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Acute Poststreptococcal Glomerulonephritis
 

Acute Poststreptococcal Glomerulonephritis

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    Acute Poststreptococcal Glomerulonephritis Acute Poststreptococcal Glomerulonephritis Presentation Transcript

    • ACUTE NEPHRITIC SYNDROME
      By Hakimah KhaniBintiSuhaimi
    • 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.
    • ACUTE POST-STREPTOCOCCAL GLOMERULONEPHRITIS
    • Outline
      Definition
      Epidemiology
      Etiology and Pathogenesis
      Clinical Features
      Complication
      Investigation
      Diagnosis
      Differential Diagnosis
      Treatment and Management
      Prognosis
    • 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
    • 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
    • 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).
    • 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
    • Clinical Features
    • 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
    • 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.
    • 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.
    • Complications in severe cases
      • Circulatory hypervolemia / Congestive heart failure
      • Encephalopathy
      • Acute renal failure
    • Laboratory Investigations
      Urinalysis
      Bacteriological and Serological test
      Renal function test
      Full blood count
      Serum complement levels
      Kidney ultrasound
    • Laboratory Investigations
      Urinalysis
      • Macroscopic hematuria: Rusty or tea-color.
      • Microscopy: leukocytes, red blood cell casts (pathognomonic), and granular casts.
      • Proteinuria 2+. (Nephrotic-range proteinuria occurs in <5% of patients.)
      • Pyuria. The urine contains large amounts of fibrin degradation products, and fibrinopeptides.
    • Laboratory Investigations
      • Evidences of streptococcal infection
      • Throat or skin cultures.
      • Antistreptolysin O (ASO) titer. Pharyngitis (80%), skin infections (<50%).
      • Anti-deoxyribonuclease (DNase) B level. Pharyngitis (98%), skin infections (80%).
      • Renal function Test
      • 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.
      • Hyperkalemia, hypocalcaemia, hyponatremia, and metabolic acidosis are seen only in severe patients.
    • Laboratory Investigations
      • Full Blood Count
      • A mild normochromic anemia may be present from hemodilution and low-grade hemolysis.
      • Leococytosis maybe present.
      • Activation of complements
      • Serum C3 level, decrease (90%), return to normal within 6 weeks.
      • Serum C4 levels are typically normal.
      • Kidney ultrasound
      • 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
    • Light microscopeNot specific for post streptococcal nephritis
      • Glomeruli appear enlarged and hypercellular.
      • Diffuse mesangial cell proliferation with an increase in mesangial matrix.
      • 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).
      • 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.
      • 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
    • Differential Diagnosis
      © Hakimah
    • Differential Diagnosis
      © Hakimah
    • 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
    • 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
    • Treatment for complications
      Significant asymptomatic hypertension
      symptomatic, severe hypertension or hypertensive emergency / encephalopathy
      Paediatric Protocols, 12th Edition
    • Paediatric Protocols, 12th Edition
    • Treatment for complications
      Acute pulmonary edema
      Paediatric Protocols, 12th Edition
    • Treatment for complications
      Acute Renal Failure
      Paediatric Protocols, 12th Edition
    • 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
    • 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