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Hey @cardionerds! Have you ever been in this situation?
A 60 yo man w/ HTN is incidentally found to have renal artery stenosis (RAS) on imaging. Do we need to call the cath lab? Or is medication the answer?
Check out this #tweetorial on Renal Artery Stenosis to learn more!
A 60 yo man w/ HTN is incidentally found to have renal artery stenosis (RAS) on imaging. Do we need to call the cath lab? Or is medication the answer?
Check out this #tweetorial on Renal Artery Stenosis to learn more!
In this 
, we'll cover:
1) A primer on RAS pathophysiology
2) The data surrounding revascularization of RAS
3) Current society guidelines on Renal Artery Stenting
, we'll cover: 1) A primer on RAS pathophysiology
2) The data surrounding revascularization of RAS
3) Current society guidelines on Renal Artery Stenting
Poll time!
I feel comfortable with determining which patients may be a candidate for Renal Artery Stenting:
I feel comfortable with determining which patients may be a candidate for Renal Artery Stenting:
Let's start w/ a brief pathophys review!
Atherosclerotic RAS causes renal hypoperfusion. This activates the RAAS system, leading to:
Renin
Angiotensin II (AII)
SVR
Remember, RAS is a common cause of secondary HTN!
Atherosclerotic RAS causes renal hypoperfusion. This activates the RAAS system, leading to:
Renin Angiotensin II (AII) SVRRemember, RAS is a common cause of secondary HTN!
Unilateral RAS leads to HTN via AII, though increased perfusion of the opposite kidney preserves natriuresis and euvolemia.
In bilateral RAS, you get volume overload (via
natriuresis) and HTN (independent of AII due to relative RAAS inhibition from volume)!
AII, though increased perfusion of the opposite kidney preserves natriuresis and euvolemia. In bilateral RAS, you get volume overload (via
natriuresis) and HTN (independent of AII due to relative RAAS inhibition from volume)!
PEARL: in b/l RAS, there is decreased flow through the afferent arteriole, & glomerular pressures depend on efferent arteriole constriction via AII. If AII is reduced by an ACEi, GFR drops and Crt will
!
Volume overload and HTN lead to several cardiac destabilizing syndromes, including:
ACS
Decompensated Heart Failure
Flash Pulmonary Edema/Pickering Syndrome
ACS Decompensated Heart Failure Flash Pulmonary Edema/Pickering Syndrome
1st line management in these settings are anti-hypertensives;
However, since the pathology is 2/2 decreased renal perfusion, does improving perfusion via stenting make a difference?
However, since the pathology is 2/2 decreased renal perfusion, does improving perfusion via stenting make a difference?
3 Trials of RA stenting v. 
: all negative!
STAR: 140 pts w/CrCl ≤80, RAS ≥ 50%, but controlled BP
ASTRAL: 806 pts w/RAS+clinical dz (HTN, Kidney Dz) where potential clinical benefit of stenting was unclear
CORAL: 948 pts with RAS 60-100%, HTN on ≥ 2 drugs or GFR<60
: all negative!STAR: 140 pts w/CrCl ≤80, RAS ≥ 50%, but controlled BPASTRAL: 806 pts w/RAS+clinical dz (HTN, Kidney Dz) where potential clinical benefit of stenting was unclearCORAL: 948 pts with RAS 60-100%, HTN on ≥ 2 drugs or GFR<60
However! These trials may have under-represented pts with very severe, hemodynamically significant stenoses. How do we identify these pts?
This review by @MPrinceMD suggests trans-lesional pressure gradients can confirm hemodynamic significance, and aid in patient selection.
This review by @MPrinceMD suggests trans-lesional pressure gradients can confirm hemodynamic significance, and aid in patient selection.
Given the controversy, what are the current guidelines on RAS revascularization?
Current AHA/ACC appropriate use criteria (AUC) list the following indications for revascularization of hemodynamically significant RAS:
Current AHA/ACC appropriate use criteria (AUC) list the following indications for revascularization of hemodynamically significant RAS:
Accelerating in renal function in b/l RAS (or RAS of solitary kidney)Failure to control BP despite max doses of 3 agents (including a diuretic)Recurrent heart failure despite max medical therapy Sudden pulmonary edemaUncontrolled UA despite max medical therapy
Lets summarize!
RAS 
destabilization syndromes via BP ± volume
Current data shows 
benefit for RAS stenting, though lacks physiologic assessment
AUC support stenting in settings of hemodynamically significant RAS, including destabilization, resistant HTN, CKD
RAS destabilization syndromes via BP ± volumeCurrent data shows benefit for RAS stenting, though lacks physiologic assessmentAUC support stenting in settings of hemodynamically significant RAS, including destabilization, resistant HTN, CKD
Poll Time, part 2!
I feel comfortable with determining which patients may be a candidate for Renal Artery Stenting:
I feel comfortable with determining which patients may be a candidate for Renal Artery Stenting:
I learned something in this Tweetorial that may change my clinical practice.
This is the tip of the iceberg of renovascular hypertension! Much more could be said about RAS due to fibromuscular dysplasia (which typically DOES respond to revascularization), methods of determining RAS physiologic significance, and renal denervation!
As always, big thanks to the @cardionerds team (especially @AmitGoyalMD and @karanpdesai) for their assistance in this #tweetorial; any and all feedback or thoughts are appreciated!
