Renal Insufficiency and Renal Artery Occlusive Disease Kimberley J. Hansen Until the early 1960s, the pathophysiology and management of atherosclerotic renovascular disease focused solely on hypertension. However, current management of renal artery atherosclerosis considers the relationship between renal artery occlusive disease and renal insufficiency, a relationship recognized by the term ischemic nephropathy. In 1962, Morris and associates reported on eight azotemic patients with global renal ischemia who had improved blood pressure and kidney function after renal revascularization. Subsequently, Dean, Libertino, and Novick and their groups demonstrated beneficial function response after surgical correction of bilateral renal artery lesions. Despite a growing enthusiasm for correction of atherosclerotic renovascular disease to improve excretory kidney function, critical questions of patient selection and best management remain unanswered. Pathophysiology The pathophysiology of ischemic nephropathy remains incompletely understood. The earliest clinical reports suggested a glomerular filtration failure based on decreased perfusion pressure within the kidney; however, the cellular and subcellular basis for ischemic nephropathy is poorly defined. Like renovascular hypertension, the renin–angiotensin system likely contributes to ischemic nephropathy through its paracrine effects, with intrarenal angiotensin peptides affecting arteriolar tone. Angiotensin peptides have also been shown to promote tubular injury and interstitial fibrosis in the presence of atherosclerotic renal artery stenosis. This observation is supported by an increase in interstitial platelet-derived growth factor β, which is associated with increased extracellular matrix and interstitial fibrosis. In addition to these possible contributors to excretory renal insufficiency, an atherosclerotic lesion may also contribute to an irreversible loss of kidney function as a source of atheroemboli. Unfortunately, studies that distinguish potentially reversible ischemic nephropathy from irreversible renal parenchymal disease are lacking. This distinction is of significant clinical importance because recovery of kidney function after correction of atherosclerotic kidney lesions associated with ischemic nephropathy has proved to be the single strongest predictor of dialysis-free survival on follow-up. Prevalence The actual contribution of atherosclerotic renovascular disease to renal insufficiency is uncertain because the prevalence of renovascular disease in this subpopulation is unknown. Past prevalence estimates of renovascular disease were drawn from case series autopsy examinations or angiography obtained to evaluate diseases of the aorta or peripheral circulation. The prevalence of renovascular disease has been estimated in participants of the Cardiovascular Health Study (CHS), which was sponsored by the National Heart, Lung, and Blood Institute. The CHS is a longitudinal, prospective, population-based study of coronary heart disease and stroke in free living men and women older than 65 years. This population-based study demonstrated that hemodynamically significant renovascular disease was present in 6.8% of this elderly cohort. In this group, renal insufficiency was associated with significant renovascular disease but only when renal artery disease coexisted with significant hypertension. When considering ischemic nephropathy, the presence of severe hypertension is the single strongest predictor for the presence of significant atherosclerotic renovascular disease. In evaluation of 629 consecutive newly defined hypertensive adults, the author’s center defined significant renovascular disease in 25% of all subjects. In subjects older than 60 years with diastolic pressure greater than 110 mm Hg, 52% of subjects screened had significant renal artery stenosis or occlusion. When serum creatinine of 1.8 mg/dL or greater was present in conjunction with advanced age and severe hypertension, 71% of subjects demonstrated hemodynamically significant renovascular disease. In one half of this latter subgroup, renovascular disease was present to both kidneys, suggesting potentially reversible renal insufficiency. Among hypertensive patients with excretory renal insufficiency, the prevalence of renovascular disease (i.e., ischemic nephropathy) varies. In a series of randomly selected patients 45 to 75 years of age with serum creatinine greater than 2.0 mg/dL, the author’s center found a 14% prevalence of unsuspected renovascular disease. In a prospective study of 90 consecutive patients older than 50 years with new-onset end-stage kidney disease, 22% demonstrated renal artery stenosis or occlusion. In this group, dialysis-dependent ischemic nephropathy demonstrated significant ethnic differences. Forty percent of patients of European ancestry who were in the atherosclerotic age range and had end-stage kidney failure had unsuspected renovascular disease, and 20% percent had global renal ischemia consistent with potentially reversible dialysis-dependent kidney failure. Collectively, these data suggest that persons with renal insufficiency do not demonstrate equal risk for the presence of renovascular disease or ischemic nephropathy. Rather, the probability of finding clinically significant