Acute Poststreptococcal Glomerulonephritis

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  • 1. ACUTE NEPHRITIC SYNDROME
    By Hakimah KhaniBintiSuhaimi
  • 2. Introduction
    Synonyms: acute nephritis,
    acute nephritic syndrome
    An immunologic mechanism: the result of an immune process that injures the glomeruli of the kidney.
    Clinical features:
    A sudden onset of hematuria,
    Proteinuria,
    Edema,
    Oliguria and volume overload,
    Hypertension,
    Azotemia is another common but inconstant finding.
  • 3.
  • 4. ACUTE POST-STREPTOCOCCAL GLOMERULONEPHRITIS
  • 5. Outline
    Definition
    Epidemiology
    Etiology and Pathogenesis
    Clinical Features
    Complication
    Investigation
    Diagnosis
    Differential Diagnosis
    Treatment and Management
    Prognosis
  • 6. Definition
    AGNthat follows an infection with a nephritogenic strain of group A beta hemolytic streptococci.
    The classic example of the acute nephriticsyndrome.
    Nelson Textbook of Pediatrics, 7th Edition
  • 7. Epidemiology
    121 of the 124 patients had poststreptococcal nephritis.
    Department of Pediatrics, HUSM, July 1987- June 1988
    Globally - incidence has decreased in the past three decades.
    Most commonly – sporadic.
    Despite that, epidemics and clusters of cases - in some poor or rural communities
    © 2008 American Society of Nephrology
    Peak incidence - age 5-12 y/o, uncommon <3y/o.
    Male : female ratio is 2 : 1.
    Nelson Textbook of Pediatrics, 7th Edition
  • 8. Etiology and Pathogenesis
    The child gets gets throat or skin infection bynephritogenic strain of group A beta hemolytic streptococci - serotype 12 , 4 and 1
    Antibodies to streptoccocus (egantistreptolysin O) are formed in his circulation
    Antigen-antibody circulating immune complexes are subsequently deposited along the glomerular basement membrane (GBM).
  • 9. Streptococcal infection
    immune complex formation + deposited in GBM
    complement system activated
    immune injuriescellular proliferation GBM fracturecapillary lumen narrowed hematuriaglomerular blood flow decreased proteinuriaoliguria GFR distal sodium reabsorptionretention of water & sodiumblood volume 
    edema
    hypertension
    Low serum
    complement
  • 10. Clinical Features
  • 11. Typical Manifestation
    Develop acute nephritic syndrome 1–2 wk after an antecedent streptococcal pharyngitis or 3–6 wk after a streptococcal pyoderma.
    Edema
    75% of the patients
    Face,periorbital area lowerextremities generalized (ascites, pleural effusions)
    2. Proteinuria– usu. normalize after 4 weeks
    3. Oliguria
    school child < 400ml/day
    preschool child < 300ml/day
    infant & toddler < 200ml/day
  • 12. Typical Manifestation (2)
    Gross hematuria(65% of patients)
    Smoky, tea-colored, cola-colored, or fresh bloody urine
    Microscopical hematuria (almost all patients)
    The urine appears normal, but >3 RBCs/HP are found in centrifuged urine sediment examined microscopically.
    Hypertension (50%) – mild to moderate, typically subsides promptly after diuresis
    Nonspecific symptoms:
    Such as anorexia, vomiting, general malaise, lethargy, abdominal or flank pain, low-grade fever and weight gain.
  • 13. Clinical course
    Spontaneous improvement typically begins within 1 wk with resolution of edema in 5-10 days and hypertension in 2-3 wk, but urinalysis may be abnormal (persistent microscopic hematuria) for a year.
  • 14. Complications in severe cases
    • Circulatory hypervolemia / Congestive heart failure
    • 15. Encephalopathy
    • 16. Acute renal failure
  • Laboratory Investigations
    Urinalysis
    Bacteriological and Serological test
    Renal function test
    Full blood count
    Serum complement levels
    Kidney ultrasound
  • 17. Laboratory Investigations
    Urinalysis
    • Macroscopic hematuria: Rusty or tea-color.
    • 18. Microscopy: leukocytes, red blood cell casts (pathognomonic), and granular casts.
    • 19. Proteinuria 2+. (Nephrotic-range proteinuria occurs in <5% of patients.)
    • 20. Pyuria. The urine contains large amounts of fibrin degradation products, and fibrinopeptides.
