Nephrotic Syndrome Flashcards
Defining characteristic of nephrotic syndrome
> 3.5 g protein/day lost in urine
Serum findings in nephrotic syndrome
hypoalbuminemia (edema)
hypogammaglobulinemia (infections)
hypercoagulable state (loss of antithrombin III)
hyperlipidemia and hypercholesterolemia (liver compensates and tries to thicken the blood)
3 groups of nephrotic diseases
Affecting Podocytes
minimal change disease, focal segmental glomerulosclerosis
Immune Complex Depositions
membranous nephropathy, membranoproliferative glomerulonephritis
Systemic Disorders
DM, systemic amyloidosis
Minimal Change Disease
classic presentation
children
Minimal Change Disease
basic pathology
cytokine-mediated
effacement (flattening) of podocyte foot processes
Minimal Change Disease
condition association
Hodgkin Lymphoma
causes massive release of cytokines (causing B-Sx)
⇒ can also efface podocyte foot processes
Microscopic findings of minimal change disease
normal on H & E (that’s where it got its name)
negative immunoflouresence
effacement of podocyte foot processes (epithelium) on electron microscopy
Proteinuria in minimal change disease
selective: only lose albumin NOT immunoglobulin
Tx of minimal change disease
steroids
*special: responds very well to treatment!
only nephrotic syndrome that is treatable
Untreated minimal change disease may lead to the development of this condition
focal segmental glomerulosclerosis
Focal Segmental Glomerulosclerosis
basic pathology
effacement/flattening of podocyte foot processes
(idiopathic)
Focal Segmental Glomerulosclerosis
associated condition(s)
HIV, heroin use, sickle cell disease
Focal Segmental Glomerulosclerosis
histology
focal: only some glomeruli
segmental: only parts of affected glomeruli
sclerosis: sclerotic tissue on H&E stain
Focal Segmental Glomerulosclerosis
H&E
Immunoflouresence
Electron Microscopy
H&E: focal regions of segmental sclerosis in glomerulus
IF: negative
EM: effacement of foot processes
Membranous Neuphropathy
basic pathology
immune complex deposition
subepithelial layer (under foot processes)
podocyte foot processes proliferate
⇒ membranous layer around capillaries
ie thickened capillary walls
Membranous Nephropathy
associations
_SLE*_
solid tumors
HCV, HBV, some drugs
Membranous Neuropathy
H&E
IM
EM
H&E: thick glomerular basement membrane
IM: granular immune complex depositions
EM: “spike and dome” appearance
Membranoproliferative Glomerulonephritis
Type I
basic pathology
subendothelial deposition of immune complexes
Membranoproliferative Glomerulonephritis
Type II
basic pathology
intramembranous immune complex deposition
within basement membrane
containing
C3 nephritic factor
binds C3 convertase and keeps it active, taking C3 out of the serum
Membranoproliferative Glomerulonephritis
Type I and II
histological findings
H&E: “tram-track” appearance, thick basement membrane
IF: immunoglobulins (type I), C3 staining (type II)
Membranoproliferative Disease
Type I
associations
HBV
HCV
Membranous disease
deposits in subepithelial layer
membranous nephropathy
Membranous disease
deposits in membranous layer
membranoproliferative glomerulonephritis
type II
Membranous disease
deposits in subendothelial layer
membranoproliferative glomerulonephritis
type I
Non-enzymatic glycocylation of dextrose onto vascular basement membrane causes this type of tissue damage
hyaline atherosclerosis
DM causes the most damage to what part of the kidney?
effernet arteriole
Why are ACE inhibitors best for DM patients?
hyaline atherosclerosis occurs perferentially in efferent arteriole
ATII also works on efferent arteriole
take away ATII effect negates some of the harm
prevents/lessens hyperfiltration
Kimmelstiel-Wildon nodules
sclerosis of mesangium
seen in nephrotic syndrome due to DM
Most commonly involved organ in systemic amyloidosis
kidney
Amyloid deposits where in kidney
mesangium
Amyloid under microscope
apple-green biofuringence
under polarized light
Congo red stain
