Professional Documents
Culture Documents
introduction
Characterized by a group of similar clinical
manifestations, such as proteinuria, hemoturia,
edema, and hypertension
But etiology, pathogenesis, pathology, and
prognosis are different
Primary: pathology confined to the kidney, any
systemic features are a direct consequence of
glomerular dysfunction
Secondary: are clasified as secondary when be
manifestation of systemic diseases, vascular,
metabolic or genetic disorders
Primary glomerular disease is the main cause of
chronic renal failure in china, and is the most
common in renal diseases
Clinical classification
According to their characters of clinical
symptoms, gromerular diseases divide
to five types
Acute GN
Rapidly progressive GN
Nephrotic syndrome
Latent GN
Chronic GN
Pathological classification
According to pathological standards of the
glomerular diseases, published by WHO in 1982
1.Minimal changes GN
2.Focal segmental glomerular lesions
3.Diffuse GN
4.Unclassified GN
>50% of the glomerulus are affected diffused
<50% of the glomerulus are affected focal
>50% of the capillary are affected global
<50% of the capillary are affected
segmental
Pathological classification
Diffused glomerulonephritis
a.Membranous
nephropathy
a.mesangial proliferative GN
b.endocapillary proliferative
b.Proliferative
GN c.Mesangial capillary G
glomerulonephritis
d.Dense deposit GN
e.Crescentic GN
c.Sclerosing GN
Classification of glomerulopathies
proliferative
Always be normal
in light microscopy
Without depositing
of immune
complex
Minimal change disease
On electron
microscopy,
there is a
characteristic
fusion of the
epithelial foot
processes
Focal
glomerulosclerosis
Light microscopy
shows the lesions
of focal
segmental
glomerular
sclerosis
IgAN
Light
microscopy
shows
mesangial
expansion by
increased cells
and matrix
IgAN
Detected by
immunofluoresc
ence
microscopy, IgA
deposit in
mesangium
Membranous
nephropathy
Immune
complex deposit
in the
subepithelial
cells, GBM
become thick
and distorted
Membranoproliferative
glomerulonephritis
Be
characterized
by a diffuse
increase in
mesangial cells
and matrix, and
by thichness of
the GBM
Crescentic
glomurulonephritis
2 mechanisms of cytotoxicity:
7. Ab mediate cell
destruction via
mechanism ADCC (cell
cytotoxicity dependent
on Ab)
Damage by antibodies
Damage mediate by complement
In proliferative glomerulopathy:
Proteinuria
a.Both charge and size selectivity normally
prevent virtually all of plasma albumin,
globulin, and other large-molecular-weight
proteins from the glomerular wall
b.Normal individuals excrete less than
150mg/g of total protein and only about
30mg/d of albumin
c.The remainder of the protein in the ruine is
secrete by the tubules:Tamm-horsfall, IgA,
and beta-microglobulin
Clinical manifestation
Proteinuria
d.The endocelial cell forms a barrier
penetrated by pores of about 100nm
that hold back cells and other
particles
e.The glomerular basement membrane
traps most large proteins
f.The foot processes of epithelial cells
allow molecular passage of small
solutes and water
Clinical manifestation
Proteinuria
g.Disruption of the basement
menbrane and slit diaphragms,
resulting in large amounts of
protein
h.The fusion of foot process
causes increased pressure
across the capillary basement
membrane, resulting in
Clinical manifestation
Hematuria
a.Isolated hematuria without proteinuria,
other cells, or casts is often indicative of
bleeding from the urinary tarct
b.Gross hematuria with blood clots is almost
suggests a postrenal source in the urinary
collecting system
c.Isolated painless hematuria
(nondysmorphic RBCs) often indicate
urogenital neoplasms
d.In the pediatric population, isolated
hematuria is more likely to be idiopathic
or congental anomaly
Clinical manifestation
Hematuria
e.Isolated hematuria with dysmorphic RBC
examined by phase-contrast microscopy
always indicated glomerular disease
f.The most etiologyies of glomerular
hematuria are IgA nephritis, hereditary
nephritis, and thin basement menbrane
disease.
g.Even in the absence of azotemia, these
patients should undergo serologic
evaluation and renal biopsy
Clinical manifestation
Edema
Glomerulopathy
a.First found in body parts with low tissue
tention
b.With heavy proteinuria(>3.5g/d)
c.With hypoalbuminemia and hyperlipidemia
d.With diminished colliod oncotic pressure
due to losses of large quantities of protein
into the urine, the salt and water retained
can not be restrained within the vascular
compartment
Clinical manifestation
Edema
Glomerulonephritis
a.Assosiated with hematuria, proteinuria,
and hypertension
b.Especially evident in the very soft tissue of
the eyelids and face, and tends to be most
pronounced in the morning because of the
recumbent posture during the night
d.Fluids retention is due to increased
capillary permeability, and primary
retention of sodium and water by the
kidneys owing to renal insufficency
Clinical manifestation
Hypertension
a.Fifty percent of patients have
hypertension
b.cause: salt and water retention,
hyperreninemic states and
exogenous erythropoietin
administration
c.Must be meticulously controled, fail
to do so can accelerate the
progression of renal damage and
congestive heart failure
Clinical manifestation
Clinical presentations
• develop renal failure over weeks to months
•With nephritic urinary sendiment: gross hematuria,
proteinuria, oliguria, hypervolemia, edema,
hypertension
•Headache, malaise, anorexia, weight loss, fever,
arthralgias, and myalgias
Rapidly progressive
glomerulonephritis (RPGN)
Laboratory findings
•The urinary is nephritic
•Ccr decreases progressively
•anti-GBM autoantibodies detectable by
immunoassay
•Pauci-immune glomerulonephritis have ANCA be
detected
Rapidly progressive
glomerulonephritis (RPGN)
Cause:
I.Hematuria with or without proteinuria
a.primary glomerular diseases
1.IgA nephropathy
2.mesangiocapillary glomerulonephritis
3.thin basement membrane disease
b.associated with multisystem or hereditary
1.Alports snydrome
2.fabrys disease
3.sickle cell disease
c. associated with infections
1.poststreptococcal glomerulonephritis
2.other postinfectious glomerulonephritis
Asymptomatic urinary
abnormalities
Cause:
II. Isolated nonnephrotic proteinuria
a.primary glomerular diseases
1.orthostatic proteinuria
2.focal and segmental glomerulonephritis
3.membranous glomerulonephritis
b.associated with multisystem or hereditary
1.diabetes mellitus
2.amyloidosis
3.nail-patella syndrome
Asymptomatic urinary
abnormalities