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October 17, 2008
Ross P. Davis, Jeffrey D. Pearce, Timothy E. Craven*, Matthew S. Edwards, Christopher J. Godshall*, Randolph L. Geary, Kimberley J. Hansen
Wake Forest University School of Medicine, Winston-Salem, NC
Atherosclerotic Renovascular Disease Among Hypertensive Adults
Purpose: This report describes the change in atherosclerotic renovascular disease (ASO-RVD) among hypertensive adults referred for renal duplex sonography (RDS).
Methods: From 10/1993 through 7/2008, 20,994 patients had RDS at our center. 437 hypertensive patients with two or more RDS exams without intervention for ASO-RVD comprised the study cohort. Patient demographics (blood pressures, medications, serum creatinine levels, and data from RDS) were collected. Analyses of longitudinal changes in Doppler parameters, blood pressures, and renal function were performed by fitting linear growth-curve models. After confirming the linearity of change in Doppler parameters among patients with variable number of studies, estimates of mean slopes were calculated using maximum-likelihood techniques. For changes in renal function, quadratic growth curves were required to describe longitudinal change.
Results: 434 subjects (212 men; [49%] and 222 women; [51%]; mean age: 64.6 ± 12.3 years) provided 1351 RDS studies (mean: 3.2 ± 2.4; range 2 to 18) for 863 kidneys over a mean follow-up of 34.4 ± 25.1 months. At baseline, 20.6% of kidneys demonstrated hemodynamically significant stenosis, while the remainder did not. On follow-up, 72 kidneys (9.1%) demonstrated anatomic progression of renovascular disease. 54 kidneys (6.9%) progressed to significant stenosis and 18 (2.3%) progressed to renal artery occlusion. Controlling for progression of disease, baseline renal artery status demonstrated a strong association with baseline kidney length (P=0.0006). Significant annualized change in renal length was observed (cm change/year ± SEM: 0.042 ± 0.011; P=0.0002) among both kidneys with and without critical renovascular disease at baseline, however, decline in length was significantly greater among kidneys exhibiting progression of renovascular disease (-0.152 ± 0.028 cm/yr; comparison of slopes between groups P=0.0005). In the absence of progression, the presence or absence of critical renal artery stenosis at baseline did not affect the rate of decline in renal length. Fitted models for the natural log transform of serum creatinine demonstrated a significant increase during follow-up (P<.0001). No association was observed between change in serum creatinine and the presence or absence of baseline renovascular disease or its progression.
Conclusions: 20.6% of hypertensive adults referred for RDS demonstrated hemodynamically significant renal artery stenosis. Regardless of the presence or absence of baseline disease, a small percentage of patients demonstrated anatomic progression of ASO-RVD. 9.1% demonstrated anatomic progression and 2.3% progressed to occlusion. Although anatomic progression of ASO-RVD was associated with an increased rate of decline in renal length, progression did not predict a decline in excretory renal function. These data are consistent with a hypothesis that primary renal parenchymal disease is the most important determinant of decline in renal function in the majority of hypertensive adults. Intervention for ASO-RVD should be selective and reserved for strict indications.
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Atherosclerotic Renovascular Disease Among Hypertensive Adults
Back to Annual Meeting
Back to Program
Ross P. Davis, Jeffrey D. Pearce, Timothy E. Craven*, Matthew S. Edwards, Christopher J. Godshall*, Randolph L. Geary, Kimberley J. Hansen
Wake Forest University School of Medicine, Winston-Salem, NC
Atherosclerotic Renovascular Disease Among Hypertensive Adults
Purpose: This report describes the change in atherosclerotic renovascular disease (ASO-RVD) among hypertensive adults referred for renal duplex sonography (RDS).
Methods: From 10/1993 through 7/2008, 20,994 patients had RDS at our center. 437 hypertensive patients with two or more RDS exams without intervention for ASO-RVD comprised the study cohort. Patient demographics (blood pressures, medications, serum creatinine levels, and data from RDS) were collected. Analyses of longitudinal changes in Doppler parameters, blood pressures, and renal function were performed by fitting linear growth-curve models. After confirming the linearity of change in Doppler parameters among patients with variable number of studies, estimates of mean slopes were calculated using maximum-likelihood techniques. For changes in renal function, quadratic growth curves were required to describe longitudinal change.
Results: 434 subjects (212 men; [49%] and 222 women; [51%]; mean age: 64.6 ± 12.3 years) provided 1351 RDS studies (mean: 3.2 ± 2.4; range 2 to 18) for 863 kidneys over a mean follow-up of 34.4 ± 25.1 months. At baseline, 20.6% of kidneys demonstrated hemodynamically significant stenosis, while the remainder did not. On follow-up, 72 kidneys (9.1%) demonstrated anatomic progression of renovascular disease. 54 kidneys (6.9%) progressed to significant stenosis and 18 (2.3%) progressed to renal artery occlusion. Controlling for progression of disease, baseline renal artery status demonstrated a strong association with baseline kidney length (P=0.0006). Significant annualized change in renal length was observed (cm change/year ± SEM: 0.042 ± 0.011; P=0.0002) among both kidneys with and without critical renovascular disease at baseline, however, decline in length was significantly greater among kidneys exhibiting progression of renovascular disease (-0.152 ± 0.028 cm/yr; comparison of slopes between groups P=0.0005). In the absence of progression, the presence or absence of critical renal artery stenosis at baseline did not affect the rate of decline in renal length. Fitted models for the natural log transform of serum creatinine demonstrated a significant increase during follow-up (P<.0001). No association was observed between change in serum creatinine and the presence or absence of baseline renovascular disease or its progression.
Conclusions: 20.6% of hypertensive adults referred for RDS demonstrated hemodynamically significant renal artery stenosis. Regardless of the presence or absence of baseline disease, a small percentage of patients demonstrated anatomic progression of ASO-RVD. 9.1% demonstrated anatomic progression and 2.3% progressed to occlusion. Although anatomic progression of ASO-RVD was associated with an increased rate of decline in renal length, progression did not predict a decline in excretory renal function. These data are consistent with a hypothesis that primary renal parenchymal disease is the most important determinant of decline in renal function in the majority of hypertensive adults. Intervention for ASO-RVD should be selective and reserved for strict indications.
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