This strong negative charge prevents negatively charged proteins like (1) from being filtered into the urinary space
Immunological damage to the glomeruli can either produce predominantly (1) (nephrotic symptoms and signs) or predominantly (2) (nephritic symptoms and signs).
- mainly protein loss
2. bleeding and more severe injury
Clinically, patients with heavy proteinuria have the (1) syndrome which consists of proteinuria (usually 3.5 grams of protein in a 24 hour urine collection), (2)
2. hypoalbuminemia, edema, hyperliipidemia, and lipiduria
The proteinuria leads directly to the (1) because the kidney is excreting the protein from blood into urine.
- hypoalbuminemia or low serum albumin
The hypoalbuminemia causes (2) because of the decreased plasma oncotic pressure from decreased serum proteins.
- edema (fluid within tissues)
The hyperlipidemia occurs because the (1) produces more (2) in the generalized response to produce more (3).
(1) happens because of the increased lipoproteins carrying lipid and because of loss of the filtration barrier.
- Lipiduria (lipid in urine)
There can be extensive (1) in patients without any histopathological changes that can be seen by light microscopy (MCD/lipoid nephrosis)
- selective proteinuria
However, ultra-structural changes can be seen by electron microscopy generally show (1) in nephrotic syndrome in Minimal Change disease (MCD).
- loss of the epithelial podocyte foot processes
Minimal change disease (biopsy (1) is the most common cause of nephrotic syndrome in children. Children who do not develop any complications have a completely normal life span without any later renal disease.
- H&E stains- no change in glomeruli; hyaline (protein and lipid) droplets in tubular cells
Although the cause of minimal change disease is unknown, it is thought to be the result of (1) occurring in glomeruli
lymphokines of the T cells
Membranous nephropathy can be either primary (Anti-phospholipase A2 receptor antibody) or secondary from a disease which is producing (2) within the kidney
- antigens or immune complexes
Some of the secondary causes of secondary membranous nephropathy include inflammation disorders like (1)
- SLE, infections (IE), drugs (gold, penicillamine), and adenocarcinomas, DM
An experimental animal model called Heymann nephritis suggest that (1) are more often present first in the (2) or surrounding cells before the (3) arrive to form immune complexes.
- basement membrane
Light microscopy can show (1) in membranous nephropathy (silver stains show (2) material so they can show immune complexes as areas where the silver stain is lost)
- thickened basement membranes
2. basement membrane
Electron microscopy of membranous nephropathy shows antigen-antibody complexes present in the subepithelial region between the (1)
- basement membrane and the podocyte
The course of membranous nephropathy is
- CRF to end stage renal disease
Most common (adult) cause of nephrotic syndrome is (1)
- focal segmental glomerulosclerosis (FSGS)
Immune microscopy in membranous nephropathy can show the presence of (1) antibody or (2) components including (3) and the components of the (4) which actually causes the injury
- membrane attack complex (C5b, C6-C9)
GBM predominantly of _____
2. Also laminin, fibronectin, and glycosaminoglycans.
Relative exclusion of negatively charged molecules such as albumin due to _____
type IV collagen;
polyanionic glycosaminoglycans, (heparan sulfate).
IgA deposit location
How is edema caused in nephrotic syndrome: 2 causes
Dec. _____ due to loss of albumin;
- fluid escapes into tissues causing edema;
- Dec. onc. pressure leads to dec. ____ –> dec. ____ –> INC. _____–> fluid retention–> edema
Dec. plasma oncotic pressure due to loss of albumin; 1. fluid escapes into tissues causing edema; 2. Dec. onc. pressure leads to dec. plasma volume –> dec. GFR –> INC. aldosterone–> fluid retention–> edema
Min. change disease -Occasional association with ___
and with ____ has led to the
speculation that it is a T lymphocytes disorder
Hodgkin disease; atopic asthma etc
Minimal change disease
Immunofluoresence for immunoglobulins (IF) and complement:
Light microscopy: Normal
Electron microscopy: diffuse obliteration of podocyte foot processes
In intermediate disease stages, silver stains (which demonstrate basement membrane
material) reveal multiple projections or “spikes” on the epithelial surface of BM
M embranous Nepropathy
Immunofluorescence microscopy reveals ____ staining of capillary walls for IgG and C3. There is intense staining for terminal complement components, including
the _____, which induces glomerular injury
diffuse granular; membrane attack complex;
Membranous glomerulopathy. Caused by the ____ accumulation of immune complexes and the accompanying changes in the ____.
subepithelial; basement membrane (BM)
IF- linear deposit see in glomeruli in_______
Type II hypersensitivity, Anti-GBM disease-aka CrGN (type 1)
FEATURES OF Glomerulus in DM
Nodular (PAS positive DEPOSIT) nephrosclerosis
Risk factors- FSGS
HIV, OBESITY, ETC.
C3 NEPHRITIC FACTOR POSTIVE SERUM- GLOMERULAR FINDINGS
DEPOSIT OF IGG, IGM, AND C3 IN GLOMERULI, INFECTION BY____
INFECTION WITH GROUP A-STREPTOCOCCI
RESP. INFECTION FOLLOWED BY HEMATURIA- POSSIBLE CONDITION
INFECTION, ATHEROSCLEROSIS, AND DVT- POSSIBLE COMPLICATIONS OF_______
NON SELECTIVE PROTENIRIA
HEMATURIA AND +4 PROTEINURIA
FSGS AND MGN