Glomerular- Pathology Flashcards
This is the term where is increased nitrogenous compounds in the blood (BUN and creatinine).
Azotemia
What happens to the GFR in azotemia?
it ↓
What causes prerenal aztoemia?
hypoperfusion of the kidneys (↓ blood flow)
True or False: there is parenchymal damage in prerenal azotemia,
FALSE. there is impairment of renal fxn but no parenchymal damage.
What causes postrenal azotemia?
a blockage past the kidney
This is the term when azotemia is associated with a bunch of other signs and Sx, like failure of renal exretory fxn, metabolic and endocrine alterations, and 2o involvement of other systems.
Uremia
This is the rapid and frequently reverible deteroration of renal fxn dominated by oliguria or anuria and a recent onset of azotemia.
Acute Renal Failure (ARF)
What are the 4 stages of chronic renal fialure?
- Diminished renal reserve
- Renal insufficiency
3, chronic renal failure - end-stage renal disease
In the diminshed renal reserve stage of chronic renal failure, how much is hte GFR reduced as compared to normal?
50% of normal
In the renal insufficiency stage of chronic renal failure, what is the GFR % of normal?
GFR 20-50% of normal
In the renal insufficiency stage of chronic renal failure, what are the other Sx in addition to azotemia??
anemia, HTN, polyuria and nocturia
In the chronic renal failure stage, the GFR is < 20%, and kidney fxn really sucks, causing what Sx?
Edema, metabolic acidosis, hyperkalemia, and overt uremia
What % of GFR is at the end-stage renal disease of chronic renal failure?
< 5%
This is the glomerular syndrome where there is an acute onset of hematuria, azotemia, mild/moderate proteinuria, oliguria, edema, and HTN.
Nephritic syndrome
This is the glomerular syndrome where there is acute nephritis, proteinuria, and acute renal failure.
Rapidly progressing glomerulonephritis (RPGN)
This is the glomerular syndrome where there is heavy proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, lipiduria, and severe edema.
Nephrotic syndrome
What are the 2 components of the glomerular basement membrane?
type IV collagen and glycoproteins
These are cells that are similiar to vascular smooth muscle cells and pericytes and lie between the capillaries and support the entire glomerular tuft.
Mesangial cells
What is the fxn of mesangial cells?
They’re mesenchymal in origin, contractile, phagocytotic, proliferative, and secrete biologically active mediators.
Hypercellularity in the glomerularnephropathies causes cellular proliferation and leukocyte infiltration, leading to what formation in the glomerulus?
crescents
Crescents from hypercellualrity is from the leakage of what component into the urinary space?
fibrin
In glomerulonephropathies, the deposition of amorphous, electron-dense material and increased synthesis of the GBM’s proteins causes what?
GBM thickening
What mechanisms underlie most glomerulonephropathy?
immune mechnaisms
If immune complexes are deposited in the glomeruli, what do they look like on immunflourescence (IF)?
Granular
If antibodies are directed against antigens in the GBM, what does it look like on IF?
Diffuse linear pattern
Which syndrome gives a diffus linear parrtern of immune complexes on IF?
Goodpasture syndrome
When circulating immune complexes get deposited and cause glomerulonephritis, there is leukocyte infiltration and proliferation of what 2 cells?
Mesangial and endothelial cells.
What are the 2 major histologic characteristics of progressive renal damage?
Focal Segmental Glomerulosclerosis (FSGS) Tubulointerstitial fibrosis (TIF)
Is FSGS a nephritic or nephrotic syndrome?
Nephrotic syndrome
Is the protein content in urine higher or lower than 3.5g/day in nephrotic syndrome?
> 3.5 g/day
In FSGS, where to proteins accumulate when there is endothelila and epithelial are injures causing the increased glomerular permeability to proteins?
Accumulation in mesangial matrix
What happens to the foot processes in FSGS?
They undergo effacement (thinning)
In FSGS, the accumulation of proteins in the mesangium of the glomerulus caues what change of the remaining glomeruli?
Compensatory hyperplasia
The compensatory hyperplasia then causes what change in FSGS?
segmental glomerulosclerosis
Though FSGS is usually idiopathic, what are the 3 high yield assocaitions with its etiology?
HIV, heroin use, and sickle cell disease
True or False: in FSGS, there is immune complex deposition causing a granular appearence on IF.
FALSE
True or False: FSGS patients do not respond to steroid treatment.
True.
In TIF, what causes direct injury to and activation of tubular cells?
Proteinuria
The proteinuria damage in TIF cuases activation of what mediators to cause the interstitial fibrosis?
cytokines, chemokines, and GFs
This syndrome is characterized by the inflammation of the glomeruli, and involves hematuria*, red cell casts in urine, azotemia, oliguria, and mild/moderate HTN.
Nephritic syndrome
PHAROH
This nephritic syndrome occurs 1-4 weeks after a streptococcal infection.
Poststreptococcal Glomerulonephritis (PSGN)
Which patients are at most risk for PSGN?
Kids 6-10 (adults can get it too)
Which protein on the strep bug causes the cross linking to self Ag’s?
M protein
True or False: all nephritic syndromes involve immune-complex deposition.
true
There are enlarged, hypercellular glomeruli in PSGN because of the the diffuse infiltration of what cells?
Leukocytes
What are seen in the subepithelium in PSGN as a result of Ag-Ab complex depostion?
Subepithelial humps