Renal Artery Stenosis and Cardiorenal syndrome (CRS) Flashcards

1
Q

Primary vs. secondary disease of renal artery

A
  • Primary = disease of large renal arteries. Includes atherosclerotic renal artery stenosis
  • Secondary = disease of small vessles and intrarenal vascular disease
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2
Q

Renal artery stenosis

A
  • Renal artery stenosis is the narrowing of one of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia.
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3
Q

Fibromuscular dysplasia

A
  • Noninflammatory nonatherosclerotic disorder that leads to arterial stenosis, occlusion, aneurysm, dissection, and arterial tortuosity. (Abnormal develop of collagen and smooth muscle of artery leading to bulges and narrowing throughout the artery).
  • Can be found in any aterial bed, but renal and internal carotid are most common.
  • Makes up <10% of renal artery stenosis
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4
Q

Classification of fibromuscular dysplasia

A
  • Medial fibroplasia (pathology)/multifocal fibroplasia (angiography)
    • “String of beads” apparence
    • Most common type of fibromuscular dysplasia
    • Tends to be located in middle-to-distal part of renal artery
  • Intimal fibroplasia (pathology)/ focal fibroplasia (angiography)
    • Appears as focal, concentric, stenosis
    • <10% of fibromuscular dysplasia
  • Adventital/periarterial hyperplasia
    • Appears like sharpely localized, tubular areas of stenosis
    • Very rare
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5
Q

Epidemiology of Fibromuscular Dysplasia

A
  • <10% of cases of renal artery stenosis
  • 90% of cases involve the media
  • Tends to affect girls and women between 15-50
  • Tends to involve distal 2/3rds of renal artery its branches
  • Rarely leads to renal-artery occulsion
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6
Q

Pathogensis of Fibromuscular Dysplasia

A
  • Likely a combination of genetic, mechanical, and hormonal factors
  • Ehlers-Danlors syndrome (group of disorders that affect connective tissue supporting skin, bones, blood vessles, and other tissues - suspect if patient has multiple aneurysms) has been associated with medical fibroplasia
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7
Q

Renal atherosclerosis

A
  • Accounts for 90% of renal artery stenosis and usually involves the ostium and proximal thrid of main renal artery and perirneal aorta.
  • Prevalence increases with age - especially in patients with DM, coronary artery disease, or hypertension
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8
Q

How does renal artery stenosis lead to hypertension?

A
  • Decrease in renal perfusion pressure due to narrowing of renal artery activates RAAS → renin release → angiotensin II production
    • This results in an increase in pressure throughtout the body before the renal artery stenosis, but the area after the stenosis does not see an increase in pressure. Thus, the juxtaglomerular cells keep releasing renin. The overall result is hypertension
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9
Q

Renal artery stenosis and renal failure

A
  • Affected kidney receives low blood flow - this results in that kidneys atrophying as the renal cells die and are replaced by fibrotic tissue
  • If only one kidney is effect the other can contrinue to work, but if both are effected it can lead to acute renal failure.
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10
Q

Imaging renal artery stenosis

A
  • Duplex imaging of renal arteries can detect elevated blood flow velocities.
    • Atherosclerosis tends to occur in proximal portion of renal artery, so elevations in velocity in middle-to-distal segments are usually due to fibromuscular dysplasia
    • Important to scan both anteriorly and posteriorly to visualize all parts of the renal artery
  • Catheter-based angioography is most accurate method for diagnosis (but invasive)
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11
Q

Therapy of renal artery stenosis

A
  • Standard hypertension medications
  • Revascularization can be considered in certain patients
    • Fibromuscular dysplasia: Ballon angioplasty (percutaneous transluminal angioplasty without placement of a stent) tends to be most effective procedure. Aortorenal bypass can be done if PTA fails
    • Atherosclerotic: Use to do percutaneous transluminal angioplasty with placement of a stent, however, this is no longer done because it is assocaited with worse outcomes.
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12
Q

When do you consider revascularization in renal artery stenosis?

A
  • Hypertensive children with fibromuscular dysplasia
  • Bilateral renal fibromuscular dysplasia or unilateral fibromuscular dysplasia to single functioning kidney
  • Recent onset hypertension where goal is cure of hypertension
  • Blood pressure control is difficult despite use of multiple medications
  • Patient has intolerance to antihypertensive medications
  • Patient where blood pressure control is difficult due to non-compliance
  • Patient has lost renal volume due to ischemic nephropathy
  • Recurrent flash pulmonary edema or refractory heart failure
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13
Q

Clinical clues indicating presence of renovascular disease

A
  • Recent or rapid development of severe hypertension
  • Rapid rise in aterial pressure associated with sudden development of LV failure (flash pulmonary edema; more common in bilateral renal artery stenosis).
  • Rapidly chaning serum creatinine levels, particularly following administration of ACE inhibitors or ARBs. (More common in bilateral renal artery stneosis due to hemodynamic compromise to entire renal functional mass.
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14
Q

Common signs and symptoms of renal artery stenosis

A
  • Symptoms - headache, pulsatile tinnitus, neck pain, flank or abdominal pain
  • Signs - hypertension, cervivcal bruit, abdominal bruit, transient ischemic attack, stroke
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15
Q

Cardiorenal Syndrome

A
  • There are many important interactions between heart disease and kindey disease.
    • Bidirectional interaction - acute or chronic heart dysfunction can cause acute or chronic kidney dysfunction and vice versa
  • Hear failure is commonly associated by a reduction in glomerular filtration rate (estimated by an increase in serum creatinine)
    • Important to distinguish between underlying kidney disease and reduced kidney function due to cardiorenal syndrome
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16
Q

How do you distinguish between underlying kidney disease and reduced kidney function due to cardiorenal syndrome?

A
  • Underlying kidney disease - proteinuria, active urine sediment with hematuria with or without pyuria or cellular casts, and/or small kidneys on imaging
  • CRS without underlying kidney disease - normal urinalysis
17
Q

Pathophysiology of CRS

A
  • Various factors contribute to reduced GFR in patients with heart failure
  1. Neurohumoral adaptations - imparied LV function leads to reduced SV and CO, arterial underfilling, elevated arterial pressures, and venous congestion → these trigger compensatory neurohormonal adaptations such as activation of sympathetic nervous systemm & RAAS system, release of ADH, release of endothelin-1 (increase Na+ and water rentention + systemic vasoconstriction)
    • These adapations start out being helpful by maintaining perfusion to vital organs by perserving systemic pressure via aterial vasoconstriction and increased heart contractility and rate. But, systemic vasoconstriction increases afterload, which reduces CO leading to reduced renal perfusion.
  2. Reduced renal perfusion - (due to reduced CO) leads to reduced GFR. (Activates RAAS which leads to afferent arteriol constriction decreasing glomerular perfusion)
  3. Increased renal venous pressure - leads to reduction in GFR
  4. Right ventricular dilatation and dysfunction - may adversely affect the kidney by 2 mechanisms
    • Elevation in central venous pressure (leads to increase in renal venous pressure)
    • RV dilatation impairs LV filling, reducing CO and eventally renal perfusion pressure
  5. Decrease in erythropoietin leading to anemia
18
Q

Renal dysfunction in HF with preserved ejection fraction

A
  • Renal dysfuntion is commonly seen in patients with HFpEF
    • Endothelial dysfunction and proinflammation state seem to be important mediators of this interaction
19
Q

What are the compensatory mechanisms in heart failure

A