Renal Vascular Disease + Cases-- Leah**

Question 1

Aside from hyaline arteriolosclerosis, what changes are seen in the kidney secondary to chronic hypertension? (2)
What is this process called?

Answer 1

Nephrosclerosis:

• Loss of tubules and scarring –> gross granular appearance
• “Fibroelastic hyperplasia”

Question 2

What does fibroelastic hyperplasia look like (3)?

Tell me again, what is fibroelastic hyperplasia assc with?

Answer 2

• media thickening, intima thicken myofibroblastic tissue, elastic lamina reduplication
• caused by long standing hypertension –> nephrosclerosis

Question 3

In general, what is the outcome of nephrosclerosis?

Answer 3

Proteinuria more common; renal insufficiency is rare.

Insufficiency may occur in severe HTN, other underlying disease, and more commonly in African Americans

Question 4

Gross appearance of a kidney in malignant hypertensive state (3)

Answer 4

Flea bitten
Swollen
Poor cortical demarcation

Question 5

Appearance of vasculature and Glomeruli in malignant HTN

Answer 5

Onion skinning–concentric smooth mm. and collagen (hyperplastic arteiolosclerosis)
Fibrinoid necrosis of both arterioles and glomeruli

Question 6

What happens physiologically in unilateral renal artery stenosis?

Answer 6

Decreased renal BP –> JG secretes renin –> hypertension/ salt and water retention
*Remember that stenosed kidney is protected from effects of HTN!

Question 7

Most common cause of renal artery stenosis?

Cause in young women?

Answer 7

Usually atherosclerosis, which is more common in males and diabetics
Young women may get fibromuscular dysplasia

Question 8

Result of long standing renal artery stenosis in stenosed kidney?
treatment?

Answer 8

• Kidney is protected from nephrosclerosis (HTN) but has ischemic damage
• Kidney shrinks

Can be cured with angioplasty/ stenting

Question 9

What are microangiopathic diseases?
When leading to anemia…..Are they classified as extrinsic or intrinsic?
Intravascular or Extravascular? (These two questions are based on first aid.)

Answer 9

Basic definition: microthrombi lead to obstruction/ ischemia

This can cause INTRAVASCULAR anemia since it takes place in the vessels, not the spleen.
This is EXTRINSIC, since the condition does not have to do with a deficiency/ deformity in the RBCs themselves.

*Thank you for putting this in here bc I wouldn’t have thought to do it!🙌

Question 10

Hemolytic Uremic Syndrome:

• what kind of disease is it?
• what causes the typical type? Atypical type?

Answer 10

Microangiopathic; caused by endothelial injury and subsequent thrombi

Typical: most commonly caused by a shiga like toxin KIDS
(ecoli. EHEC. O157H7)

Atypical: caused by excess complement ADULTS
(Most common: factor H regulatory protein deformed = ^ complement)

Question 11

Describe the symptomatic progression of HUS

Also: who is this common in?, what’s the long term outcome?

Answer 11

Disease common in KIDS (remember the kid at the ice cream shop on sketchy!). They need temporary dialysis but do recover.

Flu sx/ diarrhea –> bleeding –> oliguria/hematuria –> hemolytic anemia and low platelets

May or may not have neuro sx and HTN. (Distinguishes from TTP: main symptom is NEURO)

Question 12

TTP: what kind of disease is it? Who gets it? What causes it?

Answer 12

Microangiopathic; young females
Low amounts of ADAMTS13 = ^vWF (uncleaved) + clotting
(Usually an Ab against ADAMTS13, can also be genetic deficiency)

Question 13

TTP symptoms (4)–do they have diarrhea?

Answer 13

Most prominent: neuro-->disting. from HUS 
Fever 
Low platelets 
About half have renal failure 
NO diarrhea!

Question 14

Acute morphology of both microangiopathic diseases (HUS + TTP)

(Describe the cortex, capillaries and larger arteries)

Answer 14

Cortical necrosis/ petechia
Thick capillaries with disrupted mesangium
Fibrinoid necrosis of interlobular arteries

Question 15

Chronic morphology of microangiopathic disease

+ which of the diseases (HUS, TTP) does not progress to this chronic state?

Answer 15

• TYPICAL HUS doesn’t progress to chronic state; atypical + TTP do.*
• cortex scars, GBM has tram tracking like MPGN, hypoperfusion leads to renal failure

Question 16

Atheroembolic Disease of Kidney:

• effects what arteries most?
• most common timing of emboli?
• appearance of the emboli?

Answer 16

• MC in arcuate/interlobulars
• usually follows interventional procedure
• the plaques will have cholesterol clefts if they are ATHEROemboli
• look for purple toes!

Question 17

Autosomal Recessive anemia that may lead to renal failure?

Answer 17

Sickle Cell

Question 18

Diffuse Cortical Necrosis:

• When does it happen?
• what does it look like?
• What is the outcome?

Answer 18

• follows really bad HEMORRHAGE (sepsis, DIC, placental abruption in pregnancy)
• ischemia and coagulative necrosis of renal cortex
• can be FATAL

Question 19

Common cause of a renal infarct?
Appearance of a renal infarct?
Symptoms?

Answer 19

Commonly from emboli– which often originate in left heart
Morphology is the same as all non-neuro infarcts.
Yellow wedge –> scar

Can cause hematuria but are often silent

Question 20

In general, what vascular changes are seen in small vessels during prolonged hypertension? Malignant hypertension?
Why is this relevant?

Answer 20

HTN: hyaline arteriolosclerosis
Malignant: proliferative arteriolosclerosis (onion skinning)
These same changes effect small vessels in the kidney!