High blood pressure is a widespread health problem in the United States, affecting approximately 75 million adults. It is a significant concern in primary care, accounting for 8.6% of all visits. Renovascular hypertension is a common cause of secondary hypertension, which refers to high blood pressure that is caused by an underlying medical condition.
Renovascular hypertension occurs when the blood supply to the kidneys is compromised due to occlusion or blockage in the main renal artery, resulting in decreased blood flow. This condition can lead to resistant hypertension, a type of high blood pressure that is difficult to control with medication alone.
Epidemiology
Renovascular hypertension affects individuals of all ages. The most common cause of renal artery stenosis is atherosclerosis and it is more commonly observed in older adults aged over 65 years. This condition is more prevalent in individuals with atherosclerotic diseases, such as coronary artery disease, peripheral artery disease, or carotid artery stenosis.
Autopsy studies have indicated that more than 25% of patients who die of cardiovascular diseases have some degree of renal artery stenosis. Another cause of renovascular hypertension is fibromuscular dysplasia (FMD), a rare condition that affects the arteries and causes abnormal growth within the arterial walls.
FMD is typically observed in young women and accounts for around 10% of renovascular hypertension cases and 5.8% of secondary hypertension cases. This condition can affect any arterial bed, but it commonly affects the distal two-thirds of the renal artery.
Anatomy
Pathophysiology
Renovascular hypertension is characterized by decreased blood flow to the kidneys, which triggers the activation of the renin-angiotensin-aldosterone (RAAS) pathway. This process was first described by Goldblatt et al. in the 1930s, when they conducted experiments on dogs and observed that reduced blood supply to the kidneys led to persistent hypertension.
Goldblatt also proposed the existence of a substance that could act like a hormone, causing a pressor effect. This substance was later identified as renin, secreted by specialized juxtaglomerular cells in the kidneys. Renin secretion is stimulated by three main pathways: renal baroreceptors that sense reduced kidney perfusion, the macula densa that detects low sodium chloride levels, and beta-adrenergic stimulation.
Prolonged ischemia can also increase the number of renin-expressing cells in the kidney, known as JG recruitment. When renin is secreted into the bloodstream, it acts on angiotensinogen, a protein produced by the liver. Renin cleaves angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) primarily found in the vascular endothelium of the lungs and kidneys. Angiotensin II has multiple effects on the body, contributing to increased blood pressure.
It stimulates the sympathetic nervous system, releasing norepinephrine, which causes vasoconstriction and an increase in heart rate. It also causes collagen type I and III synthesis in fibroblasts, leading to the vascular wall, myocardium, and fibrosis thickening. These changes in the structure of blood vessels and heart muscles can further exacerbate hypertension and increase the risk of cardiovascular complications.
Etiology
Renovascular hypertension often occurs due to various factors such as extrinsic compression of a renal artery, radiation fibrosis, obstruction caused by aortic endovascular grafts, and fibromuscular dysplasia.
Genetics
Prognostic Factors
Atherosclerotic renal artery stenosis is a progressive condition that can lead to renal failure due to worsening stenosis. Untreated renovascular hypertension resulting from atherosclerotic renal artery stenosis can lead to end-stage renal failure. The median survival time for patients with renovascular hypertension is only 25 months, and the 4-year mortality rate is as high as 35%.
The primary management for renovascular hypertension should aim to correct the underlying cause. In the case of renovascular hypertension caused by atherosclerotic renal artery stenosis, medical management should be prioritized over invasive management. Multiple studies have failed to demonstrate renal or cardiovascular benefits with invasive management.
Clinical History
Clinical History
Patients with Renal Vascular Hypertension (RVHT) may not experience any symptoms, and their hypertension may be detected incidentally during routine check-ups or while undergoing surgical treatment for other health issues. Pediatric studies show that more than half of hypertensive children were asymptomatic or had their hypertension discovered during routine examinations.
If present, symptoms of RVHT are usually non-specific and relate to the organs most affected by high blood pressure. Neurological symptoms include changes in vision, headaches, altered mental status, seizures, coma, encephalopathy, hyperirritability, and hyperexcitability. Congestive heart failure signs and symptoms, such as edema, decreased energy, and shortness of breath, may also develop.
In patients with narrowing of the abdominal aorta, claudication may be present. Some children may experience anorexia, and infants or young children may present with failure to thrive. Rarely, patients may experience oliguric renal failure, a condition where the kidneys produce very little urine. It is essential to diagnose RVHT early to prevent complications, such as organ damage and end-stage renal disease.
Physical Examination
Physical Examination
In pediatric patients with renal vascular hypertension, their blood pressure reading during the physical examination is typically higher than the 95th percentile for their sex, age, and height. If a child’s blood pressure is over 140/100 mm Hg, they are more likely to have secondary hypertension, and higher blood pressure indicates a higher likelihood of RVHT.
