Disease

1. Acute post
streptococcal
glomerulonephritis

2. Rapidly progressive

Glomerulonephritis

3. Goodpasture
syndrome

4. Wegeners
granulomatosis

Pathophysiology
Symptoms usually occur in
children and young adults
following respiratory infections
caused by certain strains of
group A streptococcus that
contains M protein in the cell
wall. During the course of the
infection, these
Nephrogenic
strains
of
streptococci
form
immune
complexes
with
their
corresponding
circulating
antibodies
and
become
deposited on the glomerular
membranes.
The
accompanying
inflammatory
reaction affects glomerular
function.
Symptoms are initiated by deposition
of immune complexes in the
glomerulus, often as a complication of
another form of glomerulonephritis or
an immune systemic disorder such as
systemic lupus erythematosus (SLE).
Damage by macrophages to the
capillary walls releases cells and
plasma into Bowmans space, and the
production of crescentic formations
containing macrophages, fibroblasts,
and polymerized fibrin, causes
permanent damage to the capillary
tufts.
Appearance
of
a
cytotoxic
autoantibody against the glomerular
and alveolar basement membranes can
follow viral respiratory infections.
Attachment of this autoantibody to the
basement membrane, followed by
complement activation, produces the
capillary destruction. Referred to as
antiglomerular basement membrane
antibody, the autoantibody can be
detected in patient serum.
Wegeners granulomatosis causes a
granuloma-producing inflammation of
the small blood vessels of primarily
the kidney and respiratory system. Key
to the diagnosis of Wegeners
granulomatosis is the demonstration of
antineutrophilic cytoplasmic antibody
(ANCA) in the patients serum.
Binding of these autoantibodies to the

Urinalysis
findings
Macroscopic
hematuria
Proteinuria
RBC casts
Granular casts

Other tests
Antistreptolysin
O titer
Antigroup A
streptococcal
enzymes

Macroscopic
hematuria
Proteinuria
RBC casts

BUN
Creatinine
Creatinine
clearance

Macroscopic
hematuria
Proteinuria
RBC casts

Antiglomerular
basement
membrane
antibody

Macroscopic
hematuria
Proteinuria
RBC casts

Antineutrophilic
cytoplasmic
antibody

5. HenochSchonlein
purpura
6. Membranous
glomerulonephr
itis (MGN)

7. Minimal change
disease (MCD)

8. Focal segmental
glomerulosclero
sis (FSGS)

9. Membranoprolifer
ative
Glomerulonephritis

neutrophils located in the vascular

walls may initiate the immune
response and the resulting granuloma
formation.
Occurs primarily in children following
viral respiratory infections; a decrease
in platelets disrupts vascular integrity.
The predominant characteristic of
membranous glomerulonephritis is a
pronounced
thickening
of
the
glomerular
basement
membrane
resulting from the deposition of
immunoglobulin
G
immune
complexes. Disorders associated with
the development of membranous
glomerulonephritis include systemic
lupus
erythematosus,
Sjgren
syndrome,
secondary
syphilis,
hepatitis B, gold and mercury
treatments, and malignancy. Many
cases of unknown etiology have been
reported. As a rule, the disease
progresses slowly, with possible
remission;
however,
frequent
development of nephrotic
Syndrome symptoms occurs. There
may also be a tendency toward
thrombosis.
Minimal change disease (also known
as lipid nephrosis) produces little
cellular change in the glomerulus,
although the podocytes appear to be
less tightly fitting, allowing for the
increased filtration of protein.
Focal segmental glomerulosclerosis
(FSGS) affects only certain numbers
and areas of glomeruli, and the others
remain normal. Symptoms may be
similar to the nephrotic syndrome and
minimal change disease owing to
damaged podocytes. Immune deposits,
primarily immunoglobulins M and C3,
are a frequent finding and can be seen
in undamaged glomeruli. FSGS is
often seen in association with abuse of
heroin and analgesics and with AIDS.
Moderate to heavy proteinuria and
microscopic hematuria are the most
consistent urinalysis findings.
Membranoproliferative
glomerulonephritis
(MPGN)
is
marked by two different alterations in
the cellularity of the glomerulus and
peripheral capillaries. Type 1 displays

Macroscopic
hematuria
Proteinuria
RBC casts
Microscopic
hematuria
Proteinuria

Stool occult
blood
Antinuclear
antibody
Hepatitis B
surface antigen
Fluorescent
treponemal
antibodyabsorpti
on test (FTAABS)

Heavy
proteinuria
Transient
hematuria
Fat droplets

Serum albumin
Cholesterol
Triglycerides

Proteinuria
Microscopic
hematuria
Macroscopic or
Microscopic
hematuria

Drugs of abuse
HIV tests
Genetic testing

Hematuria
Proteinuria

Serum
complement
levels

10. IgA

nephropathy

11.
Chronic
glomerulonephr
itis

increased
cellularity
in
the
subendothelial cells of the
Mesangium (interstitial area of
Bowmans
capsule),
causing
thickening of the capillary walls,
whereas type 2 displays extremely
dense deposits in the glomerular
basement membrane.
Also known as Berger disease, IgA
nephropathy, in which immune
complexes containing IgA are
deposited
on
the
glomerular
membrane, is the most common cause
of glomerulonephritis. Patients have
increased serum levels of IgA, which
may be a result of a mucosal infection.
Marked decrease in renal function
resulting from glomerular damage
precipitated by other renal disorders.

Macroscopic or
microscopic
hematuria

Serum IgA

Hematuria
Proteinuria
Glucosuria
Cellular and
granular casts
Waxy and broad
casts

BUN
Serum creatinine
Creatinine
clearance
Electrolytes