Acute Glomerulonephritis

By- HANAN, MD
August, 2016
 Course Outline
•
Introduction to a child with Hematuria
•
Etiology & Epidemiology
•
Pathogenesis & pathology
•
Clinical manifestation
•
Diagnosis
•
Treatment
•
Complications & prognosis
 Introduction to Hematuria
•
Definition- presence of atleast 5 RBCs/microliter of
urine.
•
Significant hematuria- > 50 RBCs/ml of urine.
•
Upper urinary tract sources of hematuria originate
within the nephron (glomerulus, convoluted or
collecting tubules, and interstitium).
•
Lower urinary tract sources of hematuria originate
from the pelvocalyceal system, ureter, bladder, or
urethra
 Introduction to Hematuria…
•
Common causes of gross hematuria:-

*Urinary tract infection

*Meatal stenosis
*Perineal irritation
*Trauma
*Urolithiasis
*Hypercalciiuria
*Coagulopathy
*Tumor
 Introduction to Hematuria…
•
Glomerular

*Postinfectious glomerulonephritis
*Henoch-Schonlein purpura nephritis
*IgA nephropathy
*Alport syndrome (hereditary nephritis)
*Thin glomerular basement membrane disease
*Systemic lupus erythematosus nephritis
 Acute Post Streptococcal
Glomerulonephritis

•
Acute poststreptococcal glomerulonephritis
(APSGN) is a classic example of the acute
nephritic syndrome characterized by the
sudden onset of gross hematuria, edema,
hypertension, and renal insufficiency.
 Etiology & Epidemiology
•
APSGN follows infection of the throat or skin by
certain “nephritogenic” strains of GAS(Group A β-
hemolytic streptococcal)

•
97% of cases occur in less-developed countries
•
Epidemics of nephritis have been described in
association with throat (serotype 12) and skin
(serotype 49) infections,but most commonly is
sporadic.
 Pathology & Pathogenesis
•
The kidneys appear symmetrically enlarged.
Glomeruli appear enlarged and relatively bloodless
and show diffuse mesangial cell proliferation, with an
increase in mesangial matrix.

•
Immunofluorescence microscopy reveals a pattern of
“lumpy-bumpy” deposits of immunoglobulin and
complement on the glomerular basement membrane
(GBM) and in the mesangium.
 Pathology & Pathogenesis…
•
On electron microscopy, electron-dense deposits, or
“humps,” are observed on the epithelial side of the
GBM.

•
Morphologic studies and a depression in the serum
complement (C3) level provide strong evidence that
ASPGN is mediated by immune complexes.
 Pathology & Pathogenesis…
•
Several mechanisms of immune injury:-

1) circulating immune complex formation

with streptococcal antigens and subsequent
glomerular deposition,

2) molecular mimicry whereby circulating

antibodies elicited by streptococcal antigens
react with normal glomerular antigens,
 Pathology & Pathogenesis…
3)in situ immune complex formation of
antistreptococcal antibodies with glomerular
deposited antigen, and

4) complement activation by directly

deposited streptococcal antigens.
 Clinical manifestation
•
Poststreptococcal GN is most common in
children aged 5-12 yr and uncommon before
the age of 3 yr.

•
The typical patient develops an acute
nephritic syndrome 1-2 wk after an
antecedent streptococcal pharyngitis or 3-
6 wk after a streptococcal pyoderma.
 Clinical manifestation…
•
Hypertension-70%, transient ARF-50%
•
Non-specific symptoms-malaise,lethargy, abdominal
& flank pain.
•
Heart failure, pulmonary edema
•
Nephrotic syndrome-10-20%
•
The acute phase generally resolves within 6-8 wk.
•
Although urinary protein excretion and hypertension
usually normalize by 4-6 wk after onset, persistent
microscopic hematuria can persist for 1-2 yr after the
initial presentation.
 Diagnosis
•
Urinalysis demonstrates red blood cells
(RBCs), often in association with RBC casts,
proteinuria, and polymorphonuclear
leukocytes.

•
The serum C3 level is significantly reduced in
>90% of patients. C4 is most often normal in
APSGN, or only mildly depressed.
 Diagnosis…
•
Confirmation of the diagnosis requires clear
evidence of a prior streptococcal infection.

•
Antistreptolysin O titer(ASO titer), anti-
deoxyribonuclease (DNase) B level. If
available, a positive streptozyme screen
(which measures multiple antibodies to
different streptococcal antigens) is a valuable
diagnostic tool.
 Diagnosis…
•
Chest x-ray is indicated in those with signs of heart
failure or respiratory distress, or physical exam
findings of a heart gallop, decreased breath sounds,
rales, or hypoxemia.
•
Renal biopsy- indicated in patients with:-
1) NS
2)Absence of evidence of streptococcal
infection
3)Normal complement levels
4)Hematuria,proteinuria,diminished renal
function, &/or low C3 levels persisting >2 months.
 Diagnosis…
•
Persistent hypocomplementemia can indicate a
chronic form of postinfectious GN or another disease
such as membranoproliferative GN.

•
Bacterial endocarditis can produce a
hypocomplementemic GN with renal failure. Acute
GN can occur after certain fungal, rickettsial, and
viral diseases, particularly influenza.
 Treatment
•
Sodium restriction, diuresis usually with intravenous
furosemide, and pharmacotherapy with calcium
channel antagonists, vasodilators, or angiotensin-
converting enzyme inhibitors are standard therapies
used to treat hypertension.

•
N.B-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 GN.
 Complications & Prognosis
•
Acute complications- Hypertension(60-70%),
hypertensive encephalopathy(10%), intracranial
bleeding, heart failure,
hyperkalemia,hyperphosphatemia, hypocalcemia,
acidosis, seizures and uremia.
•
Complete recovery- in >95% of patients.
•
5% rapidly progressive GN or slowly progressive
•
CKD occurs in <2%.
•
Reading Assignments-

*IgA nephropathy and

*Rapidly progressive GN( crescentric GN)
THANK YOU!!!