Acute Glomerulonephritis

1. POST STREPTOCOCCAL
GLOMERULONEPHRITIS
PRAVEEN RK
NO: 75

2. DEFINITION
• Acute inflammation of renal glomerular parenchyma due to deposition of
immune complexes characterized by sudden onset of
Oliguria
Hematuria
Hypertension
Edema

3. ETIOLOGY
• PSGN follows infection of the throat or skin by certain
“nephritogenic” strains of group A β‐hemolytic streptococci
• Usually occurs
7 – 14 days after pharyngitis
2 wks – 6 wks after skin infection

4. • Epidemics of nephritis have been described in association with throat (serotypes
M1, M4, M25, M12) and skin (serotype M49) infections

5. • Throat infection: Winter or early spring
• Pyoderma : late summer or fall
• Overall risk of infection: 15%, regardless of site
• Risk of infection after pyoderma: 25%
• Asymptomatic carriers: 20%, may thus occur in absence of prodrome
• Peak incidence in pre‐school children. Clinically apparent GN occurs
in < 2% of children infected with strep infection
RISK FACTORS

6. PATHOGENESIS
• Trapping of circulating immune complexes in glomeruli
• Molecular mimicry between streptococcal antigens and renal antigens
(glomerular tissue acts as auto antigen reacts with circulating antibodies formed
against strep antigens)
• In situ immune complex formation against anti strep antibodies and glomeruli
• Direct complement activation

7. PATHOLOGY
• GROSS
Kidney symmetrically enlarged

8. LIGHT MICROSCOPY
• Glomeruli enlarged and ischaemic
• Capillary loops narrowed – it make glomeruli appeared as bloodless
• Diffuse proliferation of mesangial cells
• Polymorphonuclear leukocyte infiltration
• Crescents and interstitial inflammation in severe cases

10. IMMUNOFLUORESCENCE MICROSCOPY
• Immunofluorescence microscopy reveals a pattern of “lumpy‐bumpy”
deposits of immunoglobulin and complement on the glomerular
basement membrane and in the mesangium.

11. ELECTRON MICROSCOPY
• Electron microscopy, electron‐dense deposits, or “humps,” are
observed on the epithelial side of the glomerular basement
membrane

13. 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 in freshly spun urine

14. PROTEINURIA
• Mild to moderate but nephrotic range is rare
OLIGURIA
• Transient – 50%, Anuria rare

15. EDEMA : 85%
• Mild : periorbital or pedal
• Severe : hypertension, pleural effusion or ascites
• Adolescents : more likely face and legs
HYPERTENSION: in 80%
• Headache, Somnolence
• Changes in mental status
• Anorexia, Nausea , Convulsions

16. HYPERTENSIVE EMERGENCY: 10%
• BP > 30% increased for age &sex
• Evidence of encephalopathy
• Heart failure or pulmonary edema
AZOTEMIA : varying degrees
CIRCULATORY CONGESTION : 20%
• Dyspnoea, Orthopnoea
• Cough, Tachycardia, Gallop rhythm
• Basal crepitations, CCF, Pulmonary edema

17. ATYPICAL PRESENTATION
• Pulmonary edema
• Congestive cardiac failure
• Hypertensive encephalopathy
• Renal failure
• Nephrotic syndrome

18. INVESTIGATIONS
URINE
• Dysmorphic or crenated RBC and RBC casts
• Moderate proteinuria ; 5‐10% nephrotic range (Lasts for approximately 5 month)
• Leukocyte or granular or hyaline casts
BLOOD
• Transient elevation of urea and creatinine
• Low complement S.C3 in >90% ‐ in first 2 weeks(normalises in 6‐8 weeks)
• Serum CH50 is commonly depressed, C4 is most often normal or mildly depresed
in PSGN.

19. • ASO titres elevated 1‐5 weeks after infection in 80%, four fold rise,
• Return to normal after several months
• The best single antibody titer to document cutaneous streptococcal nfection is
the antideoxyribonuclease B level
Chest Xray may show pulmonary congestion, cardiomegaly
Tubular function is preserved, or mildly reduced

20. INVESTIGATIONS FOR ETIOLOGIC FACTORS
• Culture of organisms in throat or skin
• ASO titre - ↑ (only in throat infection)
• Single most specific test – Anti DNAase B ↑
(Skin infections)

21. MANAGEMENT
PRINCIPLES
• Eliminate streptococcal infection with antibiotics
• Supportive therapy
• Diuretics and anti-hypertensives to control BP and ECF volume

22. DIET
• The intake of sodium, potassium and fluids should be restricted until blood levels
of urea reduce and urine output increases

23. DIURETICS
• Oral FUROSEMIDE( 1- 3 mg /kg) – for edema
• IV FUROSEMIDE ( 2- 4 mg /kg) – pulmonary edema

24. HYPERTENSION
• Mild – restriction of salt and water
• Anti hypertensive agents – AMLODIPINE
NIFEDIPINE
DIURETICS
• Hypertensive emergencies – IV NITROPRUSSIDE or LABETALOL

25. LVF
• Hypertension control
• IV furosemide as diuretics
• This will lead to improvement in LVF
• If no diuresis – dialysis initiated
• Respiratory support – positive end expiratory pressure

26. PROLONGED OLIGURIA
• Dialysis
Severe renal failure
Hyperkalemia
Severe metabolic acidosis
Uremic pericarditis and encephalopathy
Intoxications- methanol,Li
Fluid overload
Life threatening electolyte disturbances

27. DAILY MONITORING
• Clinical : Edema, JVP, BP
Fluid intake and output
Weight
Respiratory status
Neurological status
ECG if hyperkalemic
• Biochemical: Urine microscopy, Blood Urea, Creatinine, Electrolytes

28. OUTCOME AND PROGNOSIS
• Excellent prognosis in childhood
• Edema and BP ↓ - 1 st week
• Gross hematuria and significant proteinuria – Disappear within 2 weeks
• Hypertension subsides within 2-3 wks
• Non streptococcal GN – Unpredictable outcome

29. INDICATIONS‐ RENAL BIOPSY
• Nephrotic range proteinuria in acute
stage
• Normal serum complement
• Progressively increasing S creatinine
• Prolonged hypocomplementemia > 3
m
• Ongoing macrohematuria
• Long lasting proteinuria
• Persistent azotemia
• Associated symptoms of systemic
disease
• Persistent azotemia
• Associated symptoms of systemic
disease
• Postinfectious GN and secondary causes
• Hepatitis B infection
• Shunt Nephritis
• Infective endocarditis
• Associated with HSP

30. THANK YOU