  • Laboratory Investigations
    • Evidences of streptococcal infection
    • 21. Throat or skin cultures.
    • 22. Antistreptolysin O (ASO) titer. Pharyngitis (80%), skin infections (<50%).
    • 23. Anti-deoxyribonuclease (DNase) B level. Pharyngitis (98%), skin infections (80%).
    • 24. Renal function Test
    • 25. The BUN concentration is elevated in 75% of patients, and serum creatinine level is increased in one half of the patients, but profound decrease in GFR is uncommon in children.
    • 26. Hyperkalemia, hypocalcaemia, hyponatremia, and metabolic acidosis are seen only in severe patients.
  • Laboratory Investigations
    • Full Blood Count
    • 27. A mild normochromic anemia may be present from hemodilution and low-grade hemolysis.
    • 28. Leococytosis maybe present.
    • 29. Activation of complements
    • 30. Serum C3 level, decrease (90%), return to normal within 6 weeks.
    • 31. Serum C4 levels are typically normal.
    • 32. Kidney ultrasound
    • 33. Not necessary if patient has clear cut acute nephritic syndrome
  • Renal Biopsy
    • Patients whose clinical presentation, laboratory findings, or course is atypical.
    Delay resolution
    o oliguria > 2 weeks
    o Azotaemia > 3 weeks
    o Gross haematuria > 3 weeks
    o Persistent proteinuria > 6 months
    Paediatric Protocols, 12th Edition
  • 34. Light microscopeNot specific for post streptococcal nephritis
    • Glomeruli appear enlarged and hypercellular.
    • 35. Diffuse mesangial cell proliferation with an increase in mesangial matrix.
    • 36. Polymorphonuclear leukocytes are common in glomeruli during the early stage of the disease.
  • Electron microscope
    • Subepithelial electron-dense deposits or “humps” are present which are observed on the epithelial side of the glomerular basement membrane (GBM).
    • 37. Gaps or discontinuities of GBM, which is likely indicative of proteinuria and hematuria.
  • Immunofluorescence microscopy
    • Lumpy-bumpy deposits of immunoglobulin G and complement 3 along the capillary loops and within the mesangium.
    • 38. It is helpful in the differential diagnosis of other entities that may mimic APSGN clinically, particularly IgA nephropathy.
  • Diagnosis
    Acute onset
    Symptoms: edema, oliguria, dark urine, hypertension
    Urinalysis: RBCs, protein, casts
    Evidences of streptococcal infection:
    Prodromes
    Elavated serum titers of Abs to streptozymes(ASO)
    Serum C3 - Reduced
  • 39. Differential Diagnosis
    © Hakimah
  • 40. Differential Diagnosis
    © Hakimah
  • 41. Treatment
    Treatment of APSGN is largely that of supportive care.
    Usually, patients undergo a spontaneous diuresis within 7 to 10 days after the onset of their illness - strict monitoring – nephrotic chart + fluid restriction until diuresis
    Management is directed at treating the acute effects of renal insufficiency and hypertension
  • 42. Diuretics
    Diet
    Fluid restriction – during oliguric phase
    Sodium restriction is necessary
    Protein restriction is unnecessary
    Antibiotics
    A 10-day course of systemic antibiotic therapy with penicillin V is recommended to limit the spread of the nephritogenic organisms.
    Antibiotic therapy does not affect the natural history of glomerulonephritis.
    Paediatric Protocols, 12th Edition
  • 43. Treatment for complications
    Significant asymptomatic hypertension
    symptomatic, severe hypertension or hypertensive emergency / encephalopathy
    Paediatric Protocols, 12th Edition
  • 44. Paediatric Protocols, 12th Edition
  • 45. Treatment for complications
    Acute pulmonary edema
    Paediatric Protocols, 12th Edition
  • 46. Treatment for complications
    Acute Renal Failure
    Paediatric Protocols, 12th Edition
  • 47. Follow-up
    • for at least 1 year.
    • monitor BP at every visit
    • do urinalysis and renal func􀆟 on
    to evaluate recovery.
    • repeat C3 levels 6 weeks later if not already normalised by time of discharge
    Paediatric Protocols, 12th Edition
  • 48. Prognosis
    short term outcome: excellent, mortality <0.5%.
    long term outcome: 1.8% of children develop chronic kidney disease
    following post streptococcal AGN. These children should be referred to the paediatric nephrologists for further evaluation and management.
    Paediatric Protocols, 12th Edition