This document provides information about Acute Poststreptococcal Glomerulonephritis (APSGN). It begins by describing the features of acute nephritic syndrome which is characterized by gross hematuria, edema, hypertension, and renal insufficiency. It then discusses the pathology, clinical manifestations, diagnosis, and management of APSGN. APSGN is caused by a previous streptococcal infection and results in immune complex deposition in the glomeruli. It presents abruptly with hematuria, edema, hypertension, and sometimes renal insufficiency. Treatment focuses on supporting kidney function and controlling blood pressure while the patient recovers over 6-8 weeks. Prognosis is generally good with complete recovery in over 95
6. Acute Poststreptococcal Glomerulonephritis
ďź APSGN ďź
ďClassic example of the acute nephritic syndrome
ďcharacterized by sudden onset of:
ďźGross hematuria
ďźEdema
ďźHypertension, and
ďźRenal insufficiency
ď2nd
most common glomerular causes of gross
hematuria in children (1st
IgA nephropathy) 6
7. ⢠APSGN follows infection of the throat or
skin by certain ânephritogenicâ strains of
group A β-hemolytic streptococci
â Throat (serotype 12) , cold weather months.
â skin (serotype 49) , warm weather months.
BUT
⢠APSGN is most commonly sporadic
⢠Epidemics of nephritis -reported
Etiology and epidemiology
8. PATHOLOGY
⢠Kidneys âsymmetrically enlarged
⢠Light microscopy,
⢠All glomeruli appear enlarged & relatively bloodless
⢠Diffuse mesangial cell proliferation
⢠Increase mesangial matrix
⢠Polymorphonuclear leukocytes in glomeruli
⢠Crescents and interstitial inflammation
⢠These changes are not specific for
poststreptococcal glomerulonephritis
8
9. (A) ultrastructural features of a normal glomerular capillary loop ,
(B)ultrastructural features of APSGN, Note the subepithelial hump
like dense deposits and endocapillary hypercellularity
A B
12. EM glomerular capillary -APSGN showing
ďsubepithelial dense deposits and
ďa neutrophil (N) marginated
13. Immune
complexes,
antigens
Activation of
Compliments
Recruitment of
leukocytes
GBM damage,
Blood ingredients
leakage
Hematuria
Proteinuria
RBC Casts
Proliferation
of MC and
EC
Blockage of renal
capillaries and
decreased GFR
Edema
hypertention
heart failure
encephalopathy
renal failure
Oliguria, sodium
and water
retention,
hypervolemia
Inflammation
mediates, Cytokines,
proliferative F.
Infection of
streptocacci
PATHOGENESIS
14. Although
⢠Morphologic studies &
⢠â(C3) level
strongly suggest âmediated by
immune complexes
Questions still unsolved
⢠Precise mechanismsâ UNKNOWN
14
PATHOGENESIS
16. General manifestations
⢠Age:
⢠most common in children aged 5-12 yr
⢠uncommon before the age of 3 yr.
⢠Sex: more common in boys than in girls,
(M:F 2 : 1)
⢠Antecedent infection:
⢠1-2 wk after pharyngitis
⢠3-6 wk after pyoderma
21. Clinical course
â Spontaneous improvement begins within 1 wk
â Edema-- resolves in 5-10 days
â Hypertension-- normalize by 4-6 wk after onset
â Proteinuria -- normalize by 4-6 wk
⢠Acute phase resolves within 6-8 wk.
⢠Microscopic hematuria may persist 1-2 yr
26. Antibodies to streptococcal
antigen(s)
⢠Anti-streptolysin O titer (ASOT) >333 TOD
Units
⢠COMMONLY elevated after a pharyngeal infection but
⢠RARELY increases after streptococcal skin infections.
⢠Anti deoxyribonuclease (DNase) B antibodies
(best single antibody titer to document cutaneous
streptococcal infection)
⢠Anti-hyaluronidase antibodies
⢠Anti-streptokinase antibodies
27. Renal biopsy
⢠Acute renal failure
⢠Nephrotic syndrome
⢠Absence of evidence of streptococcal
infection
⢠Normal complement levels
ALSO if
⢠Hematuria and proteinuria, diminished
renal function, and/or low C3 level
persist > 2 mo after onset
30. ⢠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.
⢠Management is directed at treating the
acute effects of renal insufficiency and
hypertension
Therapeutic Principle
31. Treatment
Management is directed at
â˘Treat renal insufficiency
â˘Treat hypertension
â˘Antibiotic therapy
ďŽ
Diet
ďŽ
Protein, sodium and water intake
-ARF
ďŽ
32. Treat renal insufficiency
ďCareful intake and output record
ďDaily weight measurement
ďMonitor & treat HTN
ďWater and sodium restriction
ďProtein restriction
ďPotassium and phosphate restriction
ďAdjust medication dosages
32
TREAT if any
ďHyperkalemia
ďHyponatremia
ďSeizures
ďAcidosis
ďHypocalcemia
34. Antibiotics
ďSystemic antibiotic therapy to limit
spread of nephritogenic organisms
ď10-day course of systemic antibiotic
therapy with Penicillin OR
ďSingle I.M Inj Benzathin Penicillin
ďNOTE: Antibiotic therapy does not affect
natural history of glomerulonephritis
Â
35. Indications for dialysis
ďŽ Volume overload with evidence of
hypertension and/or pulmonary edema
refractory to diuretic therapy
ďŽ Persistent hyperkalemia
ďŽ Severe metabolic acidosis unresponsive to
medical management
ďŽ Neurologic symptoms (altered mental
status, seizures)
ďŽ Blood urea nitrogen greater than 100â150
mg/dL
ďŽ Calcium/phosphorus imbalance, with
hypocalcemic tetany.
37. Mortality
Can be avoided by appropriate
management of:
â˘Acute renal failure
â˘Cardiac failure
â˘Hypertension 37
38. Prevention ??
⢠Early systemic antibiotic therapy for
streptococcal throat and skin infections
does not eliminate the risk of
glomerulonephritis
⢠Family members of patients with acute
glomerulonephritis should be cultured
for group-A β-hemolytic streptococci and
treated if culture positive 38
39. IgA nephropathy
(IgAN)
⢠Recurrent painless gross hematuria.
⢠Preceded by (usually 1-3 days ) infections
(URTI , Ac GE).
⢠HTN & renal insufficiency --- uncommon
⢠C3 level ----- normal
⢠ASO or anti DNase B ---- not elevated