ACUTE GLOMERULONEPHRITIS

(NEPHRITIC SYNDROME)

DR.DEEPAK SARRAF
MDGP & EMERGENCY MEDICINE
RESIDENT 1ST YEAR
INTRODUCTION
Acute glomerulonephritis comprises a specific set
of renal diseases in which an immunologic
mechanism triggers inflammation & proliferation of
glomerular tissue that can result in damage to the
basement membrane , mesangium , or capillary
endothelium. Acute nephritic syndrome is the most
serious & potentially devastating form of the various
renal syndromes.
DEFINATION
Acute glomerulonephritis is characterized by abrupt
onset of hematuria , oliguria , edema & hypertension.
Mild disease may go undetected; severe cases have
anuria , hypertensive encephalopathy & heart failure.
. ESSENTIALS OF DIAGNOSIS :

i) Glomerular hematuria(dysmorphic red blood cells)

ii) Modest proteinuria(0.3-3g/day)
iii) Red blood cell casts may be present if glomerular
bleeding is heavy.
iv) Nephritic syndrome in more severe/inflammatory
cases :
 Glomerular hematuria & proteinuria
 Hypertension
 Edema
 Rising creatinine over days to months.
EPIDEMIOLOGY
GN represents 10-15% of glomerular diseases. The
incidence of PSGN has fallen over the past few
decades in most developed countries.GN comprises
25-30% of all cases of end-stage renal disease(ESRD).
Most cases that progress do so relatively quickly,&
end-stage renal failure may occur within weeks or
months of the onset of acute nephritic syndrome.
Worldwide , IgA Nephropathy(Berger disease) is the
most common cause of GN. PSGN remains much
more common in regions such as India , Pakistan ,
Nepal , Malaysia & South America. Postinfectious
GN can occur at any age but usually develops in
children. Most cases occur in patients aged 5-15
years.
. ETIOLOGY
1.Postinfectious :
 Streptococcus , staphylococcus , pneumococci ,
meningococci , Treponema pallidum , Salmonella ,
Leptospira.
 P. malariae, P.falciparum , toxoplasma , filaria.
 Hepatitis B & C, cytomegalovirus , parvovirus,
EBV , coxasackievirus , varicella.
 Associated with severe infections , infection of
shunts , prostheses , bacterial endocarditis.
2. Systemic vasculitis :
 Henoch-schonlein purpura
 Microscopic polyarteritis,Wegener granulomatosis.
3. Others :
 Membranoproliferative glomerulonephritis

 IgA nephropathy

 Hereditary nephropathy

 Systemic lupus erythematous.

. INVESTIGATIONS
i) CBC – Polymorphonuclear leucocytosis
ii) Serum C3 level is reduced.
iii) Urinalysis – RBC , RBC casts , proteinuria
iv) Evidence of streptococcal infection : Positive
throat swab culture , raised ASO titre , positive
streptozyme test.
v) Renal biopsy : Usually not required , may be done in
atypical presentation e.g. mixed features of GN &
nephrotic syndrome , ARF , absence of evidence of
streptococcus infection , normal levels of C3 level in
acute stage of illness , persistence of marked hematuria
or proteinuria or both or a low C3 level for more than 3
months after onset.

.POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
Acute GN following infection by group A beta-
hemolytic streptococci is a common disorder.
Streptococcal infection of the throat or skin precedes the
onset of nephritis by 1- 4 weeks. Only a few strains of
streptococci are nephritogenic e.g. types 4 & 12 causing
pharyngitis & type 49 causing pyoderma.
. Pathology :
i) On light microscopy- glomeruli are enlarged &
ischemic & capillary loops narrowed , making
glomeruli appear bloodless.
ii) Electron microscope- shows deposits(humps) on
the subepithelial side of the glomerular
basement membrane.
. Clinical features :
 Mild proteinuria & microscopic hematuria.
 Puffiness around the eyes & pedal edema.
 Urine is cola-colored.
 Hypertension , present in over half the patients.
. Investigation :
i) Urinalysis – shows 1-2+ protein , red cells , RBC
cast & granular cast.
ii) Serum C3 level is reduced.
iii) RFT – Blood urea & creatinine raised ,
hyponatremia , hyperkalemia.
iv) Chest X-ray – Shows vascular markings
suggesting hypervolemia.
v) Serological evidence of streptococcus infection:
Positive throat swab culture , raised ASO
titre , positive streptozyme test.
. Treatment :
No specific treatment , treatment is symptomatic
& supportive.
i) In mild cases(mild oliguria , normal BP),only
careful monitoring of BP , fluid intake &
restriction of potassium intake is required.
ii) A 10-day course of penicillin is recommended to
limit the spread of nephritogenic streptococcus ,
however it doesn’t affect the natural course of
GN.
iii) Diet – The intake of sodium , potassium & fluid
should be restricted until blood urea is reduce &
urine output increases.
iv) Diuretics : Oral frusemide 1-3mg/kg for modest edema.
v) Hypertension : Mild HTN can be controlled by salt & water
restriction. Effective anti-HTN agents includes amlodipine ,
nifedipine or diuretics.
vi) Dialysis : Dialysis is required in children severe renal failure &
prolong oligoanuria , fluid overload & life threatening
electrolyte disturbances.
. Outcome & prognosis :
Acute PSGN has an excellent prognosis in childhood. The
symptoms begin to resolve in the 1st week with loss of edema &
fall in blood pressure. Gross hematuria & significant
proteinuria disappear within 2 weeks , although microscopic
hematuria & slight proteinuria may persist for several months.
Hypertension subsides within 2-3 weeks. Patients with acute
GN of nonstreptococcus etiology have variable & unpredictable
outcome.
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