Chapter 272 - Renovascular Disease Flashcards
Vascular disorders that commonly
threaten the blood supply of the kidney
large-vessel atherosclerosis,
fibromuscular diseases, and embolic disorders
predictive of
systemic atherosclerotic disease events.
Rates of urinary albumin excretion (UAE)
reduces UAE and risk of cardiovascular events
statins
causes of Large-vessel renal artery occlusive disease
extrinsic
compression of the vessel, intimal dissection, fibromuscular dysplasia
(FMD), atherosclerotic disease (most common)
considered a specifically treatable
“secondary” cause of hypertension.
renal artery stenosis
common and often has only minor hemodynamic
effects
Renal artery stenosis
reported in 3–5% of normal subjects presenting
as potential kidney donors without hypertension
FMD
It may present clinically
with hypertension in younger individuals (between age 15 and
50), most often women
FMD
does not often threaten kidney function,
but sometimes produces total occlusion and can be associated with
renal artery aneurysms
FMD
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%).
Atherosclerotic renal artery stenosis (ARAS)
It appears to slow these rates of total occlusion in ARAS and
improve clinical outcomes
Intensive treatment of arterial
blood pressure and statin therapy
results of Critical levels of stenosis
reduction in perfusion pressure
that activates the renin-angiotensin system, reduces sodium excretion,
and activates sympathetic adrenergic pathways
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
systemic hypertension
treatment of renovascular HPN
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
tend to affect both the post-stenotic
and contralateral kidneys, reducing overall glomerular filtration rate
(GFR) in ARAS.
ARAS and systemic hypertension
When kidney function is threatened by large-vessel
disease primarily
ischemic nephropathy
Moderately
reduced blood flow that develops gradually
reduced GFR and limited oxygen consumption with preserved tissue
oxygenation
what happens with more advanced disease in ARAS and systemic HPN
reductions
in cortical perfusion and frank tissue hypoxia develop
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.
ARAS
Nearly 85% of patients considered for renal revascularization have
what stage and what rate of GFR
stage 3–5 chronic kidney disease (CKD) with GFR <60 mL/min per
1.73 m2
strong predictor of morbidity- and
mortality-related cardiovascular events, independent of whether renal
revascularization is undertaken.
Diagnostic approaches to renal
presence of ARAS
Levels of renin activity are therefore subjected to what?
timing,
the effects of drugs, and sodium intake
Renal artery velocities by Doppler
ultrasound _____ generally predict hemodynamically important
lesions (>60% vessel lumen occlusion)
> 200 cm/s
although some treatment trials
require velocity >300 cm/s to avoid false positives
has predictive value regarding the viability of the kidney
It remains operator- and institution-dependent
renal resistive
index
has a strong negative predictive value when
entirely normal.
Captopril-enhanced
renography
less
often used, as gadolinium contrast has been associated with nephrogenic
systemic fibrosis
Magnetic resonance angiography (MRA)
provides excellent vascular images
and functional assessment, but carries a small risk of contrast toxicity.
Contrast-enhanced computed tomography
(CT) with vascular reconstruction
treatment for patients with FMD that are commonly
younger females with otherwise normal vessels and a long life
expectancy
percutaneous renal
artery angioplasty
Medical therapy for Renal Artery Stenosis
blockade of the renin-angiotensin
system, attainment of goal BPs, cessation of tobacco, statins, and
aspirin
Follow-up requires surveillance for progressive occlusion criteria??
worsening renal function and/or loss of BP control
often reserved for patients failing
medical therapy or developing additional complications
Renal revascularization
major complications in renal revascularization
renal artery dissection, capsular perforation, hemorrhage,
and occasional atheroembolic disease
can be catastrophic and accelerate both hypertension
and kidney failure, precisely the events that revascularization is intended to prevent
atheroembolic
disease
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
treatment for hypertension is refractory to effective therapy
revascularization
arise most frequently as a result of cholesterol
crystals breaking free of atherosclerotic vascular plaque and lodging
in downstream microvessels.
Emboli to the kidneys
suspected in >3% of elderly subjects
with end-stage renal disease (ESRD) and is likely underdiagnosed
Atheroembolic renal disease
risk factors for atheroembolic renal disease
males with a history of diabetes, hypertension,
and ischemic cardiac disease
precipitating events in atheroembolic renal disease
angiography,
vascular surgery, anticoagulation with heparin, thrombolytic
therapy, or trauma
days where clinical manifestations of this syndrome (atheroembolic disease) commonly
develop
between 1 and 14 days
Systemic embolic disease manifestations
fever, abdominal pain, and weight loss
cutaneous manifestations of systemic embolic disease
livedo reticularis and localized toe gangrene
require dialytic support
Progressive renal failure
laboratory findings of systemic embolic disease
rising creatinine, transient eosinophilia (60–80%), elevated sedimentation rate, and hypocomplementemia
Definitive diagnosis for systemic embolic disease
kidney biopsy demonstrating microvessel occlusion with
cholesterol crystals that leave a “cleft” in the vessel
can lead to
declining renal function and hypertension
Thrombotic occlusion of renal vessels or branch arteries
causes of thrombosis
local vessel abnormalities, such as local
dissection, trauma, or inflammatory vasculitis
patchy, transient areas of infarctions
segmental
arteriolar mediolysis
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
Cardiac sources that causes thromboembolic renal disease
vegetations from subacute bacterial endocarditis
venous circulation if right-to-left
shunting - patent foramen ovale
Clinical manifestations of acute arterial thrombosis
flank pain,
fever, leukocytosis, nausea, and vomiting
sign of kidney infarction
lactate dehydrogenase (LDH) rise to extreme levels
sign of kidney infarction, both kidneys affected
renal function will decline precipitously with
a drop in urine output
Diagnosis of
renal infarction
vascular imaging with MRI, CT
angiography, or arteriography
Options for interventions of newly detected arterial occlusion
surgical reconstruction, anticoagulation, thrombolytic therapy,
endovascular procedures, antihypertensive
drug therapy
treatment for unilateral disease - arterial dissection with thrombosis
supportive care
with anticoagulation
It is potentially
catastrophic, producing anuric renal failure
Acute, bilateral occlusion of kidney
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
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
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.
It can led
to obliteration of glomeruli and loss of tubular structures.
fibrinoid necrosis
mainstay of therapy for malignant
hypertension
Antihypertensive therapy
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
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.
African-American males
more likely to develop rapidly progressive hypertension and kidney
failure than are whites in the United States
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
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
Pathologic examination for hypertensive nephrosclerosis
afferent arteriolar
thickening with deposition of homogeneous eosinophilic material
(hyaline arteriolosclerosis) associated with narrowing of vascular
lumina
Clinical manifestations of hypertensive nephrosclerosis
retinal vessel changes associated with hypertension (arteriolar narrowing, arteriovenous crossing changes), left ventricular hypertrophy, and elevated BP
