1) Poststreptococcal glomerulonephritis (PSGN) is an acute inflammation of the renal glomeruli that occurs after infection with certain strains of Streptococcus. 2) It is characterized by hematuria, edema, hypertension, and oliguria. 3) The pathogenesis involves molecular mimicry between streptococcal antigens and renal antigens, resulting in the trapping of immune complexes in the glomeruli.

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