Post-Streptococcus Glomerulonephritis

Name :CHOW MIEN CHINGroup :88

Post-streptococcal glomerulonephritis (PSGN)

EpidemiologyCommonest cause of nephritic syndromePeak incidence age : age 6-12 y/oMale : female ratio is 2:1Immune mediated inflammation.Most commonly-sporadic.

EtiologyUsually appear after infected by

“nephritogenic” Group A beta hemolytic streptococci (GAHS)-

serotype 12,4,1.GAHS typically can be found on skin and

throat

Impetigo Strep. throat

Pathogenesis Throat/skin infection by GAHS (serotype 12,4,1 )

Antibodies to streptococcus (anti-streptolysin O) are formed in the circulation.

Antigen- antibody circulating immune complexes are deposited at glomerular basement membrane

Acute nephritic syndrome develop

1-2weeks

3-4weeks

Streptococcus

pharyngitis

Streptococcus

pyoderma

Signs and symptoms 1) Edema (90%) : typically found on face,

periorbital and upper extremities.acites and anasarca mayb occur in children.

2) Macroscopical hematuria (65%) : meat-colored

3) Proteinuria : usual ,normalize after 4 weeks

4) Hypertension (75%) : mild- moderate , subside after diuresis.

5) Oligouria : in children <0.5mL/day/hr (minimum urine output 0.5 -1 mL/day/hr)

Non specific symptoms :Such as high blood pressure, tachycardia,anorexia, nausea & vomit, general malaise, lethargy, low grade fever, pallor due to edema/ anemia.

Complication in severe cases 1. Circulatory hypervolumia/congestive

heart failure2. Hypertensive encephalopathy3. Acute renal failure4. Pulmonary edema

Lab. investigation1. Urinalysis2. Bacteriological and serological test3. Renal function test4. Full blood count5. Serum complement level

Urinalysis Macroscopic hematouria : rusty / tea- colour.Microscopic hematouria:leucocyte, RBC castsPyuria :fibrin degrade products.

Evidences of streptococcus infection• Skin and throat culture.• high (anti-streptolysin)O and (anti-

deoxyribonuclease)B titer

Renal f(n) test • Increased creatinine, BUN level.• Decrease GFR unlikely to be found in children.• Hyperkalemia, hypocalcaemia, metabolic acidosis

and hyponatremia seen only in severe patients.

FBC• Mild normochromic anemia ,leucocytosis

mayb present.

Activation of complements• Serum C3 lvl decrease (90%) , return to

normal within 6weeks.• Serum C4 lvl are typically normal.

*complement-group of protein work with immune system and move freely in bloodstream, complement level decrease during inflammation.*

Electron microscope

Immune deposits on the epithelial side of glomerular basement membrane form “Humps” .

Immunofluoroscence microscopy

Granular (lumpy, bumpy) deposition of C3 and IgG alone the capillaries loops and the mesangium.

Differential diagnosis Ig A NephropathyHematouriaCrescentic glonerulonephritisDiffuse proliferative glomerulonephritisChronic nephritis

TreatmentTreatment of PSGN is mainly on supportive

care, restriction of fluid and sodium.Usually patient undergo spontaneous

diuresis within 7-10 days aft onset of illness.

10 days systemic AB therapy with penicillin V to limit the spread of nephritogenic organisms.

Management is direct to treat the acute effect of renal insufficiency and HPT.

Anti-hypertensive :

**Anti- aggregant & anti-coagulant are given to prevent micro-thrombosis.**

Anti- aggregant :(eg: aspirin, dipyridamole, clopidegol)

Anti –coagulant: (eg: heparin) subcutaneously or I.V, 2-4times/day

Extra- corporal method:(eg: plasmapheresis are given to remove immune complexeswith combination of strong medication.)

Pulse therapy:

Complication Nephrosclerosis.

Prognosis Short term outcome : excellent, mortality

<0.5%Long term outcome : 2% children deve.

Chronic kidney disease.