Post streptococcal glomerulonephritis

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

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

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

11. 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

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

13. 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

14. 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

15. Atypical presentation Pulmonary edema Congestive cardiac failure Hypertensive encephalopathy Renal failure Nephrotic syndrome

16. 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.

17. 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

18. 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)

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

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

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

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

23. 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

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

25. 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

26. 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

27. 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

28. Thank you