Chapter 272 - Renovascular Disease Flashcards

(69 cards)

1
Q

Vascular disorders that commonly

threaten the blood supply of the kidney

A

large-vessel atherosclerosis,

fibromuscular diseases, and embolic disorders

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2
Q

predictive of

systemic atherosclerotic disease events.

A

Rates of urinary albumin excretion (UAE)

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3
Q

reduces UAE and risk of cardiovascular events

A

statins

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4
Q

causes of Large-vessel renal artery occlusive disease

A

extrinsic
compression of the vessel, intimal dissection, fibromuscular dysplasia
(FMD), atherosclerotic disease (most common)

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5
Q

considered a specifically treatable

“secondary” cause of hypertension.

A

renal artery stenosis

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6
Q

common and often has only minor hemodynamic

effects

A

Renal artery stenosis

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7
Q

reported in 3–5% of normal subjects presenting

as potential kidney donors without hypertension

A

FMD

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8
Q

It may present clinically
with hypertension in younger individuals (between age 15 and
50), most often women

A

FMD

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9
Q

does not often threaten kidney function,
but sometimes produces total occlusion and can be associated with
renal artery aneurysms

A

FMD

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10
Q

common in the general population (6.8% of a community-based
sample above age 65).

The prevalence increases with age and for
patients with other vascular conditions such as coronary artery disease
(18–23%) and/or peripheral aortic or lower extremity disease (>30%).

A

Atherosclerotic renal artery stenosis (ARAS)

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11
Q

It appears to slow these rates of total occlusion in ARAS and
improve clinical outcomes

A

Intensive treatment of arterial

blood pressure and statin therapy

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12
Q

results of Critical levels of stenosis

A

reduction in perfusion pressure
that activates the renin-angiotensin system, reduces sodium excretion,
and activates sympathetic adrenergic pathways

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13
Q

characterized by angiotensin dependence in the
early stages, widely varying pressures, loss of circadian blood pressure
(BP) rhythms, and accelerated target organ injury, including left
ventricular hypertrophy and renal fibrosis

A

systemic hypertension

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14
Q

treatment of renovascular HPN

A

agents that block the renin-angiotensin system and
other drugs that modify these pressor pathways

restoration of renal blood flow by either endovascular or surgical
revascularization

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15
Q

tend to affect both the post-stenotic
and contralateral kidneys, reducing overall glomerular filtration rate
(GFR) in ARAS.

A

ARAS and systemic hypertension

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16
Q

When kidney function is threatened by large-vessel

disease primarily

A

ischemic nephropathy

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17
Q

Moderately

reduced blood flow that develops gradually

A

reduced GFR and limited oxygen consumption with preserved tissue
oxygenation

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18
Q

what happens with more advanced disease in ARAS and systemic HPN

A

reductions

in cortical perfusion and frank tissue hypoxia develop

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19
Q

It develops in patients with other risk factors for atherosclerosis
and is commonly superimposed upon preexisting small-vessel
disease in the kidney resulting from hypertension, aging, and diabetes.

A

ARAS

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20
Q

Nearly 85% of patients considered for renal revascularization have
what stage and what rate of GFR

A

stage 3–5 chronic kidney disease (CKD) with GFR <60 mL/min per
1.73 m2

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21
Q

strong predictor of morbidity- and
mortality-related cardiovascular events, independent of whether renal
revascularization is undertaken.
Diagnostic approaches to renal

A

presence of ARAS

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22
Q

Levels of renin activity are therefore subjected to what?

A

timing,

the effects of drugs, and sodium intake

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23
Q

Renal artery velocities by Doppler
ultrasound _____ generally predict hemodynamically important
lesions (>60% vessel lumen occlusion)

A

> 200 cm/s

although some treatment trials
require velocity >300 cm/s to avoid false positives

