The document summarizes acute post-streptococcal glomerulonephritis (APSGN). It describes the etiology as an immune complex mediated glomerulonephritis following a streptococcal infection. Clinical manifestations include edema, hematuria, proteinuria, and hypertension. Diagnosis is based on urinalysis and serologic testing. Treatment focuses on controlling hypertension and edema. Prognosis is generally good with complete recovery in over 95% of cases.
The document summarizes acute post-streptococcal glomerulonephritis (APSGN). It describes the etiology as an immune complex mediated glomerulonephritis following a streptococcal infection. Clinical manifestations include edema, hematuria, proteinuria, and hypertension. Diagnosis is based on urinalysis and serologic testing. Treatment focuses on controlling hypertension and edema. Prognosis is generally good with complete recovery in over 95% of cases.
The document summarizes acute post-streptococcal glomerulonephritis (APSGN). It describes the etiology as an immune complex mediated glomerulonephritis following a streptococcal infection. Clinical manifestations include edema, hematuria, proteinuria, and hypertension. Diagnosis is based on urinalysis and serologic testing. Treatment focuses on controlling hypertension and edema. Prognosis is generally good with complete recovery in over 95% of cases.
The document summarizes acute post-streptococcal glomerulonephritis (APSGN). It describes the etiology as an immune complex mediated glomerulonephritis following a streptococcal infection. Clinical manifestations include edema, hematuria, proteinuria, and hypertension. Diagnosis is based on urinalysis and serologic testing. Treatment focuses on controlling hypertension and edema. Prognosis is generally good with complete recovery in over 95% of cases.
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ER
CBC (01/30/17) Result Serology Result
Hgb 106 (01/30/17) ASO Hct 0.32 RBC 3.7 Plt Ct 601 WBC 8.4 Basophils 0.01 Segmenters 0.66 Lymphocytes 0.24 Monocytes 0.09 ER Urinalysis Urinalysis Color Amber Urobilinogen Normal Transparency Cloudy Nitrite Negative Glucose Trace Leukocytes Negative Bilirubin Small Red blood cells Ketone Negative White blood cells 22 Sp. Gravity 1.023 Mucus threads Occasional pH 5.5 Bacteria Few Blood Large Hyaline Cast 2-5 Protein Fine granular cast 1-2 Clinical Manifestation Post-Streptococcal GN Age and Sex All ages (Mean 7 yr); 2:1 male Acute Nephritic Syndrome 90% Asymptomatic hematuria Occasionally Nephrotic Syndrome 10-20% Hypertension 70% Acute Renal Failure 50% (Transient) Other Latent period of 1-3 wks Laboratory findings Inc. ASO titers (70%) (+) Streptozyme (95%) Dec. C3-C9; Normal C1, C4 Immunogenetics HLA-B12 Nelson Textbook of Pediatrics, 7th Edition Acute Post-Streptococcal Glomerulonephritis Definition • AGN that follows an infection with nephritogenic strain of group A beta hemolytic streptococci. • The classic example of the acute nephritic syndrome
Nelson Textbook of Pediatrics, 7th Edition
Anatomy and Physiology • Lie in the retroperitoneal space above the level of umbilicus • Length: ~6cm (full-term newborn) to >/= 12cm (adult) • Weight: ~24g (full-term newborn) to 150g (adult)
Blood supply: Main renal artery
Each kidney: 1 million nephrons Formation of nephrons is completed at 36-40 weak of gestation • Filtering mechanism of the kidney (cap) Capillary (En) Endothelium (f) Fenestrations (B) Glomerular basement membrane (LD) Lamina densa (LRI) Lamina rara interna (LRE) Lamina rara externa (fp) Foot processes (c) Cell coat (Black arrow) Filtration slits Etiology and Pathogenesis • The child gets gets throat or skin infection by nephritogenic strain of group A beta hemolytic streptococci -serotype 12, 4 and 1
• Antibodies to streptoccocus (eg antistreptolysin O)are formed in his
deposited alongtheglomerular basement membrane (GBM). (+) ASO titer Streptococcal Infection (+) anti DNAse B (+) Streptozyme test Immune complex formation
Activation of complement Consumption of
system complement proteins
Decreased C3, C5 Cellular proliferation Damage to GBM