renal artery disease correlates with age, severity of hypertension, and the presence and severity of renal insufficiency. This is especially true when the progression of renal insufficiency and decline in glomerular filtration rate is rapid. Natural History Available information regarding the natural history of renal artery atherosclerosis has been extrapolated from angiographic case series and ultrasound examinations from retrospective reviews or from prospective studies from selected hypertensive patients. The quality of these studies and their interpretation has varied widely. In the past, many have considered anatomic progression of atherosclerotic renovascular disease a certainty, one associated with an inevitable decline in kidney size and function. This view has been used to support renal artery intervention whenever disease was discovered, even in the absence of hypertension or renal insufficiency. However, the author does not favor prophylactic intervention for asymptomatic renovascular disease. This view is supported by a recent longitudinal cohort study that included 110 CHS participants. These subjects had two renal duplex sonography examinations 8.5 years apart. With 235 kidneys for study, no kidney with significant disease at first duplex progressed to an occlusion, although incident disease was defined in 4% of subjects. In these CHS participants, progression to hemodynamically significant renal artery stenosis was observed at a rate of 0.5% per year. These data suggest that patients with mild to moderate hypertension demonstrate little anatomic progression of atherosclerotic renovascular disease and lend no support to “prophylactic” intervention by any method. Few data are available defining the mortality risk associated with untreated atherosclerotic renovascular disease associated with renal insufficiency. Conlon and colleagues reported on all-cause mortality among patients chosen for cardiac catheterization studied simultaneously with abdominal aortography. Among patients with renovascular disease, the 4-year estimated survival was 65%, which is significantly decreased in comparison with that for age- and sex-matched controls without renal artery stenosis. By multivariate analysis significant, and independent predictors of mortality include renal artery disease with an elevated serum creatinine and decreased left ventricular performance. In addition, an increased mortality for untreated ischemic nephropathy was suggested by Baboolal and coworkers. Over an 8-year period these authors identified 51 patients with angiographic evidence of bilateral renovascular disease consisting of more than 90% diameter reducing renal artery stenosis with at least 50% contralateral stenosis. Each of these patients had received medical treatment, but none had received renal artery repair or catheter-based intervention. By product-limit estimates, 40% of these patients died within 2 years of diagnosis and 35% progressed to dialysis dependence at 5 years. Despite the absence of prospective data, clinical experience suggests that ischemic nephropathy can mediate a rapid decline in kidney function. The rate of decline in function has been described for a patient subgroup characterized by a preoperative serum creatinine level of at least 1.8 mg/dL with at least three measures of kidney function before and after surgery. Among patients with ischemic nephropathy proved by increased kidney function measured 3 weeks after surgery, the preoperative decline in estimated glomerular filtration rate (GFR) exceeded 5% per week. Immediate improvement in kidney function was associated with a significant decrease in rate of decline in postoperative estimated GFR. Conversely, in patients with kidney function unimproved after operation, estimated GFR continued to decline at a rate that was unchanged. Only patients with an incremental increase in estimated GFR after operation have demonstrated decreased rate of decline in subsequent kidney function and improved dialysis-free survival on follow-up. The relationship between early kidney function response and dialysis-free survival has important implications. First, the method of intervention for ischemic nephropathy should be selected that provides maximum retrieval of kidney function. This selection should consider the pattern of atherosclerotic disease typically found in this patient population. Ostial atherosclerosis accounts for 98% of renal artery lesions, one third of renal artery disease is represented by complete renal artery occlusion, and two thirds of patients demonstrate bilateral renal artery stenosis or occlusion. Second, clinical benefit after renal artery intervention probably applies only to patients who demonstrate an incremental increase in excretory kidney function. The common practice of considering patients with unchanged kidney function after treatment to be “preserved” or “protected” should be abandoned. Patients with unimproved kidney function remain at high risk for both dialysis dependence and death. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Dyslipidemia and Hypertriglyceridemia Endovascular Renal Denervation Stay updated, free articles. Join our Telegram channel Join Tags: Current Therapy in Vascular and Endovascular Surgery Aug 25, 2016 | Posted by admin in CARDIOLOGY | Comments Off on Renal Insufficiency and Renal Artery Occlusive Disease Full access? Get Clinical Tree
