When is Renovascular Hypertension Amenable to Revascularization

Last Updated: June 16, 2022


Disclosure: none
Pub Date: Thursday, Jun 16, 2022
Author: George Bakris, MD
Affiliation: University of Chicago Medicine; American Heart Association Comprehensive Hypertension Center

Dr. Bhalla and colleagues' updated scientific statement on renovascular disease is comprehensive, thorough, and practical, providing an excellent summary of diagnostic tips in the document1. Renal artery stenosis is an important and sometimes overlooked cause of secondary hypertension that, in many cases, can be treated, and hypertension management is made much easier for both the physician and the patient.

Renovascular hypertension results primarily from fibromuscular dysplasia in young people and atherosclerotic disease in older individuals. Renovascular hypertension is a well-known cause of secondary hypertension, and etiologies related to the atherosclerotic process are a more common cause of secondary hypertension. Historically, this was especially true among those between 45-60 years of age in the decades up until 2010. The slow reduction in smoking over the past three decades and the advent of statin therapy for hypercholesterolemia are attributed, in part, to the reduced incidence of clinically significant renal artery stenosis. However, atherosclerotic renovascular hypertension, while accounting for a much smaller fraction of secondary hypertension than 30 years ago in this age group, is rivaled by the higher incidence shifted to those between the ages of 65-80 years2.

It is essential to note that occult renal arterial disease is likely also present if peripheral artery disease or multivessel coronary artery disease are present3. A renal Doppler ultrasound can frequently reveal significant flow abnormalities in the renal arteries as a screening test. However, a difference in size between the two kidneys of one centimeter or more suggests long-standing reduced flow and pressure in that kidney4. A greater than a one-centimeter difference in kidney size should prompt an investigation for renal arterial stenosis5.

Anyone who has a substantial drop in blood pressure with blockers of the renin-angiotensin system (RAS) and/or a significant >30% rise in serum creatinine within a week of drug initiation should be evaluated for renal artery stenosis. A greater than 30% rise in serum creatinine with RAS blockade is more likely if significant bilateral renal artery stenosis is present.

Another indication for renal artery stenosis screening is unexplained flash pulmonary edema or recurrent heart failure6. This diagnosis should be considered, especially among those who smoke and/or have poorly treated cholesterol values over a long period. Suppose the clinical picture fits, and 70% or greater stenosis is present with a post stenotic gradient on an angiogram. In that case, an interventional procedure is strongly indicated to preserve the kidney and reduce blood pressure. The previous statement may be at odds with the current evidence-based guidelines; however, my experience is consistent with the current guidance.

While prior randomized trials did not show incremental benefit of performing percutaneous renal artery revascularization among those with optimal medical therapy, the results of those trials could not be extrapolated to all patients with high-grade stenosis who were excluded from the trials7, 8. These trials did not assess the excellent utility of percutaneous revascularization in certain high-risk groups with progressively worsening renal function, resistant hypertension, or flash pulmonary edema compared to real-world clinical practice.

In a referral practice of resistant hypertension patients, we found renal artery stenting very effective in a subgroup of patients who failed adequate blood pressure control or had significant >50% increases in serum creatinine following treatment with RAS blockers. Additionally, those with hypertension and a greater than 1 cm difference in kidney size benefit from preserving the smaller kidney and controlling blood pressure.

Singular tight, i.e., >70% stenotic lesions due to medical therapy, but as any nephrologist or renal physiologist knows, it will dramatically reduce kidney function in the affected kidney. The reduced blood flow and pressure are not restored, the affected kidney function will slowly be lost. Hence, reductions in glomerular filtration rates well above 60-70% are seen when blockers of the RAS are applied since the RAS system’s activation is driving the blood pressure. Blood pressure is also significantly reduced with these agents, an event not commonly seen in the absence of significant stenosis in a euvolemic patient. These reductions in kidney function are reversed within a few weeks of stopping the RAS blockers. Using other agents to control BP will work. Still, on average, three to four drugs will be needed, and, unappreciated by many physicians, there will be a breakthrough of blood pressure to previous levels within three to four months of treatment. If this is seen and renovascular disease has not been ruled out, it must be investigated. Hence, while blood pressure can reduce with non-RAS agents, the effects are short-lived, and kidney function will continue to decline unless blood supply and, importantly, higher pressure to that kidney is not restored.

