Renal artery stenosis resident survival guide: Difference between revisions
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{{familytree | | | | | | | | | | A01 | | | A01= ❑ '''Determine if one or more of the following is present:'''}} | {{familytree | | | | | | | | | | A01 | | | A01= ❑ '''Determine if one or more of the following is present:'''}} | ||
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<tr><td>'''1.'''Onset of hypertension before the age of 30 years or severe hypertension after the age of 55</td></tr> | <tr><td>'''1.'''Onset of hypertension before the age of 30 years or severe hypertension after the age of 55</td></tr> | ||
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{{familytree | | | H01 | | |!| | | | | | | |!| H01= <div style="height: 2em; width: 10em; padding:1em;">Go to invasive imaging</div>}} | {{familytree | | | H01 | | |!| | | | | | | |!| H01= <div style="height: 2em; width: 10em; padding:1em;">Go to invasive imaging</div>}} | ||
{{familytree | | | | | | | I01 | I01= <div style="height: 2em; width: 10em; padding:1em;">Evidence of RAS</div>}} | {{familytree | | | | | | | I01 | | I01= <div style="height: 2em; width: 10em; padding:1em;">Evidence of RAS</div>}} | ||
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{{familytree | | | | | | | |`|-|-| J01 |-|-|'| J01= <div style="height: 7.5em; width: 10em; padding:1em;">'''Confirmed RAS: | {{familytree | | | | | | | |`|-|-| J01 |-|-|'| J01= <div style="height: 7.5em; width: 10em; padding:1em;">'''Confirmed RAS: |
Revision as of 17:27, 8 January 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]
Definition
Renal artery stenosis is defined as a dimished diameter of the lumen of the renal artery. Renal artery stenosis can also be classified by hemodynamic function. Shown below there is a table rewarding hemodynamic function.[1]
Hemodynamically significant RAS |
≥70% by visual estimation |
≥70% by intravascular ultrasound measurement |
50-70% RAS with a systolic gradient of ≥20 mm Hg or a mean gradient of ≥10 mm Hg. |
Causes
Life Threatening Causes
Renal artery stenosis is caused by a heterogenous group of entities, that if left unattended may lead to ischemic nephropathy and consecuently death due to end stage renal disease.
- Atherosclerosis
- Fibromuscular dysplasia
- Neurofibromatosis
- Vasculitis
- Congenital bands
- Radiation
Common Causes
- Atherosclerosis
- Fibromuscular dysplasia
Managment of RAS
Clinical Clues to the Diagnosis of RAS
❑ Determine if one or more of the following is present: | |||||||||||||||||||||||||||||||||||||||||||||
| |||||||||||||||||||||||||||||||||||||||||||||
❑If one of the above are present, proceed with Non- invasive imaging
| ❑If there are no clinical clues, proceed with invasive renal arteriography
| ||||||||||||||||||||||||||||||||||||||||||||
Is patient allergic to contrast
| {{{ }}} | ||||||||||||||||||||||||||||||||||||||||||||
If yes proceed with US | If no check for:
❑ Implanted devices:
| ❑ Abdominal aortography to assess the renal arteries during coronary and peripheralangiography | |||||||||||||||||||||||||||||||||||||||||||
If none of the above proceed with MRA
| If yes to any of the above, proceed with CT | ||||||||||||||||||||||||||||||||||||||||||||
Negative noninvasive test but with high clinical suspicion | Evidence of RAS | Evidence of RAS | |||||||||||||||||||||||||||||||||||||||||||
Go to invasive imaging | |||||||||||||||||||||||||||||||||||||||||||||
Evidence of RAS | |||||||||||||||||||||||||||||||||||||||||||||
Confirmed RAS:
❑Proceed to medical therapy ❑Consider revascularization | |||||||||||||||||||||||||||||||||||||||||||||
Algorithm based on the 2013 AHA Guidelines Recommendations for Management of Patients with PAD.[1]
Treatment
Medical/Pharmacological Therapy
The 4 main components of the BMT (best medical therapy) are:
Also, statins, optimal glycemic control, and smoking cessation are of supreme importance.
Indications for Renal Revascularization
Indication | Level of Evidence |
1.Hemodynamically significant RAS (see table above) with recurrent, unexplained CHF or sudden, unexplained pulmonary edema | Class I; LOE B |
2. RAS with:
|
Class IIa; LOE B |
3.RAS and CRI with bilateral RAS or RAS to solitary functioning kidney | Class IIa; LOE B |
4. RAS and unstable angina | Class IIa; LOE B |
5. Asymptomatic bilateral or solitary viableʰ kidney with a hemodynamically significant RAS | Class IIb; LOE C |
6. Asymptomatic unilateral hemodynamically significant RAS in a viable kidney (>7cm) | Class IIb; LOE C |
7. RAS and CRI with unilateral RAS (2 kidneys present) | Class IIb; LOE C |
Shown below there is an algorithm of therapeutic options to consider after any of the indications for revascularization are met.
❑ Presence of one or more indications for revascularization: | |||||||||||||||||||||||||||||||||
❑Renal Angioplasty/Stent | ❑ Renal artery surgery | ||||||||||||||||||||||||||||||||
Atherosclerotic RAS
| Fibromuscular dysplasia RAS
| ||||||||||||||||||||||||||||||||
Renal stent placement is indicated for ostial atherosclerotic RAS lesions that meet the clinical criteria for intervention | Balloon angioplasty with bailout stent placement if necessary is recommended for fibromuscular dysplasia lesions | ||||||||||||||||||||||||||||||||
Algorithm based on the 2013 AHA Guidelines Recommendations for Management of Patients with PAD.[1]
References
- ↑ 1.0 1.1 1.2 Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH; et al. (2013). "Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. 127 (13): 1425–43. doi:10.1161/CIR.0b013e31828b82aa. PMID 23457117.