Management of Heart Failure with Renal Artery Ischemia Madhav V. Rao, MD, Patrick Murray, MD, Clyde W. Yancy, MD  Heart Failure Clinics  Volume 4, Issue 4, Pages 465-478 (October 2008) DOI: 10.1016/j.hfc.2008.03.010 Copyright © 2008 Elsevier Inc. Terms and Conditions

Fig. 1 Interrelation among RAS, hypertension, and chronic renal failure. RAS may occur alone (isolated anatomic RAS) or in combination with hypertension (renovascular or essential hypertension), renal insufficiency (ischemic nephropathy), or both. Patients who have RAS alone may benefit from revascularization to prevent loss of renal mass. In patients who have RAS and hypertension, hypertension seldom is cured by revascularization, except in those who have FMD. In patients who have RAS and chronic renal failure, renal revascularization may improve or stabilize renal function. (From Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med 2001;344[6]:431–42; with permission. Copyright © 2001, Massachusetts Medical Society.) Heart Failure Clinics 2008 4, 465-478DOI: (10.1016/j.hfc.2008.03.010) Copyright © 2008 Elsevier Inc. Terms and Conditions

Fig. 2 Progressive atherosclerosis, RAS, and ischemic nephropathy. In the early phase (A), there is mild atherosclerosis of the perirenal abdominal aorta and normal renal function. Renal blood flow, renal mass, and the serum creatinine concentration are normal. The dimensions of the kidneys are normal, and there is no cortical atrophy. The total GFR (100 mL per minute) and the GFR in each kidney (50 mL per minute) are normal. As the disease progresses (B), there is progressive aortic atherosclerosis and severe unilateral RAS. The left kidney is smaller than the right kidney, and there may be cortical thinning and asymmetry in renal blood flow. The serum creatinine concentration remains normal as long as the right kidney is normal, despite the loss of renal mass. The total GFR may be normal (100 mL per minute) or only slightly depressed owing to compensatory changes in the right kidney, but renal blood flow is decreased in the left kidney (35 mL per minute). In advanced disease (C), there is bulky atherosclerotic plaque in the perirenal aorta and severe bilateral RAS. Both kidneys are small, and there is marked cortical thinning and irregularity. Loss of more than 50% of renal mass usually is associated with an elevation in the serum creatinine concentration (ischemic nephropathy), which may not be reversible. The total GFR (30 mL per minute) and the GFR in each kidney (15 mL per minute) are depressed. (From Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med 2001;344[6]:431–42; with permission. Copyright © 2001, Massachusetts Medical Society.) Heart Failure Clinics 2008 4, 465-478DOI: (10.1016/j.hfc.2008.03.010) Copyright © 2008 Elsevier Inc. Terms and Conditions

Fig. 3 Renal angiogram showing the typical string-of-beads appearance of FMD. (From Cheung CM, Hegarty J, Kalra PA. Dilemmas in the management of renal artery stenosis. Br Med Bull 2005;73–4:35–55; with permission.) Heart Failure Clinics 2008 4, 465-478DOI: (10.1016/j.hfc.2008.03.010) Copyright © 2008 Elsevier Inc. Terms and Conditions

Fig. 4 Two-kidney, one-clip model of renovascular hypertension. ATI, angiotensin I; AT1I, angiotensin II; JGA, juxtaglomerular apparatus. (From Rundback JH, Murphy TP, Cooper C, et al. Chronic renal ischemia: pathophysiologic mechanisms of cardiovascular and renal disease. J Vasc Interv Radiol 2002;13[11]:1085–92; with permission.) Heart Failure Clinics 2008 4, 465-478DOI: (10.1016/j.hfc.2008.03.010) Copyright © 2008 Elsevier Inc. Terms and Conditions

Fig. 5 Two-kidney, two-clip model of renovascular hypertension. AT, angiotensin; JGA, juxtaglomerular apparatus. (From Rundback JH, Murphy TP, Cooper C, et al. Chronic renal ischemia: pathophysiologic mechanisms of cardiovascular and renal disease. J Vasc Interv Radiol 2002;13(11):1085–92; with permission.) Heart Failure Clinics 2008 4, 465-478DOI: (10.1016/j.hfc.2008.03.010) Copyright © 2008 Elsevier Inc. Terms and Conditions