Downloaded 1,015 times
Uploaded byPraveen RK
Post streptococcal glomerulonephritis
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.
In this document
Powered by AI
Introduction to PSGN, presented by Praveen RK, highlighting its significance.
PSGN is characterized by acute renal inflammation, presenting with oliguria, hematuria, hypertension, and edema.
PSGN typically follows throat or skin infections by nephritogenic group A streptococci, with a notable risk factor statistics.
Describes the immune complex deposition and interactions that lead to PSGN.
Gros anatomical features and microscopic changes in tissues, showcasing enlarged kidneys and glomerular abnormalities.
Advanced microscopy techniques (Immunofluorescence and Electron) highlight specific deposit patterns in glomeruli.
Details on symptoms like hematuria, proteinuria, edema, and hypertension with specific demographic data.
Laboratory findings related to urine and blood tests needed to assess PSGN's presence and etiology.
Outlines the approach to PSGN management including antibiotic therapy and supportive care.
Emphasizes dietary restrictions and medications like diuretics and antihypertensives for effective management.
Management of prolonged oliguria and complications requiring dialysis intervention.
Important monitoring aspects for PSGN patients and favorable outcomes typically seen in children.
Situations describing when renal biopsy is warranted in PSGN cases, indicating potential complications.
Concluding remarks from the presentation.
More Related Content
Similar to Post streptococcal glomerulonephritis
Post streptococcal glomerulonephritis
- 1.
- 2. DEFINITION • Acute inflammationof renal glomerular parenchyma due to deposition of immune complexes characterized by sudden onset of Oliguria Hematuria Hypertension Edema
- 3. ETIOLOGY • PSGN followsinfection 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 ofnephritis 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 ofcirculating 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.
- 8. LIGHT MICROSCOPY • Glomerulienlarged 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 • Immunofluorescencemicroscopy reveals a pattern of “lumpy‐bumpy” deposits of immunoglobulin and complement on the glomerular basement membrane and in the mesangium.
- 11. ELECTRON MICROSCOPY • Electronmicroscopy, electron‐dense deposits, or “humps,” are observed on the epithelial side of the glomerular basement membrane
- 13. CLINICAL FEATURES • Abruptonset • 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 tomoderate 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 • Pulmonaryedema • Congestive cardiac failure • Hypertensive encephalopathy • Renal failure • Nephrotic syndrome
- 18. INVESTIGATIONS URINE • Dysmorphic orcrenated 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 titreselevated 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 ETIOLOGICFACTORS • 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 streptococcalinfection with antibiotics • Supportive therapy • Diuretics and anti-hypertensives to control BP and ECF volume
- 22. DIET • The intakeof 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 Severerenal 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.