Chapter 125 - Renovascular disease introduction Flashcards

1
Q

Rate of atherosclerotic renal artery stenosis in elderly

A

7%

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2
Q

Etiology of renal artery stenosis

A

1) atherosclerosis
2) FMD
3) dissection
4) aneurysm
5) trauma
6) arteritis
7) developmental abnormalities

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3
Q

Primary importance of renal vascular disease

A

1) hypertension

2) loss of renal function

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4
Q

Discovery of Renin

A

19th century

Tigerstedt, Bergman isolated from rabbit kidney

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5
Q

Goldblatt 1930 landmark experiment

A

HTN from RAS can be reversed by removing ipsilateral kidney

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6
Q

Leadbetter 1938 on renal artery stenosis

A

normalized BP after removing ectopic kidney in child with severe HTN

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7
Q

Freeman 1954 on renal artery stenosis

A

Successful renal artery reconstruction in someone with bilateral ostial stenosis

HTN normalized

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8
Q

Ischemic nephropathy definition

A

Renal insufficiency from RAS or occlusion

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9
Q

Wake Forest study on RAS reconstruction mortality

A

30 day mortality 4.6%

7% in ones with ischemic nephropathy

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10
Q

NIS data on renal bypass mortality

A

10%

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11
Q

Improvements in BP following renal bypass

A

85% improved

15% no better or worse

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12
Q

Post-op marker for improved dialysis free survival

A

eGFR stability or improvement

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13
Q

RCT on renal artery stenting

A

1) ASTRAL

2) CORAL

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14
Q

Characteristic of atherosclerotic RVD

A

1) most severe at renal ostia

2) contiguous with sheet of aortic plaque

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15
Q

Characteristic of FMD PVD

A

1) main artery and branches away from ostia
2) web-like stenosis (string of beads)
3) in children it’s mostly intimal fibroplasia subtype (no string of beads)

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16
Q

Pathophysiology of renovascular HTN

A

1) flow limiting RAS –> pressure drop
2) juxtaglomerular cells release renin
3) Angiotensinogen converted to angiotensin I
4) angiotensin I converted to Angiotensin II by ACE in pulmonary circulation
5) Ang II = peripheral vasoconstruction and blood volume expansion

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17
Q

Effects of angiotensin II

A

1) activates vasoconstriction and mitogenic response
2) forms reactive oxygen species that inactivate NO
cross talk with GF to amplify smooth muscle cell vasoconstrictor and proliferative signaling pathways
3) Upregulate NE and endothelin 1
4) renal tubules for Na and H2O reabsorption
5) adrenal release of aldosterone –> Na reabsorption
6) vasopressin release of pituitary

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18
Q

Non-RAAS mediated renovascular HTN

A

Chronic structural changes with hypertrophic remodelling

19
Q

Goldblatt volume-dependent renovascular HTN

A

Patients with bilateral RAS or RAS in solitary kidney that cannot compensate to volume expansion

20
Q

Risk factors for ischemic nephropathy

A

1) HTN
2) diabetes
3) atherosclerosis
4) dyslipidemia
5) smoking

21
Q

Prevalence of RAS in at risk individual

A

7%

1/8 has bilateral disease

6% < 55 years old
40% > 75 years old

22
Q

Association with RVD in presence of other stenotic arterial beds

A

CAD - 22%
Carotid - 27%
PAD - 40%

23
Q

Anatomic progression of RAS in 3 years

A

43% progression, 7% occlude

24
Q

How much renal function loss before creatinine rise

A

50%

25
Q

Other measures of renal function

A

kidney length

26
Q

Rate of progression to dialysis in RAS in 3-4 years

A

7-12%

27
Q

Differential diagnosis in patients with renovascular HTN

A

1) essential HTN
2) glomerulonephritis
3) nephrotic syndrome
4) primary aldosteronism
5) cushing
6) pheochromocytoma
7) carcinoid
8) hyperthyroidism
9) coarctation of the aorta
10) sleep apnea
11) increased intracranial pressure
12) volume overload

28
Q

Spontaneous hypokalemia or severe hypokalemia after diuretics suggests this disease

A

Conn syndrome

hyperaldosteronism

29
Q

Diseases that may be associated with pheochromocytoma

A

1) MEN2
2) neurofibromatosis type 1
3) von Hippel-Lindau

30
Q

Accuracy of US to detect RAS

A

> 90%

31
Q

Critical stenosis of RAS defined as

A

PSV > 200 cm/s in main renal artery
equals > 60% stenosis

RAR = renal artery PSV / aortic PSV
significant if > 3.5

32
Q

Blunted waveform with delayed systolic upstroke in RAS US

A

> 100 ms suggest RAS

PPV 97%; low sensitivity

33
Q

Resistive index in RAS US

A

normal < 0.7

>0.8 critical RAS

34
Q

How much more radiation does a CTA do compared to CXR

A

87-260 times more

35
Q

How much contrast used in CTA of renal

A

120-140 ml

36
Q

FDA black box warning on gadolinium

A

Not use in eGFR < 30 unless absolutely necessary

37
Q

Access site bleeding for DSA for renal artery based on CORAL study

A

13%

38
Q

Radionuclide renography key points

A

1) quantify uptake and excretion of radiolabeled molecules (Tc 99m-mercaptoacetyltriglycine)
2) ACEi renography (captopril renography) to unmask intrinsic renal compensation to RAS
3) diseased kidney will show decline in excretion of radiolabel; normal kidney will show increase GFR and more excertion
4) less accurate in patients with azotemia or small kidneys

39
Q

Renal vein renin assay key points

A

1) start with low-sodium diet and stop antiHTN meds except diuretic and CCB 5 days before
2) furosemid given evening prior 40 mg
3) bedrest 4 hours prior to study
4) sample from renal veins and IVC as control

1.5 times higher renin considered positive

40
Q

Medical management of RAS

A

1) statins
2) improve cardiovascular risks
3) ACEi and ARBs
4) diuretics
5) CCB
6) beta blockers

41
Q

Patency of open repair in RAS

A

better than endo

> 90%

42
Q

Restenosis of RAS after stenting

A

> 10%

43
Q

Factors to lower threshold for RAS revascularization

A

1) children with severe RVD
2) FMD complicated by HTN
3) failure of conservative mgnt with ongoing eGFR reduction and HTN problem
4) hypertensive crisis