An eye examination may show signs of retinopathy and retinal hemorrhages. Patients with heart failure may have symptoms such as cardiomyopathy, rapid breathing, and vasomotor instability, which can cause skin discoloration and mottling. In cases of aortic coarctation, lower-extremity pulses may be weak. An enlarged liver and abdominal bruit may also be present.
Children with tumors that affect the renal vasculature may have an abdominal mass near the kidney. Although rare, there may be signs of visceral artery involvement due to extensive collateralization. Neurofibromatosis can present with café-au-lait macules, as well as other symptoms such as neurofibromas, macrocephaly, dermal neurofibromas, and freckling in the axillary region.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Obstructive sleep apnea
Coarctation of the aorta
Cushing syndrome
Pheochromocytoma
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Renovascular hypertension is mainly caused by the RAAS pathway, and the primary treatment options are ACE and ARB, which are considered a Class 1a indications. Often, multiple medications are required to control blood pressure. Other medications, such as calcium channel blockers, thiazides, beta-blockers, and hydralazine, have also effectively managed hypertension in patients with RAS.
Direct renin inhibitors like aliskiren have been studied as monotherapy or in combination with ACE inhibitors or ARBs for hypertension treatment. However, their efficacy in treating renovascular hypertension is still uncertain. ACEIs and ARBs promote vasodilation and sodium and water excretion by inhibiting the action of angiotensin II.
However, these medications are not recommended for patients with a single-functioning kidney or bilateral lesions as they can cause efferent arteriolar vasodilatation, leading to a reduction in autoregulation and glomerular filtration. Although they are effective in controlling blood pressure, these medications can also worsen renal function.
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High blood pressure is a widespread health problem in the United States, affecting approximately 75 million adults. It is a significant concern in primary care, accounting for 8.6% of all visits. Renovascular hypertension is a common cause of secondary hypertension, which refers to high blood pressure that is caused by an underlying medical condition.
Renovascular hypertension occurs when the blood supply to the kidneys is compromised due to occlusion or blockage in the main renal artery, resulting in decreased blood flow. This condition can lead to resistant hypertension, a type of high blood pressure that is difficult to control with medication alone.
Renovascular hypertension affects individuals of all ages. The most common cause of renal artery stenosis is atherosclerosis and it is more commonly observed in older adults aged over 65 years. This condition is more prevalent in individuals with atherosclerotic diseases, such as coronary artery disease, peripheral artery disease, or carotid artery stenosis.
Autopsy studies have indicated that more than 25% of patients who die of cardiovascular diseases have some degree of renal artery stenosis. Another cause of renovascular hypertension is fibromuscular dysplasia (FMD), a rare condition that affects the arteries and causes abnormal growth within the arterial walls.
FMD is typically observed in young women and accounts for around 10% of renovascular hypertension cases and 5.8% of secondary hypertension cases. This condition can affect any arterial bed, but it commonly affects the distal two-thirds of the renal artery.
Renovascular hypertension is characterized by decreased blood flow to the kidneys, which triggers the activation of the renin-angiotensin-aldosterone (RAAS) pathway. This process was first described by Goldblatt et al. in the 1930s, when they conducted experiments on dogs and observed that reduced blood supply to the kidneys led to persistent hypertension.
Goldblatt also proposed the existence of a substance that could act like a hormone, causing a pressor effect. This substance was later identified as renin, secreted by specialized juxtaglomerular cells in the kidneys. Renin secretion is stimulated by three main pathways: renal baroreceptors that sense reduced kidney perfusion, the macula densa that detects low sodium chloride levels, and beta-adrenergic stimulation.
Prolonged ischemia can also increase the number of renin-expressing cells in the kidney, known as JG recruitment. When renin is secreted into the bloodstream, it acts on angiotensinogen, a protein produced by the liver. Renin cleaves angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) primarily found in the vascular endothelium of the lungs and kidneys. Angiotensin II has multiple effects on the body, contributing to increased blood pressure.
It stimulates the sympathetic nervous system, releasing norepinephrine, which causes vasoconstriction and an increase in heart rate. It also causes collagen type I and III synthesis in fibroblasts, leading to the vascular wall, myocardium, and fibrosis thickening. These changes in the structure of blood vessels and heart muscles can further exacerbate hypertension and increase the risk of cardiovascular complications.
Renovascular hypertension often occurs due to various factors such as extrinsic compression of a renal artery, radiation fibrosis, obstruction caused by aortic endovascular grafts, and fibromuscular dysplasia.
Atherosclerotic renal artery stenosis is a progressive condition that can lead to renal failure due to worsening stenosis. Untreated renovascular hypertension resulting from atherosclerotic renal artery stenosis can lead to end-stage renal failure. The median survival time for patients with renovascular hypertension is only 25 months, and the 4-year mortality rate is as high as 35%.
