Renal Vascular Pathology Flashcards
3 HTN-related kidney vascular disorders?
“Benign” nephrosclerosis.
Malignant nephrosclerosis.
Collagen problems (e.g. scleroderma)
3 main categories of vascular disorders affecting the kidney?
Hypertension.
Decreased renal blood flow.
Thrombotic microangiopathies.
Why is “benign” nephrosclerosis called “benign”?
It shouldn’t be. I guess it’s to distinguish it from malignant nephrosclerosis caused by malignant HTN… but benign nephrosclerosis does a lot of damage.
What drives “benign” nephrosclerosis?
Longstanding mild to moderate HTN.
Gross appearance of kidney with “benign” glomerulosclerosis? (4 specific things)
Coarse, granular cortical surface (they showed one of these on the path cart).
Reduced kidney weight.
Reduced nephron mass.
Mild thinning of cortex.
3 microscopic changes seen in “benign” nephrosclerosis?
Hyaline arteriosclerosis.
Patchy interstitial fibrosis and tubular atrophy.
Global glomerulosclerosis.
What is the “hyaline” in hyaline arteriosclerosis?
An insudate of plasma proteins that moves into vessel walls -> narrowing of lumen.
What does global glomerulosclerosis refer to?
There’s sclerosis of the entirety of each individual affected glomerulus (in contrast to “segmental”).
What changes happen to larger vessels (not arterioles) of the kidney in “benign” nephrosclerosis?
Intimal fibrosis and medial thickening -> narrowed lumen.
Gross appearance of a kidney with malignant nephrosclerosis?
“Flea bitten” appearance - multiple pinpoint petechial hemorrhages.
Major process that you see in histology of malignant nephrosclerosis (that you wouldn’t see in “benign”)?
Necrosis, especially fibrinoid necrosis.
and some other things
What is fibrinoid necrosis? What’s the eosinophilic stuff?
how can you distinguish this from hyaline, if you’re confused
Necrosis of small vessels in kidney with fibrin deposition.
the fibrin is rough on RBCs, so you can see some RBC fragments in affected vessels
Why do you see “onion-skinning” in arterioles in malignant nephrosclerosis?
as an adaptation to the very high pressures, but it causes vessel lumen narrowing.
(thombus can also occur in these)
What kills people with malignant HTN?
Kidney failure.
Cerebral hemorrhage.
Heart failure.
How can scleroderma cause malignant HTN?
Collagen deposition in vessels -> reduced flow -> renin release -> HTN.
Pattern of damage seen on histology of kidney affected by scleroderma?
Fibrinoid necrosis, mucoid changes, some onion-skinning…
2 renal lesions that cause reduced renal blood flow?
Stenosis of renal artery.
Atheroembolus.
2 causes of stenosis of renal arteries?
Atherosclerosis.
Fibromuscular dysplasia.
(and… you could have some mass effect occluding the artery from outside)
How do atherosclerosis and fibromuscular dysplasia causing renal artery stenosis differ in appearance?
Atherosclerosis: usually one focal area of stenosis.
Fibromuscular dysplaia: alternating areas of stenosis and dilation.
3 changes (visible by histology) that happen in the underperfused kidney in renal artery stenosis?
Tubular atrophy.
Interstitial fibrosis.
Juxtaglomerular apparatus hyperplasia.
Does unilateral renal artery stenosis affect the opposite kidney?
Yes - renin -> increased BP can cause arteriosclerosis on the opposite kidney.
(more on this in the HTN lecture)
And the other kidney tends to get much bigger. “Goldblatt kidney”
Cholesterol emboli… what do they look like in histology?
They’re hard to see… shadows of washed out crystals surrounded by giant cells. (another one of these “why do we care if we’re not going to be pathologists?” things)
What kind of infarct would cause a wedge-shaped area of necrosis/scar in the kidney?
Occlusion of an interlobar artery.
What pattern of kidney damage will be seen in the context of acute blood loss? (e.g. obstetric emergency)
Cortical necrosis.
(this is confusing, given other lecturers said outer medulla is most susceptible to ischemia… perhaps the cortex is less able to adjust to acute changes? chronic ischemia would more affect medulla? Unclear.)
