急性链球菌感染后肾小球肾炎

Hyperkalemia, hypocalcaemia, hyponatremia, and metabolic acidosis are seen only in severe patients. A mild normochromic anemia may be present from hemodilution and low-grade hemolysis.
Diet
Protein, sodium and water intake should be restricted in patients with acute renal failure. Sodium and water restriction is also needed in treating hypertension.
Thank you
Oliguria, sodium and water retention, hypervolemia Blockage of renal capillaries and decreased GFR Proliferation of MC and EC
GBM damage, Blood ingredients leakage

Proteinuria: Many patients have significant
proteinuria, but <5% of symptomatic patients develop frank nephrotic syndrome.

Laboratory Findings (1) Urinalysis

Hematuria is nearly always present in APSGN. Other findings on microscopy are those of leukocytes, red blood cell casts, and granular casts. Macroscopic hematuria typically has a rusty or tea-color. Proteinuria is nearly always present but typically in the sub-nephrotic range. Nephrotic-range proteinuria occurs in <5% of patients. The urine contains large amounts of fibrin degradation products, and fibrinopeptides.
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PATHOGENESIS
Infection of streptocacci Immune complexes antigens Activation of Compliments Recruitment of leukocytes Hematuria Proteinuria RBC Casts
Edema hypertention heart failure encephalopathy renal failure


Laboratory Findings (2)

GFR and Blood chemistory

The BUN concentration is elevated in 75% of patients, and serum creatinine level is increased in one half of the patients, but profound decrease in GFR is uncommon in children.
Inflammation mediates, Cytokines, proliferative F.
Typical manifestations

Hematuria: Gross hematuria (30-50%),
microscopic hematuria are more common.

Edema(90%): typically presents in the face and



Bed rest




Bed rest is indicated as long as there are clinical manifestation of active disease, such as edema, hypertension, or gross hematuria. The acute phase generally resolves within 2-3 wk. Children could go back school after ESR returns to normal. But, exhausting and competive activites are prohibited until the Addis count returns to normal.

Throat (serotype 12) , cold weather months.

skin (serotype 49) , warm weather months.
Diagrams depicting the ultrastructural features of a normal glomerular capillary loop (A) , and the ultrastructural features of APSGN (B), Note the subepithelial hump like dense deposits and endocapillary hypercellularity.
upper extremities. Ascites and anasarca may occur in children.

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Hypertension(75% ): usually mild to moderate,
and most evident at the onset of nephritis and typically subsides promptly after diuresis.


Laboratory Findings (3)

evidences of streptococcal infection


Throat or skin cultures. Antistreptolysin O (ASO) titer. Pharyngitis (80%), skin infections (<50%). Anti-deoxyribonuclease (DNase) B level. Pharyngitis (98%), skin infections (80%). IT ’s the best single antibody titer to document cutaneous streptococcal infection .

Activation of complements


Serum C3 level, decrease (90%), return to normal within 4-8 wk. Serum C4 levels are typically normal.
Treatments

Treatment of APSGN is largely that of supportive care. Usually, patients undergo a spontaneous diuresis within 7 to 10 days after the onset of their illness. Management is directed at treating the acute effects of renal insufficiency and hypertension
Acute Poststreptococcal Glomerulonephritis (APSGN)
Etiology

APSGN follows infection of the throat or skin
by certain “nephritogenic” strains of
group A β-hemolytic streptococci
Antibiotics
A 10-day course of systemic antibiotic therapy with penicillin is recommended to limit the spread of the nephritogenic organisms. Antibiotic therapy does not affect the natural history of glomerulonephritis.