Pathology 1, 2, 3 Flashcards
What is azotemia?
Elevation of the blood urea nitrogen (BUN) and creatinine levels
Decreased glomerular filtration rate
What is prerenal azotemia?
Hypoperfusion of the kidneys–> Impairs renal function in the absence of parenchymal damage
What can cause prerenal azotemia?
Hemorrhage, shock, volume depletion, and CHF
This is when urine flow is obstructed beyond the level of the kidney.
Postrenal azotemia
What is it when you have azotemia associated with a constellation of clinical signs, symptoms, and biochemical abnormalities
Uremia
Describe diminished renal reserve.
GFR 50% notmal
BUN creatinine normal
Patient asymptomatic
What is seen in renal insufficiency?
GFR 20-50% normal
Azotemia (anemia and HTN)
Polyuria and nocturia (decreased concentrating ability)
What is the GFR in chronic renal failure
Less than 20-25% normal
Kidneys cant regulate volume and solute concentration
What symptoms are seen with chronic renal failure?
Edema, metabolic acidosis, and hyperkalemia
What is it called when the GFR is less than 5% normal and the patient is in the terminal stage of uremia?
End-stage renal disease
Nephritic?
- Hematuria (RBC casts)
- HTN
- Azotemia
- Oliguria
- Proteinuria (under 3.5g/day)
Nephrotic?
- Severe proteinuria (more than 3.5/day)
- Hypoalbuminemia (less than 3g/dL)
- Generalized edema
- Hyperlipidemia
- Lipiduria
4 types of histologic alterations?
- Hypercellularity
- BM Thickening
- Hyalinosis
- Sclerosis
What diseases is hypercellularity associated with?
Inflammatory diseases
What are the cellular changes seen in hypercellularity?
- Cellular proliferation (increased cellularity) in the mesagnial or endothelial cells
- Leukocytic infilatration (neutrophils, monocytes, lymphocytes)
- Crescent formation
What’s a crescent?
Acuumulation of cells composed of proliferating parietal epithelial cells and infiltrating leukocytes
(dark proliferation of cells)
Do the proximal convoluted tubules have a lot of cytoplasm?
YES
Remember, the DCT aren’t as big and puffy as the PCT
What do you see in light mycroscopy for basement membrane thickening?
Thickening of the capillary walls
What is seen deposited on EM for basement membrane thickening?
Amorphous electron-dense material (usually immune complexes)
Where are the amorphous electron-dense material (immune complexes) seen in EM for basement membran thickening seen?
Endothelial or epithelial side of the BM or withing the GBM itself
What else can be seen in EM for basement membreane thickening
Thickening of the basement membrane (due to increased synthesis of protein components (glomerulosclerosis)
What is seen on light microscopy and electron microscope in hyalinosis
Light: Accumulation of homogenous, eoinsophilic material
Electron: Extracellular and amorphous material
What hyalinosis composed of?
Plasma proteins insudated from circulation into glomerular structures
What can hyalinosis cause?
Extensive change…it can obliterate capillary lumens of the glomerular tuft
What is hyalinosis a consequence of and where is it commonly seen?
Consequence of glomerular damage and is common seen in focal segmental glomerulosclerosis (also diabetes)
What is sclerosis?
Accumulations of extracellular collagenous matrix confined to the mesangium (diabetic glomerulosclerosis)/involving capillary loops
What happens to the capillary lumens in sclerosis?
They are obliterated (some or all) in affected glomeruli
What is formed in capillary lumens in affected glomeruli in sclerosis?
Formation of fibrous adhesions
-Sclerotic portions of glomerulus and parietal epithelium of Bowman’s capsule
What is seen in acute proliferative (poststreptococcal/postinfectious) glomerulonephritis?
Diffuse proliferation of glomerular cells and influx of leukocytes
What is the cause of acute proliferative glomerulonephritis?
Immune complexes depositing
When can you see acute proliferative glomerulonephritis?
1-4 weeks after streptococcal infection (pharynx or skin)
What ages do you see acute proliferative glomerulonephritis in?
6-10
-Adults can be affected too
What is seen on light microscopy for acute proliferative glomerulonephritis?
- Enlarged, hypercellular glomeruli (infiltration by leukocytes, proliferation of endothelial and mesangial cells, and crescent formation)
- Interstitial edema and inflammation
- Tubules have red cell casts
What is seen on IF for acute proliferative glomerulonephritis?
Granular deposits of IgG, IgM, and C3 in the mesangium and along the GBM
What is seen on EM for acute proliferative glomerulonephritis?
Discrete, amorphous, electon-dense deposits on the epithelial side of the membrane (subepithelial) –> HUMPS
What is the clinical presentation for acute proliferative glomerulonephritis?
- Young child
- Abrupt development of malaise, fever, nausea, oliguria, and hematuria
- 1-2 weeks after recovery from a sore throat
- Red cell casts in the urine
- Mild proteinuria (usually less than 1gm/day
- Periorbital edema
- Mild-moderate HTN
What lab findings are seen with acute proliferative glomerulonephritis?
- Elevations of antistreptococcal antibody titers
- Decline in serum concentrations of C3
3 central features of rapidly progressive glomerulonephritis (crescentic glomerulonephritis)?
- Severe glomerular injury
- Rapid and progressive loss of renal function
- Severe oliguria and signs of nephritic syndrome
What is the most common histologic picture of rapidly progressive glomerulonephritis?
Presence of crescents
- Proliferation of parietal epithelial cells lining Bowman’s capsule
- Infiltration of monocytes and macrophages
Does rapidly progressive glomerulonephritis cause death?
YES… death from renal failure occurs in weeks to months if untreated
What are the 3 groups of rapidly progressive glomerulonephritis?
- Anti-GBM antibody induced disease (Goodpasture Syndrome)
- Immune complex deposition
- Pauci-immune type
What is seen in anti-GBM antibody-induced disease (Goodpasture syndrome)?
Linear deposits of IgG and C3 in the GBM
How is anti-GBM antibody-induced diseases (Goodpasture syndrome) treated?
Plasmapheresis
When do you see immune complex deposition associated with crescentic glomerulonephritis?
Post-infections, LN, IgA nephropathy, HSP
What kind of staining is seen with immune complex deposition associated with crescentic glomerulonephritis?
Granular pattern
What do you do to treat immune complex deposition associated with crescentic glomerulonephritis?
Treat underlying disease
What 2 things are characteristic of pauci-immune type rapidly progressive glomerulonephritis?
- Lack of anti-GMB antibodies or immune complexes by IF and EM
- Circulating antineutrophil cytoplasmic antibodies (ANCAs)