CASE DISCUSSION

INTRODUCTION
• Acute glomerulonephritis (GN) comprises a specific set of renal diseases in which an immunologic
mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage
to the basement membrane, mesangium, or capillary endothelium.
• Acute GN is defined as the sudden onset of hematuria, proteinuria, and red blood cell (RBC) casts
in the urine. This clinical picture is often accompanied by hypertension, edema, azotemia, and
renal salt and water retention.
• Treatment of PSGN is mainly supportive, because there is no specific therapy for renal disease.
When acute GN is associated with chronic infections, the underlying infections must be treated.

ETIOLOGY
• APSGN follows infection of the throat or skin by certain “nephritogenic” strains of group A B
haemolytic streptococci.
• Usually occurs:
– 7 to 14 days after pharyngitis
– 2 weeks – 6 weeks after skin infection
– Throat:
– Serotypes M1, M4, M25, M12

RISK FACTORS
• Pyoderma: Summer
• Throat infection: Cold seasons
• Peak incidence in pre- school children
PATHOPHYSIOLOGY

LIGHT MICROSCOPY
• Glomeruli are enlarged and ischemic
• Capillary loops are narrowed which makes the glomeruli appear bloodless
• Diffuse proliferation of mesangial cells
• Polymorphonuclear leukocyte infiltration
• Crescents and interstitial inflammation in severe cases

CLINICAL FEATURES
• Abrupt onset
• Age 4-12 years, M>F
• Latent period:
– Throat infection (1-2 weeks)
– Skin infection (3-6 weeks)
• Hematuria
– Smoky brown or cola colored
– Glomerular: dysmorphic RBC, casts seen on spun urine
• Azotemia
• Circulatory congestion
 • Proteinuria
– Mild to moderate
• Oliguria
– Transient
• Edema (85%)
– Mild: periorbital or pedal
– Severe: hypertension, pleural effusion or ascites
– Adolescents: face and legs
• Hypertension
– Headache, somnolence
– Changes in mental status
– Anorexia, nausea, convulsions

INVESTIGATIONS FOR ETIOLOGIC FACTORS

• Culture of organisms in throat or skin
• ASO titer
• Anti DNAse B

MANAGEMENT
• Eliminate streptococcal infection with antibiotics
– Penicillin (250 mg qid for 7-10 d)
– Erythromycin (250 mg qid for 7-10 d)
• Supportive therapy
• Diuretics
– Oral furosemide
• 1-3 mg/ kg for edema
– IV furosemide
• 2-4 mg/kg for pulmonary edema
• Anti hypertensives to control BP and ECF volume
– Amlodipine, Nifedipine
– Emergencies: IV Nitroprusside or Labetalol
• Diet:
– The intake of Na, K and fluids should be restricted until blood levels of urea reduce and
urine output increases

PROLONGED OLIGURIA
• Dialysis
– Severe renal failure
– Hyperkalemia
– Severe metabolic acidosis
– Uremic pericarditis and encephalopathy
– Intoxications (methanol)
– Fluid overload
– Life threatening electrolyte disturbances
OUTCOME AND PROGNOSIS
• Excellent prognosis in childhood
• Edema and BP decreased in first week
• Gross hematuria and significant proteinuria (disappear within 2 weeks)
• Hypertension subsides within 2-3 weeks
• Non streptococcal GN – unpredictable outcome

INDICATIONS FOR RENAL BIOPSY

• Nephrotic range proteinuria in acute stage
• Normal serum complement
• Progressively increasing creatinine
• Prolonged hyppocomplementemia > 3months
• Ongoing macrohematuria
• Long lasting proteinuria
• Persistent azotemia
• Hepatitis B infection
• Infective endocarditis