Renal Insufficiency and Renal Artery Occlusive Disease Kimberley J. Hansen Until the early 1960s, the pathophysiology and management of atherosclerotic renovascular disease focused solely on hypertension. However, current management of renal artery atherosclerosis considers the relationship between renal artery occlusive disease and renal insufficiency, a relationship recognized by the term ischemic nephropathy. In 1962, Morris and associates reported on eight azotemic patients with global renal ischemia who had improved blood pressure and kidney function after renal revascularization. Subsequently, Dean, Libertino, and Novick and their groups demonstrated beneficial function response after surgical correction of bilateral renal artery lesions. Despite a growing enthusiasm for correction of atherosclerotic renovascular disease to improve excretory kidney function, critical questions of patient selection and best management remain unanswered. Pathophysiology The pathophysiology of ischemic nephropathy remains incompletely understood. The earliest clinical reports suggested a glomerular filtration failure based on decreased perfusion pressure within the kidney; however, the cellular and subcellular basis for ischemic nephropathy is poorly defined. Like renovascular hypertension, the renin–angiotensin system likely contributes to ischemic nephropathy through its paracrine effects, with intrarenal angiotensin peptides affecting arteriolar tone. Angiotensin peptides have also been shown to promote tubular injury and interstitial fibrosis in the presence of atherosclerotic renal artery stenosis. This observation is supported by an increase in interstitial platelet-derived growth factor β, which is associated with increased extracellular matrix and interstitial fibrosis. In addition to these possible contributors to excretory renal insufficiency, an atherosclerotic lesion may also contribute to an irreversible loss of kidney function as a source of atheroemboli. Unfortunately, studies that distinguish potentially reversible ischemic nephropathy from irreversible renal parenchymal disease are lacking. This distinction is of significant clinical importance because recovery of kidney function after correction of atherosclerotic kidney lesions associated with ischemic nephropathy has proved to be the single strongest predictor of dialysis-free survival on follow-up. Prevalence The actual contribution of atherosclerotic renovascular disease to renal insufficiency is uncertain because the prevalence of renovascular disease in this subpopulation is unknown. Past prevalence estimates of renovascular disease were drawn from case series autopsy examinations or angiography obtained to evaluate diseases of the aorta or peripheral circulation. The prevalence of renovascular disease has been estimated in participants of the Cardiovascular Health Study (CHS), which was sponsored by the National Heart, Lung, and Blood Institute. The CHS is a longitudinal, prospective, population-based study of coronary heart disease and stroke in free living men and women older than 65 years. This population-based study demonstrated that hemodynamically significant renovascular disease was present in 6.8% of this elderly cohort. In this group, renal insufficiency was associated with significant renovascular disease but only when renal artery disease coexisted with significant hypertension. When considering ischemic nephropathy, the presence of severe hypertension is the single strongest predictor for the presence of significant atherosclerotic renovascular disease. In evaluation of 629 consecutive newly defined hypertensive adults, the author’s center defined significant renovascular disease in 25% of all subjects. In subjects older than 60 years with diastolic pressure greater than 110 mm Hg, 52% of subjects screened had significant renal artery stenosis or occlusion. When serum creatinine of 1.8 mg/dL or greater was present in conjunction with advanced age and severe hypertension, 71% of subjects demonstrated hemodynamically significant renovascular disease. In one half of this latter subgroup, renovascular disease was present to both kidneys, suggesting potentially reversible renal insufficiency. Among hypertensive patients with excretory renal insufficiency, the prevalence of renovascular disease (i.e., ischemic nephropathy) varies. In a series of randomly selected patients 45 to 75 years of age with serum creatinine greater than 2.0 mg/dL, the author’s center found a 14% prevalence of unsuspected renovascular disease. In a prospective study of 90 consecutive patients older than 50 years with new-onset end-stage kidney disease, 22% demonstrated renal artery stenosis or occlusion. In this group, dialysis-dependent ischemic nephropathy demonstrated significant ethnic differences. Forty percent of patients of European ancestry who were in the atherosclerotic age range and had end-stage kidney failure had unsuspected renovascular disease, and 20% percent had global renal ischemia consistent with potentially reversible dialysis-dependent kidney failure. Collectively, these data suggest that persons with renal insufficiency do not demonstrate equal risk for the presence of