9/21- Histopathology Review and ATN & IS Nephritis Flashcards
(43 cards)
What are the overall characteristics (clinical findings) in Nephrotic Syndrome?
- Proteinuria
- Edema
- Hypoalbuminemia
- Hypercholesterolemia
- Lipiduria
What are the overall characteristics (clinical findings) in Nephritic Syndrome?
- Hematuria
- Mild proteinuria
- HTN
What are the overall characteristics (clinical findings) in Acute Renal Failure?
- Oliguria or anuria
- Elevated BUN and creatinine
What are the overall characteristics (clinical findings) in Chronic Renal Failure?
- Chronic elevation of BUN and creatinine
What is seen here?
V = vessel
G = glomerulus
- Can see vascular pole on lower left of glomerulus
- Normal loops are open; nothing within (including blood)
- Can see mesangium (“branches of trees”)
pT = proximal tubule
- pink, much cytoplasm, big lumen
dT = distal tubule
- less pink, smaller lumen
What is seen here?
pT = proximal tubule
dT = distal tubule
Into what 3 categories can renal diseases be divided?
Diseases affecting:
- Glomeruli
- Tubulo-interstitium
- Vessels
What are the glomerular patterns of injury?
Hypercellularity
- Mesangial cells
- Endothelial cells
- Leukocyte infiltrates
- Crescents
Basement membrane abnormalities
- Too thick, too thin, abnormal structure
Hyalinosis and Sclerosis
What is seen here?
Left (A): Mesangial hypercellularity ( > 3 cells per mesangial region)
- Cap loops nice and open, but too many nuclei in mesangial region
Right (B): Endocapillary proliferation; hypercellularity occludes capillary lumens
- Not too many open capillary loops
- Cellularity occluding loop
What is seen here?
Intracapillary neutrophils
- Can see tri-lobed nucleus
What is seen here?
Cellular crescent
- Cellularity in tubular/lumen space
What is seen here?
Left: Normal thickness glomerular basement membranes with preserved foot processes
- Podocyte foot processes can be seen angling down toward bottom right, covering GBM
- Foot processes standing straight and upright (“like Stonehenge”)
- Hazy gray area is intra-cap
Right: thin and irregular GBM with a basket-woven appearance
- Hereditary nephritis- Alports
What is seen here?
Left: Thickened glomerular basement membranes with effaced foot processes
- Altered charge potential and selective permeability
- Diabetes
Right: Thin, but normal structure GBM (B, note size measurement of 87 nm, normal is 350 nm in adult)
- RBCs can squeeze across these thin GBM
- Benign familial hematuria
What is seen here?
Left: Globally sclerotic glomerulus
- Typically accompanied by:
Right: tubular atrophy and interstitial fibrosis
The atrophic tubules have cast material and resemble thyroid tissue (“thyroidization”).
Immunofluorescence (IF) stains are used to highlight what processes? Examples?
Antibody mediated diseases
- anti-GBM disease
- membranoproliferative GN (type II)
- *pauci-immune GN is antibody mediated but IF is negative Immune complex mediated diseases
- systemic lupus erythematosus
- postinfectious glomerulonephritis
What is seen here?
Linear GBM staining, IgG
- “Linearly” green
- Typically seen in anti-GBM disease (evenly distributed along basement membrane)
What is seen here?
Mesangial staining
- SLE (could be IgA, IgG…)
Electron microscopy is necessary to detect what types of abnormalities?
- Confirm IF findings (electron dense deposits)
- Evaluation of foot processes: effaced or preserved, only way to diagnosis minimal change disease
- Evaluation of basement membrane thickness and composition
- Drug effects (mitochondrial alterations)
- Viral infections
- Storage disease
What is seen here?
- Electron dense deposits
- Left: Mesangial; could be lupus, IgA/IgG nephropathy… just showing mesangial electron dense deposits
- Right: Epimembranous (“humps”); very characteristic of post-glomerulonephritis
What is seen here?
Effaced foot processes
- Can see endothelial cell nucleus protruding into cap lumen
- Foot processes look like “melted Hershey kisses”)
What is seen here?
Viral (BK) particles
- Commonly seen in kidney biopsies in transplant population
Case 1)
- 61 year-old lawyer was admitted for a triple coronary bypass surgery for coronary atherosclerosis; op was successful and the pt recovered from the surgery
- Two days post-postoperatively, he developed progressive SOB and chest pain and a diagnosis of ARDS was made - At the same time, urine output was decreased and he became anuric.
- The serum creatinine was 6.5 mg/dl but there was no protein excretion in his urine.
- The serum creatinine before the operation was 0.9 mg/dl and there was no proteinuria by dip stick.
- The patient was put on hemodialysis, but multiorgan failure developed and he expired 5 days after surgery. An autopsy was performed.
What syndrome does this pt have?
Possible causes overall and then in this patient?
Syndrome of acute renal failure
- This syndrome is characterized by decreased renal function and anuria of sudden onset.
- The normal renal function before the operation also supports the diagnosis of acute renal failure - The absence of protein is also a characteristic feature of acute renal failure.
Possible causes of acute renal failure are multiple and can be classified into 3 categories: Pre-renal, renal, and post-renal
- Pre-renal causes are related to sudden and bilateral loss of renal perfusion
- The renal causes are mainly related to severe involvement of one of the three main renal compartments (glomerular, tubulointerstitial, or vascular)
- The post-renal causes are related to sudden bilateral obstruction of the urine outflow.
In this patient: hypoperfusion leading to acute tubular necrosis
There are two types of acute tubular necrosis.
- One is related to ischemic injury secondary to severe and prolonged renal hypoperfusion, and the other is related to nephrotoxins.
- Acute tubular necrosis of ischemic type is much more frequent and is most probably the cause of acute renal failure in this patient.
What are nephrotoxic drugs associated with ATN?
- Aminoglycosides
- Contrast agents
…
Case 1 cont’d)
For the pt with ischemic injury 2ndary to severe/prolonged renal hypoperfusion causing acute renal failure
Tubular changes are mostly related to apoptosis, necrosis, and regeneration of the tubular epithelial cells and vary according to the stages of disease
- There is focal necrosis or flattening of the tubular epithelial cells
- Interstitial edema, vascular congestion, and minimal interstitial inflammation, may also be present in ischemic acute tubular necrosis
