Ch299: Renovascular Disease Flashcards
What region of the kidney has less blood supply and hence less oxygen: cortical or medullary?
Medullary region are at the margin of hypoxemia
Predictive of systemic atherosclerotic disease events
urinary albumin excretion (UAE)
Increased UAE increases risk of atherosclerotic events
Pharmacologic therapy to reduce UAE and risk of CV events
Statins
Causes of large-vessel renal artery occlusive disease
- Extrinsic compression of vessel
- Fibromuscular dysplasia
- Atherosclerotic disease
The systemic effect produced by the kidneys, trying to restore the renal pressure secondary to disorders that reduced it
Systemic hypertension
May present as hypertension in younger individuals (age 15-50) most often women
Fibromuscular dysplasia
Prevalence of this condition increases with age and history of CAD and/or peripheral aortic or lower ext disease
Atherosclerotic renal artery stenosis (ARAS)
Slows the rate of ARAS and improve clinical outcome
- Intensive treatment of arterial BP
2. Statin therapy
Treatment for renovascular hypertension
- Agents that block renin-angiotensin system
2. Endovascular or surgical revascularization to restore renal blood flow
T or F: Patients who underwent revascularization often don’t need to continue their antihypertensive drugs
False
Revascularization rarely lowers BP to normal
Strong predictor of morbidity and mortality related CV events, independent of whether renal revascularization is undertaken
ARAS
Vascular studies to evaluate renal arteries
- Duplex ultrasonography
- Magnetic resonance angiography (w/ gadolinium)
- Computed tomographic angiography
- Intraarterial angiography - considered “GOLD STANDARD” for diagnosis of large-vessel disease
Treatment for FMD
Percutaneous renal artery angiography
T or F: Renal revascularization is now often reserved for patients failing medical therapy or developing additional complications
True
Factors favoring revascularization for renal artery stenosis
- Progressive decline in GFR during treatment of systemic hpn
- Medical failure
- Rapid or recurrent decline in GFR in assoc with reduction in systemic pressure
- Decline in GFR dueing therapy with ACE inhibitors or ARBs
- Recurrent CHF in patient whom adequacy of LV function does not explain a cause
Table 299-2, p.1629
T or F: Atheroembolic renal disease are often caused by angiographic procedures (coronary vessels)
True
Definitive diagnosis for atheroembolic renal disease
Kidney biopsy
Most common emboli to kidneys causing atheroembolic renal disease
Cholesterol crystals
T or F: Once atheroembolic disease developed, anticoagulation should be continued.
False
Withdrawal of anticoagulation is recommended
Role of statin therapy in atheroembolic dse in kidneys
MAY improve outcome
Role of embolic protection devices in renal circulation
Unclear. Few trials failed to show major benefits
Causes of thrombotic occlusion of renal vessels or branch arteries
- Local vessel abnormalities (local dissection, trauma, vasculitis)
- Hypercoagulability conditions (rare)
- Distant embolic events (left atrium in AF, fat emboli fr large bone fractures)
- Cardiac source (vegetations fr subacute bacterial endocarditis)
- Systemic emboli (venous circulation in right-to-left shunt in patent foramen ovale)
T or F: Acute arterial thrombosis do not produce flank pain and fever.
False
It produces flank pain, fever, leukocytosis, nausea, vomiting
Diagnosis of renal infarction
MRI
CT angiography
CT arteriography
Management of arterial thrombosis of kidney
- Surgical reconstruction
- Anticoagulation
- Thrombolytic therapy
- Endovascular procedures
- Supportive care (including antihypertensive drug therapy)
Postmortem findings in kidneys of pt with “malignant” hypertension
- “Fibrinoid necrosis” - vascular lesions with breakdown of vessel wall, deposition of eosinophilic materials (fibrin), perivascular infiltrate
- “Onionskin” lesions - larger interlobular arteries with hyperplastic proliferation of vascular wall cellular elements, deposition of collagen, separation of layers
Mainstay of therapy for malignant hypertension
Antihypertensive therapy
Renal abnormalities in malignant hypertension
- Rising serum crea
2. Occasionally hematuria & proteinuria
Gene responsible for predisposition of African-American population to subtle focal sclerosing glomerular disease
APOL1 previously identified as MYH9
Afferent arteriolar thickening with deposition of homogenous eosinophilic material (hyaline arteriosclerosis) associated with narrowing of vascular lumina
Hypertensive nephrosclerosis