renovascular disease or ischemic nephropathy. Rather, the probability of finding clinically significant renal artery disease correlates with age, severity of hypertension, and the presence and severity of renal insufficiency. This is especially true when the progression of renal insufficiency and decline in glomerular filtration rate is rapid. Natural History Available information regarding the natural history of renal artery atherosclerosis has been extrapolated from angiographic case series and ultrasound examinations from retrospective reviews or from prospective studies from selected hypertensive patients. The quality of these studies and their interpretation has varied widely. In the past, many have considered anatomic progression of atherosclerotic renovascular disease a certainty, one associated with an inevitable decline in kidney size and function. This view has been used to support renal artery intervention whenever disease was discovered, even in the absence of hypertension or renal insufficiency. However, the author does not favor prophylactic intervention for asymptomatic renovascular disease. This view is supported by a recent longitudinal cohort study that included 110 CHS participants. These subjects had two renal duplex sonography examinations 8.5 years apart. With 235 kidneys for study, no kidney with significant disease at first duplex progressed to an occlusion, although incident disease was defined in 4% of subjects. In these CHS participants, progression to hemodynamically significant renal artery stenosis was observed at a rate of 0.5% per year. These data suggest that patients with mild to moderate hypertension demonstrate little anatomic progression of atherosclerotic renovascular disease and lend no support to “prophylactic” intervention by any method. Few data are available defining the mortality risk associated with untreated atherosclerotic renovascular disease associated with renal insufficiency. Conlon and colleagues reported on all-cause mortality among patients chosen for cardiac catheterization studied simultaneously with abdominal aortography. Among patients with renovascular disease, the 4-year estimated survival was 65%, which is significantly decreased in comparison with that for age- and sex-matched controls without renal artery stenosis. By multivariate analysis significant, and independent predictors of mortality include renal artery disease with an elevated serum creatinine and decreased left ventricular performance. In addition, an increased mortality for untreated ischemic nephropathy was suggested by Baboolal and coworkers. Over an 8-year period these authors identified 51 patients with angiographic evidence of bilateral renovascular disease consisting of more than 90% diameter reducing renal artery stenosis with at least 50% contralateral stenosis. Each of these patients had received medical treatment, but none had received renal artery repair or catheter-based intervention. By product-limit estimates, 40% of these patients died within 2 years of diagnosis and 35% progressed to dialysis dependence at 5 years. Despite the absence of prospective data, clinical experience suggests that ischemic nephropathy can mediate a rapid decline in kidney function. The rate of decline in function has been described for a patient subgroup characterized by a preoperative serum creatinine level of at least 1.8 mg/dL with at least three measures of kidney function before and after surgery. Among patients with ischemic nephropathy proved by increased kidney function measured 3 weeks after surgery, the preoperative decline in estimated glomerular filtration rate (GFR) exceeded 5% per week. Immediate improvement in kidney function was associated with a significant decrease in rate of decline in postoperative estimated GFR. Conversely, in patients with kidney function unimproved after operation, estimated GFR continued to decline at a rate that was unchanged. Only patients with an incremental increase in estimated GFR after operation have demonstrated decreased rate of decline in subsequent kidney function and improved dialysis-free survival on follow-up. The relationship between early kidney function response and dialysis-free survival has important implications. First, the method of intervention for ischemic nephropathy should be selected that provides maximum retrieval of kidney function. This selection should consider the pattern of atherosclerotic disease typically found in this patient population. Ostial atherosclerosis accounts for 98% of renal artery lesions, one third of renal artery disease is represented by complete renal artery occlusion, and two thirds of patients demonstrate bilateral renal artery stenosis or occlusion. Second, clinical benefit after renal artery intervention probably applies only to patients who demonstrate an incremental increase in excretory kidney function. The common practice of considering patients with unchanged kidney function after treatment to be “preserved” or “protected” should be abandoned. Patients with unimproved kidney function remain at high risk for both dialysis dependence and death. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Dyslipidemia and Hypertriglyceridemia Endovascular Renal Denervation Stay updated, free articles. Join our Telegram channel Join
