ACUTE POSTSTREPTOCOCCAL

GLOMERULONEPHRITIS (APSGN) IN
CHILDREN
dr. HM Heru Muryawan,SpAK
Group A beta-hemolytic Streptococci are the most common etiologic organism,
pharingitis and pyoderma are the common antecendents of APSGN
Terminology
Acute proliferative glomerulonephritis
is charaterized by the histo-pathologic findings of capillary wall and mesangial
hypercellularity accompanied by invading polymorpho-nuclear cells.
Acute nephritic syndrome consist of
haematuria, proteinuria, edema, hypertension, volume overload, and varying degree
of renal insufficiency (oliguria, azotemia, hyper-creatininemia)
Epidemiology
Two antigenitically distinct proteins, M and T. Streptococcal pharyngitis
occurs primarily in school-aged children from to ! years of age, most commonly in
the winter and spring. Streptococcal-induced s"in lesions, occur more often in the
summer and fall in temperate climates, and are less seasonally associated in the
tropical areas
Table Diseases Presenting with Acute Proliferative Glomerulo-nephritis and
the Acute Nephritic Syndrome in hildren!
ommon
#ost infectious glomerulonephritis
#oststreptococcal
$ther systemic infections
%enoch-Sch&nlein purpura
"ess common
Membranoproliferative glomewrulonephritides
'g( nephropathy
Systemic lupus erythematosus
)amilial nephritis
'nfective endocarditis-related
Shunt nephritis
#ncommon
*egener+s granulomatosus
#olyarteritis nodosa
Table $ %rganisms &mplicated as Etiologic 'actors in Acute Proliverative
Glomerulonephritis
(acteria $ )iruses ,
Streptococcus, group ( b-hemolyic -aricella
Streptococcus viridans .ubeolla
Streptococcus pneumonia /ytomegalovirus
Staphylococcus aureus 0pstein-1arr virus
Staphylococcus epidermidis
/orynebacterium Parasites
#ropionibacterium To2oplasma
(typical mycobacterium Trichinella
Mycoplasma .ic"ettsia
1rucella .. ric"ettsiae
Meningococcus


3eptospira
Pathology
The process is diffuse and generalised in that all the observed glomeruli and
all the lobules in each glomerulus.
4uring the acute stage, the glomeruli are enlarged, with pronounced lobular
configuration that results from the proliferation.
Thus, the designations of intracapillary and endocapillary glomerulonephritis
are appropriate
Pathogenesis
The first element necessary in the production of disease are the host genetic
factors that determine the immune response to the streptococcal antigen.
The second element, the susceptible host must be presented with the
inciting antigen.
%ypothesis , the streptococcal antigens may deposit within glomeruli and
stimulate the fi2ation of complement and specific antibody (5,6,7,8)
Pathophysiology
9lomerular filtration rate (9).) is reduced
Tubular function is preserved
$liguria results clinically due to enchanced absorption of fluid and solute in
the distal tubule and collecting tubule.
%ypertension and edema result from vascular, and subse:uently, interstitial
volume e2pansion
(zotemia,acidemia, hyper"alemia, hyperphosphatemia
Frequency of clinical manifestations
; 9ross hematuria 6-77<
; -olume overload , 0dema =<
%ypertension !>-=><
; /irculatory congestion (congestive heart
failure, pulmonari edema) 6><
; /entral nerveous systems (headache,
somnolence, coma, seizure) 5><
; 1ac" or abdominal pain, nausea, vomiting occasionally
; (nore2ia, malaise, lethargy uncommon
; (cute nephritic syndrome, ?S some
; .apidly progressive glomerulonephritis 5<
"aboratory 'indings
#rinalysis $ 0arly in the course of (#S9? urine osmolality is high.
#roteinuria usually light.
Microscopic e2amination ,
@ .ed blood cells - mostly small
- dysmorphic
@ .ed blood cells cast in fresh urine (pathognomonic), hyaline cast
granular cast
@ *hite blood cells.
*enal 'unction$ 9lomerular filtration rate, renal blood flow decreased.
Serum urea nitrogen, creatinine usually elevated.
)ree water retension may lead to hyponatremia.


omplete (lood ount $
(nemia caused by volume e2pansion.
Trombocytopenia may be present.
3eucocytosis is found in patients with intercurrent infection.
Antistreptolysin % +AS%, titer will increase the precentage of positive diagnostic
results.
Third complement +-, is generally but not universally profoundly decreased
Treatment
The treatment of the child with (#S9? is largerly supportive.
)irst comes the decision of whether hospitalization is re:uired.
'ndication for hospitalization ,
$bvious edema, hypertension.
0levated blood urea nitrigen (1A?) and creatinine levels.
?o indication for hospitalization ,
Must be followed for fre:uent observation of deterioration.
0valuation must include the serologic e2amination that will substantiate
the diagnosis of poststeptococcal disease.
There is no reason to "eep the children in bed.
)or patient with acute nephritic syndrome , hypertension and other signs of volume
overload, azotemia must be managed promptly and properly.
There should be strict fluid and sodium restriction because volume overload is
generally present.
-olume overload sufficient to produce congestive heart failure, severe hyper"alemia
must be dialysed, which in children peritoneally is preferable
Table$ Treatment Strategy for Acute Glomerulonephritis
5. 1ed rest as necessary
6. )luid and salt restriction
7. Specific intervention for the following ,
a. %ypertension and other signs of volume overload, including
encephalopathy
b. %ypercalemia
c. (cidemia
d. %yperphosphatemia
8. /onfirm li"ehood of psotstreptococcal disease
. *atch for inde2 of suspicion for diseases other than
post streptococcal 9?
%utcome of APSGN
There is a good correlation between the
severity of the initial clinical syndrome, histologic abnormalities, and
prolonged abnormal renal function.
Those patients with the most severe clinical
findings
have the most severe histologic
findings, with glomerular capillary obliteration and epithelial cell
proliferation.
permanently decreased renal
function.
yet, some of the patiens
recovered.


55< of patients did not heal
within 7 years or more of the acute disease.
Those with milder clinical features , all patients appear to improve.
$n the whole greater than B>< of (#S9? should e2pected to
recover.
>, - 6,>< may have a rapid progressive disease, reaching end-stage
within wee"s to months
ourse of Disease Process!
'n general, the acute phase of illness in (#S9? with its most severe
manifestations last 6-7 wee"s.
The fre:uency of need for follow-up e2aminations will depend on the
individual patient and the severity of the disease



Groos haematuria
Oliguria, azotemia
Hypertension
Depression of C
!ersistent proteinuria
Mi"ros"opi" haematuria
#ntermittent or
orthostati" proteinuria
$ % $ & '
$
wee(s wee(s months months
year years
)igure . *ime "ourse of resolution for the usual "lini"al+"hemi"al features of
post,strepto"o""al glomerulonephritis