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24
Q

has predictive value regarding the viability of the kidney

It remains operator- and institution-dependent

A

renal resistive

index

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25
has a strong negative predictive value when | entirely normal.
Captopril-enhanced | renography
26
less often used, as gadolinium contrast has been associated with nephrogenic systemic fibrosis
Magnetic resonance angiography (MRA)
27
provides excellent vascular images | and functional assessment, but carries a small risk of contrast toxicity.
Contrast-enhanced computed tomography | (CT) with vascular reconstruction
28
treatment for patients with FMD that are commonly younger females with otherwise normal vessels and a long life expectancy
percutaneous renal | artery angioplasty
29
Medical therapy for Renal Artery Stenosis
blockade of the renin-angiotensin system, attainment of goal BPs, cessation of tobacco, statins, and aspirin
30
Follow-up requires surveillance for progressive occlusion criteria??
worsening renal function and/or loss of BP control
31
often reserved for patients failing | medical therapy or developing additional complications
Renal revascularization
32
major complications in renal revascularization
renal artery dissection, capsular perforation, hemorrhage, | and occasional atheroembolic disease
33
can be catastrophic and accelerate both hypertension | and kidney failure, precisely the events that revascularization is intended to prevent
atheroembolic | disease
34
they are more likely to recover function after restoring blood flow
Patients with rapid loss of kidney function, sometimes associated with antihypertensive drug therapy, or with vascular disease affecting the entire functioning kidney mass
35
treatment for hypertension is refractory to effective therapy
revascularization
36
arise most frequently as a result of cholesterol crystals breaking free of atherosclerotic vascular plaque and lodging in downstream microvessels.
Emboli to the kidneys
37
suspected in >3% of elderly subjects | with end-stage renal disease (ESRD) and is likely underdiagnosed
Atheroembolic renal disease
38
risk factors for atheroembolic renal disease
males with a history of diabetes, hypertension, | and ischemic cardiac disease
39
precipitating events in atheroembolic renal disease
angiography, vascular surgery, anticoagulation with heparin, thrombolytic therapy, or trauma
40
days where clinical manifestations of this syndrome (atheroembolic disease) commonly develop
between 1 and 14 days
41
Systemic embolic disease manifestations
fever, abdominal pain, and weight loss
42
cutaneous manifestations of systemic embolic disease
livedo reticularis and localized toe gangrene
43
require dialytic support
Progressive renal failure
44
laboratory findings of systemic embolic disease
rising creatinine, transient eosinophilia (60–80%), elevated sedimentation rate, and hypocomplementemia
45
Definitive diagnosis for systemic embolic disease
kidney biopsy demonstrating microvessel occlusion with | cholesterol crystals that leave a “cleft” in the vessel
46
can lead to | declining renal function and hypertension
Thrombotic occlusion of renal vessels or branch arteries
47
causes of thrombosis
local vessel abnormalities, such as local | dissection, trauma, or inflammatory vasculitis
48
patchy, transient areas of infarctions
segmental | arteriolar mediolysis
49
distant embolic events that causes thromboembolic renal disease
left atrium in patients with atrial fibrillation fat emboli originating from traumatized tissue, most commonly large bone fractures
50
Cardiac sources that causes thromboembolic renal disease
vegetations from subacute bacterial endocarditis venous circulation if right-to-left shunting - patent foramen ovale
51
Clinical manifestations of acute arterial thrombosis
flank pain, | fever, leukocytosis, nausea, and vomiting
52
sign of kidney infarction
lactate dehydrogenase (LDH) rise to extreme levels
53
sign of kidney infarction, both kidneys affected
renal function will decline precipitously with | a drop in urine output
54
Diagnosis of | renal infarction
vascular imaging with MRI, CT | angiography, or arteriography
55
Options for interventions of newly detected arterial occlusion
surgical reconstruction, anticoagulation, thrombolytic therapy, endovascular procedures, antihypertensive drug therapy
56
treatment for unilateral disease - arterial dissection with thrombosis
supportive care | with anticoagulation
57
It is potentially | catastrophic, producing anuric renal failure
Acute, bilateral occlusion of kidney
58
rapidly progressive BP elevations with target organ injury including retinal hemorrhages, encephalopathy, and declining kidney function.
“Malignant” Hypertension note: mortality rates in excess of 50% over 6–12 months
59
Postmortem studies of such patients identified vascular lesions, with breakdown of the vessel wall, deposition of eosinophilic material including fibrin, and a perivascular cellular infiltrate.
fibrinoid necrosis
60
separate lesion was identified in the larger interlobular arteries in many patients with hyperplastic proliferation of the vascular wall cellular elements, deposition of collagen, and separation of layers
“onionskin” lesion.
61
It can led | to obliteration of glomeruli and loss of tubular structures.
fibrinoid necrosis
62
mainstay of therapy for malignant | hypertension
Antihypertensive therapy
63
It most commonly develops in patients with treated hypertension who neglect to take medications or who may use vasospastic drugs, such as cocaine
Malignant hypertension
64
findings in renal abnormalities
rising serum creatinine hematuria and proteinuria biochemical findings: evidence of hemolysis (anemia, schistocytes, and reticulocytosis) and changes associated with kidney failure.
65
African-American males
more likely to develop rapidly progressive hypertension and kidney failure than are whites in the United States
66
type of Genetic polymorphisms common in the African-American population predispose to subtle focal sclerosing glomerular disease, with severe hypertension developing at younger ages secondary to renal disease in this instance
APOL1
67
lesser degrees of hypertension induce less severe, but prevalent, changes in kidney vessels and loss of kidney function large portion of patients reaching ESRD without a specific etiologic diagnosis are assigned the designation
hypertensive nephrosclerosis
68
Pathologic examination for hypertensive nephrosclerosis
afferent arteriolar thickening with deposition of homogeneous eosinophilic material (hyaline arteriolosclerosis) associated with narrowing of vascular lumina
69
Clinical manifestations of hypertensive nephrosclerosis
``` retinal vessel changes associated with hypertension (arteriolar narrowing, arteriovenous crossing changes), left ventricular hypertrophy, and elevated BP ```