Narrowing of capillary lumen HEMATURIA PROTEINURIA
Dec. Glomerular blood flow Dec. in oncotic pressure Dec. Glomerular Dec. in oncotic pressure blood flow
Oliguria Fluid escapes from Uremia Dec. GFR intravascular space Inc. BUN and Crea
Activation of RAAS Inc. Na reabsorption
EDEMA Activation of ADH Inc. water retention
Inc. vasoconstriction HYPERTENSION Epidemiology
• Occur throughout the world
• 97% of cases occur in less- developed countries • Peak incidence: ages 5-12 yr • Uncommon before the age of 3 yr • Male: female ratio is 2:1 • Most commonly sporadic. Clinical Manifestation • Acute nephritic syndrome develops: • 1-2 wk after a streptococcal pharyngitis • 3-6 wk after a streptococcal pyoderma
1. Edema- face, periorbital area, peripheral
2. Oliguria- <0.5ml/kg/hr in children 3. Hypertension- occurs in 70% of patients, normalize by 4-6 weeks 4. Proteinuria- not as severe as nephrotic, normalize by 4-6 weeks 5. Gross hematuria- tea colored, cola-colored 6. Microscopic hematuria- persists for 1-2 years 7. Nonspecific symptoms such as malaise, lethargy, abdominal pain, or flank pain are common.
• The acute phase generally resolves within 6-8 wk.
• Patients are at risk of developing encephalopathy (10%) and/or heart failure sec to ypertension or hypervolemia. Diagnosis 1. Urinalysis • Macroscopic hematuria: Tea or cola colored • Microscopic hematuria: Leukocytes, RBCs, RBC cast (Pathognomonic), granular casts • Proteinuria: Nephrotic range occurs in <5% • Pyuria: due to large amounts of fibrin degradation and fibrinopeptides CBC Mild normochromic anemia may be present due to hemodilution and low grade hemolysis, resolves with diuresis Electrolytes Hyperkalemia, hyperphosphatemia, hypocalcemia in severe patients BUN/Crea Maybe elevated but profound decrease in GFR is uncommon Serum Decreased protein/albumin C3, CH50/C4 Decreased s, serum C3, normal by 6-8wks Normal Serum C4 ASO titer/antiDase Elevated B/Streptozyme test ANA Elevated in SLE Throat skin culture Support diagnosis but low sensitivity • Asymptomatic isolated microscopic hematuria on 3 uarinalysis within 2 weeks- uncommon • MRI of the brain is indicated in patients with severe neurologic symptoms • Chest x-ray is indicated in those with signs of heart failure or respiratory distress • Renal biopsy should be considered only in the presence of acute renal failure, nephrotic syndrome, absence of evidence of streptococcal infection, or normal complement levels. Treatment • Although a 10 day course of systemic antibiotic therapy with Penicillin is recommended to limit the spread of the nephritogenic organisms, antibiotic therapy does not affect the natural history of APSGN. • Standard therapies used to treat hypertension Sodium restriction Diuresis (usually with intravenous furosemide) Calcium channel antagonists (Nifedipine, Amlodipine) Vasodilators (Hydralazine) Angiotensin-converting enzyme inhibitors (Enalapril) Treatment • Diet: A low-sodium, low-protein diet should be prescribed during the acute phase, when edema and hypertension are in evidence; however, prolonged dietary restrictions are not warranted. Limitation of fluid and salt intake is recommended in the child who has either oliguria or edema. In patients with oliguric acute kidney injury, potassium intake should be restricted to prevent hyperkalemia. • Activity: Limited activity is probably indicated during the early phase of the disease, particularly if hypertension is present. Prevention • Early systemic antibiotic therapy for streptococcal throat and skin infections does not eliminate the risk of GN. • Family members of patients with acute GN, especially young children, should be considered at risk and be cultured for group A β-hemolytic streptococci and treated if positive. Prognosis • Complete recovery occurs in >95% of children with APSGN. • Recurrences are extremely rare. • Mortality in the acute stage can be avoided by appropriate management of acute renal failure, cardiac failure, and hypertension. • Infrequently, the acute phase is severe and leads to glomerulosclerosis and chronic renal disease in <2% of affected children.