The primary management for renovascular hypertension should aim to correct the underlying cause. In the case of renovascular hypertension caused by atherosclerotic renal artery stenosis, medical management should be prioritized over invasive management. Multiple studies have failed to demonstrate renal or cardiovascular benefits with invasive management.
Clinical History
Patients with Renal Vascular Hypertension (RVHT) may not experience any symptoms, and their hypertension may be detected incidentally during routine check-ups or while undergoing surgical treatment for other health issues. Pediatric studies show that more than half of hypertensive children were asymptomatic or had their hypertension discovered during routine examinations.
If present, symptoms of RVHT are usually non-specific and relate to the organs most affected by high blood pressure. Neurological symptoms include changes in vision, headaches, altered mental status, seizures, coma, encephalopathy, hyperirritability, and hyperexcitability. Congestive heart failure signs and symptoms, such as edema, decreased energy, and shortness of breath, may also develop.
In patients with narrowing of the abdominal aorta, claudication may be present. Some children may experience anorexia, and infants or young children may present with failure to thrive. Rarely, patients may experience oliguric renal failure, a condition where the kidneys produce very little urine. It is essential to diagnose RVHT early to prevent complications, such as organ damage and end-stage renal disease.
Physical Examination
In pediatric patients with renal vascular hypertension, their blood pressure reading during the physical examination is typically higher than the 95th percentile for their sex, age, and height. If a child’s blood pressure is over 140/100 mm Hg, they are more likely to have secondary hypertension, and higher blood pressure indicates a higher likelihood of RVHT.
An eye examination may show signs of retinopathy and retinal hemorrhages. Patients with heart failure may have symptoms such as cardiomyopathy, rapid breathing, and vasomotor instability, which can cause skin discoloration and mottling. In cases of aortic coarctation, lower-extremity pulses may be weak. An enlarged liver and abdominal bruit may also be present.
Children with tumors that affect the renal vasculature may have an abdominal mass near the kidney. Although rare, there may be signs of visceral artery involvement due to extensive collateralization. Neurofibromatosis can present with café-au-lait macules, as well as other symptoms such as neurofibromas, macrocephaly, dermal neurofibromas, and freckling in the axillary region.
Differential Diagnoses
Obstructive sleep apnea
Coarctation of the aorta
Cushing syndrome
Pheochromocytoma
Renovascular hypertension is mainly caused by the RAAS pathway, and the primary treatment options are ACE and ARB, which are considered a Class 1a indications. Often, multiple medications are required to control blood pressure. Other medications, such as calcium channel blockers, thiazides, beta-blockers, and hydralazine, have also effectively managed hypertension in patients with RAS.
Direct renin inhibitors like aliskiren have been studied as monotherapy or in combination with ACE inhibitors or ARBs for hypertension treatment. However, their efficacy in treating renovascular hypertension is still uncertain. ACEIs and ARBs promote vasodilation and sodium and water excretion by inhibiting the action of angiotensin II.
However, these medications are not recommended for patients with a single-functioning kidney or bilateral lesions as they can cause efferent arteriolar vasodilatation, leading to a reduction in autoregulation and glomerular filtration. Although they are effective in controlling blood pressure, these medications can also worsen renal function.
medtigo
Renovascular Hypertension
Updated :
September 6, 2023
High blood pressure is a widespread health problem in the United States, affecting approximately 75 million adults. It is a significant concern in primary care, accounting for 8.6% of all visits. Renovascular hypertension is a common cause of secondary hypertension, which refers to high blood pressure that is caused by an underlying medical condition.
Renovascular hypertension occurs when the blood supply to the kidneys is compromised due to occlusion or blockage in the main renal artery, resulting in decreased blood flow. This condition can lead to resistant hypertension, a type of high blood pressure that is difficult to control with medication alone.
Renovascular hypertension affects individuals of all ages. The most common cause of renal artery stenosis is atherosclerosis and it is more commonly observed in older adults aged over 65 years. This condition is more prevalent in individuals with atherosclerotic diseases, such as coronary artery disease, peripheral artery disease, or carotid artery stenosis.
Autopsy studies have indicated that more than 25% of patients who die of cardiovascular diseases have some degree of renal artery stenosis. Another cause of renovascular hypertension is fibromuscular dysplasia (FMD), a rare condition that affects the arteries and causes abnormal growth within the arterial walls.
FMD is typically observed in young women and accounts for around 10% of renovascular hypertension cases and 5.8% of secondary hypertension cases. This condition can affect any arterial bed, but it commonly affects the distal two-thirds of the renal artery.
Renovascular hypertension is characterized by decreased blood flow to the kidneys, which triggers the activation of the renin-angiotensin-aldosterone (RAAS) pathway. This process was first described by Goldblatt et al. in the 1930s, when they conducted experiments on dogs and observed that reduced blood supply to the kidneys led to persistent hypertension.
