Renal artery stenosis resident survival guide: Difference between revisions
Line 57: | Line 57: | ||
{{familytree | | | | | | | | A01 | |A01='''Initiate a regimen that combines:'''}} | {{familytree | | | | | | | | A01 | |A01='''Initiate a regimen that combines:'''}} | ||
{{familytree | | | | | | | | |!| | | | | | | | }} | {{familytree | | | | | | | | |!| | | | | | | | }} | ||
{{familytree | | |,|-|-|-| | {{familytree | | |,|-|-|-|^|-|^|-|^|-|-|-|.| }} | ||
{{familytree | | B01 | | B02 | | B03 | | B04 | | | B01= '''Antihypertensives''' | B02='''Statins''' | B03='''Optimal glycemic control''' | B04='''Smoking cessation counseling'''}} | {{familytree | | B01 | | B02 | | B03 | | B04 | | | B01= '''Antihypertensives''' | B02='''Statins''' | B03='''Optimal glycemic control''' | B04='''Smoking cessation counseling'''}} | ||
{{familytree | | |!| | | | | | | | | | | | | | | }} | {{familytree | | |!| | | | | | | | | | | | | | | }} | ||
{{familytree | | C01 | | | | | | | | | C01=❑ [[ARB]] <br> ❑ [[ACEI]] <br> ❑ [[CCB]] <br> ❑ [[Beta blockers]]}} | {{familytree | | C01 | | | | | | | | | C01= <div style="float: left; text-align: left"> ❑ [[ARB]] <br> ❑ [[ACEI]] <br> ❑ [[CCB]] <br> ❑ [[Beta blockers]]}} | ||
{{familytree | | |!| | | | | | | | | | | | | | }} | {{familytree | | |!| | | | | | | | | | | | | | }} | ||
{{familytree | | D01 | | | | | | | | | D01= ❑ Measure creatinine:}} | {{familytree | | D01 | | | | | | | | | D01= ❑ Measure creatinine:}} |
Revision as of 19:50, 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 of >70% is considered hemodynamically significant.[1]
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: ❑ Onset of hypertension before the age of 30 years or severe hypertension after the age of 55 ❑ Accelerated, resistant, or malignant hypertension ❑ Development of new azotemia or worsening renal function after administration of an ACE inhibitor or ARB agent ❑ Unexplained atrophic kidney or size discrepancy between kidneys >1.5 cm ❑ Sudden, unexplained pulmonary edema ❑ Unexplained renal dysfunction, including individuals starting renal replacement therapy ❑ Multi-vessel CAD ❑ Unexplained CHF ❑ Refractory angina | |||||||||||||||||||||||||||||||||||||||||||
If yes: ❑ Proceed with non-invasive imaging | If no, but multiple vessel CAD: ❑ Proceed with invasive renal arteriography | ||||||||||||||||||||||||||||||||||||||||||
Is patient allergic to contrast | |||||||||||||||||||||||||||||||||||||||||||
If yes: ❑ Proceed with US | If no check for: ❑ Implanted devices: - Pacemakers | ❑ 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 | |||||||||||||||||||||||||||||||||||||||||||
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 Therapy
Initiate a regimen that combines: | |||||||||||||||||||||||||||||||||||
Antihypertensives | Statins | Optimal glycemic control | Smoking cessation counseling | ||||||||||||||||||||||||||||||||
❑ Measure creatinine: | |||||||||||||||||||||||||||||||||||
{{{ EO1 }}} | |||||||||||||||||||||||||||||||||||
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.