Acute Poststreptococcal Glomerulonephritis


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Acute Poststreptococcal Glomerulonephritis

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