Goldblatt also proposed the existence of a substance that could act like a hormone, causing a pressor effect. This substance was later identified as renin, secreted by specialized juxtaglomerular cells in the kidneys. Renin secretion is stimulated by three main pathways: renal baroreceptors that sense reduced kidney perfusion, the macula densa that detects low sodium chloride levels, and beta-adrenergic stimulation.
Prolonged ischemia can also increase the number of renin-expressing cells in the kidney, known as JG recruitment. When renin is secreted into the bloodstream, it acts on angiotensinogen, a protein produced by the liver. Renin cleaves angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) primarily found in the vascular endothelium of the lungs and kidneys. Angiotensin II has multiple effects on the body, contributing to increased blood pressure.
It stimulates the sympathetic nervous system, releasing norepinephrine, which causes vasoconstriction and an increase in heart rate. It also causes collagen type I and III synthesis in fibroblasts, leading to the vascular wall, myocardium, and fibrosis thickening. These changes in the structure of blood vessels and heart muscles can further exacerbate hypertension and increase the risk of cardiovascular complications.
Renovascular hypertension often occurs due to various factors such as extrinsic compression of a renal artery, radiation fibrosis, obstruction caused by aortic endovascular grafts, and fibromuscular dysplasia.
Atherosclerotic renal artery stenosis is a progressive condition that can lead to renal failure due to worsening stenosis. Untreated renovascular hypertension resulting from atherosclerotic renal artery stenosis can lead to end-stage renal failure. The median survival time for patients with renovascular hypertension is only 25 months, and the 4-year mortality rate is as high as 35%.
The primary management for renovascular hypertension should aim to correct the underlying cause. In the case of renovascular hypertension caused by atherosclerotic renal artery stenosis, medical management should be prioritized over invasive management. Multiple studies have failed to demonstrate renal or cardiovascular benefits with invasive management.
Clinical History
Patients with Renal Vascular Hypertension (RVHT) may not experience any symptoms, and their hypertension may be detected incidentally during routine check-ups or while undergoing surgical treatment for other health issues. Pediatric studies show that more than half of hypertensive children were asymptomatic or had their hypertension discovered during routine examinations.
If present, symptoms of RVHT are usually non-specific and relate to the organs most affected by high blood pressure. Neurological symptoms include changes in vision, headaches, altered mental status, seizures, coma, encephalopathy, hyperirritability, and hyperexcitability. Congestive heart failure signs and symptoms, such as edema, decreased energy, and shortness of breath, may also develop.
In patients with narrowing of the abdominal aorta, claudication may be present. Some children may experience anorexia, and infants or young children may present with failure to thrive. Rarely, patients may experience oliguric renal failure, a condition where the kidneys produce very little urine. It is essential to diagnose RVHT early to prevent complications, such as organ damage and end-stage renal disease.
Physical Examination
In pediatric patients with renal vascular hypertension, their blood pressure reading during the physical examination is typically higher than the 95th percentile for their sex, age, and height. If a child’s blood pressure is over 140/100 mm Hg, they are more likely to have secondary hypertension, and higher blood pressure indicates a higher likelihood of RVHT.
An eye examination may show signs of retinopathy and retinal hemorrhages. Patients with heart failure may have symptoms such as cardiomyopathy, rapid breathing, and vasomotor instability, which can cause skin discoloration and mottling. In cases of aortic coarctation, lower-extremity pulses may be weak. An enlarged liver and abdominal bruit may also be present.
Children with tumors that affect the renal vasculature may have an abdominal mass near the kidney. Although rare, there may be signs of visceral artery involvement due to extensive collateralization. Neurofibromatosis can present with café-au-lait macules, as well as other symptoms such as neurofibromas, macrocephaly, dermal neurofibromas, and freckling in the axillary region.
Differential Diagnoses
Obstructive sleep apnea
Coarctation of the aorta
Cushing syndrome
Pheochromocytoma
Renovascular hypertension is mainly caused by the RAAS pathway, and the primary treatment options are ACE and ARB, which are considered a Class 1a indications. Often, multiple medications are required to control blood pressure. Other medications, such as calcium channel blockers, thiazides, beta-blockers, and hydralazine, have also effectively managed hypertension in patients with RAS.
Direct renin inhibitors like aliskiren have been studied as monotherapy or in combination with ACE inhibitors or ARBs for hypertension treatment. However, their efficacy in treating renovascular hypertension is still uncertain. ACEIs and ARBs promote vasodilation and sodium and water excretion by inhibiting the action of angiotensin II.
However, these medications are not recommended for patients with a single-functioning kidney or bilateral lesions as they can cause efferent arteriolar vasodilatation, leading to a reduction in autoregulation and glomerular filtration. Although they are effective in controlling blood pressure, these medications can also worsen renal function.
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