About a half-century ago, renal vein renin was used to define whether the stenosis was significant enough to warrant intervention. However, this was not always reliable, and it was expensive; thus, not routinely done today. Renal vein renin is still being explored to aid in a more precise diagnosis in the pediatric population. Saida and colleagues performed a retrospective study of plasma renin activity [PRA], aldosterone, and renal vein renin [RVR] coupled with imaging studies (computed tomography angiography [CTA], kidney ultrasonography [US]) and compared them with catheter angiography in ten pediatric patients with RVH. They noted a high sensitivity for diagnosing RVH via kidney US (89%) and PRA (80%). RVR, however, did not aid in the diagnosis of RVH.9

In short, stenting of a narrowed renal artery (>70 % with a 20 mmHg post stenotic gradient should be strongly considered, especially if associated with resistant hypertension. Medical management is effective over the short term if needed, but if hypertension breaks through to prior levels or can’t be controlled, stenting is necessary.

Citation


Bhalla V, Textor SC, Beckman JA, Casanegra AI, Cooper CJ, Kim ESH, Luther JM, Misra S, Oderich GS; on behalf of the American Heart Association Council on the Kidney in Cardiovascular Disease; Council on Hypertension; Council on Peripheral Vascular Disease; and Council on Cardiovascular Radiology and Intervention. Revascularization for renovascular disease: a scientific statement from the American Heart Association [published online ahead of print June 16, 2022]. Hypertension. doi: 10.1161/HYP.0000000000000217

References


  1. Bhalla V TS, Beckman JA, Casanegra AI, Cooper CJ, Kim ESH, Luther JM, Misra S, Oderich GS, on behalf of the American Heart Association Council on the Kidney in Cardiovascular Disease, Council on Hypertension, Council on Peripheral Vascular Disease, and Council on Cardiovascular Radiology and Intervention. Revascularization for Renovascular Disease. Hypertension. 2022;In Press.
  2. Plouin PF and Bax L. Diagnosis and treatment of renal artery stenosis. Nat Rev Nephrol. 2010;6:151-9.
  3. Aboyans V, Desormais I, Magne J, Morange G, Mohty D and Lacroix P. Renal Artery Stenosis in Patients with Peripheral Artery Disease: Prevalence, Risk Factors, and Long-term Prognosis. Eur J Vasc Endovasc Surg. 2017;53:380-385.
  4. Guzman RP, Zierler RE, Isaacson JA, Bergelin RO and Strandness DE, Jr. Renal atrophy and arterial stenosis. A prospective study with duplex ultrasound. Hypertension. 1994;23:346-50.
  5. Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, Hiratzka LF, Murphy WR, Olin JW, Puschett JB, Rosenfield KA, Sacks D, Stanley JC, Taylor LM, Jr., White CJ, White J, White RA, Antman EM, Smith SC, Jr., Adams CD, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B, American Association for Vascular S, Society for Vascular S, Society for Cardiovascular A, Interventions, Society for Vascular M, Biology, Society of Interventional R, Guidelines AATFoP, American Association of C, Pulmonary R, National Heart L, Blood I, Society for Vascular N, TransAtlantic Inter-Society C and Vascular Disease F. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. J Am Coll Cardiol. 2006;47:1239-312.
  6. Messerli FH, Bangalore S, Makani H, Rimoldi SF, Allemann Y, White CJ, Textor S and Sleight P. Flash pulmonary oedema and bilateral renal artery stenosis: the Pickering syndrome. Eur Heart J. 2011;32:2231-5.

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