare cases, it can last half a year or longer.
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Proteinuria: Nearly all patients exhibit varying degrees of proteinuria, though most cases involve less than 3.0 g/d. It may resolve within days or weeks, but a few patients may develop nephrotic-range proteinuria.
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Edema: An early symptom, often presenting as morning eyelid swelling, termed "nephritic facies." In severe cases, it may spread throughout the body but is typically non-pitting (no indentation when pressed). Diuresis and resolution usually occur within about 2 weeks.
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Hypertension: Approximately 80% of patients experience mild to moderate hypertension, primarily due to water-sodium retention and increased blood volume. The severity of hypertension often parallels the degree of edema and normalizes with diuresis and resolution of swelling.
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Oliguria: Some patients present with reduced urine output (< 400 mL/d) and transient azotemia at onset. Urine volume gradually increases after 2 weeks, with renal function recovering.
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Acute kidney injury: Most cases involve transient mild elevations in blood urea nitrogen and serum creatinine. The condition is self-limiting, with most patients recovering within weeks.
CAUSES
What are the possible causes of acute poststreptococcal glomerulonephritis?
It is caused by infection with β-hemolytic streptococcus "nephritogenic strains" (commonly group A types 12 and 49).
The main pathogenic mechanisms include: formation of streptococcal antigen-antibody immune complexes that deposit in glomeruli with complement activation; autoimmune reactions between streptococcal and renal tissue components; and autoimmune reactions triggered by altered normal renal antigens.
DIAGNOSIS
How to diagnose acute poststreptococcal glomerulonephritis?
Typically, 1-3 weeks after streptococcal infection, symptoms of acute nephritis syndrome such as hematuria, proteinuria, edema, and hypertension may occur, sometimes accompanied by oliguria and renal insufficiency, along with decreased serum C3 levels.
If the condition gradually improves and fully recovers within 8 weeks of onset, a clinical diagnosis of acute poststreptococcal glomerulonephritis can be made. If the glomerular filtration rate progressively declines or symptoms persist beyond 2 months, a renal biopsy should be performed promptly for definitive diagnosis.
What tests are needed for patients with acute poststreptococcal glomerulonephritis?
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Blood test: Elevated white blood cell count, predominantly neutrophils. Urinalysis: Presence of red blood cells, with or without proteinuria.
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Renal function: Possible transient increase in creatinine levels.
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Immunoglobulin complement and ASO titer: Typically, decreased serum C3 and elevated ASO titer, indicating recent streptococcal infection.
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Throat swab culture: About half of cases show positive culture for group A beta-hemolytic streptococci from throat or skin lesions. For patients with severe edema and heavy proteinuria, plasma total protein, albumin/globulin ratio, cholesterol, triglycerides, and lipoproteins should be measured to assess hypoalbuminemia and hyperlipidemia.
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Test for antinuclear antibodies, anti-dsDNA antibodies, anti-Sm antibodies, anti-RNP antibodies, and antihistone antibodies to rule out systemic lupus erythematosus.
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Liver function and hepatitis B virus markers to exclude hepatitis B-associated nephritis.
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Abdominal X-ray: Kidneys may appear normal or enlarged.
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Chest X-ray: Heart size may be normal or slightly enlarged, often with signs of pulmonary congestion.
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Renal biopsy: Classic findings include subepithelial "hump-like" deposits on electron microscopy, which typically disappear 6–8 weeks after onset.
Is a kidney biopsy painful? Does it require anesthesia? What precautions should be taken?
Kidney biopsy is a crucial diagnostic procedure in nephrology. Local anesthesia is administered during the procedure, and patients are asked to hold their breath briefly. The pain is generally tolerable for most individuals.
Post-biopsy care includes keeping the puncture site clean and dry, avoiding heavy physical activity for 1–3 months, monitoring urine color and vital signs (e.g., blood pressure), and follow-up ultrasounds. For details, refer to the "Kidney Biopsy" entry.
What diseases should acute poststreptococcal glomerulonephritis be differentiated from?
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Other glomerular diseases presenting as acute nephritis syndrome.
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Acute glomerulonephritis caused by other pathogens: Similar onset but lacks the characteristic C3 decrease and ASO elevation.
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Membranoproliferative glomerulonephritis: Similar clinical course but with prolonged hypocomplementemia and no spontaneous remission. Heavy proteinuria and persistent hypocomplementemia are hallmarks. Renal biopsy can confirm the diagnosis.
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Rapidly progressive glomerulonephritis: Similar onset but more severe, with progressive oliguria/anuria and rapid renal failure. Biopsy reveals crescent formation, aiding differentiation.
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Systemic diseases with renal involvement: Lupus nephritis and Henoch-Schönlein purpura nephritis may mimic acute nephritis but often feature skin rashes or joint pain. Lupus-specific antibodies or positive tourniquet tests help distinguish them.
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Non-glomerular diseases: Acute interstitial nephritis, malignant hypertension, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura may also resemble acute glomerulonephritis clinically.
TREATMENT
How to treat acute poststreptococcal glomerulonephritis?
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Rest is essential. Gradually increase activity after gross hematuria disappears, edema subsides, and blood pressure normalizes. During the acute phase, sodium intake should be limited to less than 3 g/day. Patients with normal renal function do not need protein restriction, while those with renal insufficiency should consume high-quality low-protein diets (0.6–0.8 g/kg daily).
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Active anti-infection therapy: For upper respiratory or skin infections, use antibiotics with low nephrotoxicity (e.g., penicillin, cephalosporins) for 10–14 days. Macrolides are recommended for penicillin-allergic patients. Tonsillectomy may be considered for chronic tonsillitis if necessary.
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Diuresis and blood pressure control: Restrict water and sodium intake; diuretics may be used if needed.
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For acute kidney injury, dialysis is indicated when criteria are met. Monitor electrolytes and creatinine levels, and discontinue dialysis after recovery.
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APSGN is self-limiting; glucocorticoids and cytotoxic drugs are not recommended.
Which department should patients with acute poststreptococcal glomerulonephritis visit?
Seek care at the nephrology department of a local hospital.
DIET & LIFESTYLE
What should be noted in diet and lifestyle for acute poststreptococcal glomerulonephritis?
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Limit sodium intake during the acute phase to less than 3g per day.
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Patients with normal kidney function do not need to restrict protein intake. If renal insufficiency is present, a high-quality low-protein diet should be provided, with daily protein intake controlled at 0.6–0.8 g/kg.
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Ensure adequate rest, engage in moderate activity, avoid overexertion or heavy physical labor, and prevent catching cold.
PREVENTION
How can patients with acute poststreptococcal glomerulonephritis prevent disease progression?
Seek timely diagnosis and treatment, ensure adequate rest, dynamically monitor complement levels, monitor urine output and renal function, and actively administer symptomatic treatment. The disease is self-limiting and generally has a favorable prognosis.