Symptoms of renovascular hypertension include:High blood pressure at a young age.High blood pressure that suddenly gets worse or is hard to control.Kidneys that are not working well (this can start suddenly)Narrowing of other arteries in the body, such as to the legs, the brain, the eyes and elsewhere.More items...•
The most common causes of renovascular hypertension are forms of renal artery stenosis. Atherosclerosis, which is the buildup of plaque in the arteries, is behind 90% of cases. Fibromuscular dysplasia, which is a condition that causes the narrowing of the arteries, is behind 9% of cases.
Renovascular hypertension is high blood pressure (greater than 140/80 mmHg) caused by renal artery disease. Normally, the kidneys regulate body fluid and blood pressure, as well as regulate blood chemistry and remove organic waste.
Diagnosis of Renovascular Hypertension If renovascular hypertension is suspected, ultrasonography, magnetic resonance angiography (MRA), or radionuclide imaging may be done to identify patients who should have renal angiography, the definitive test.
Suspect a renovascular cause if diastolic hypertension develops abruptly in a patient < 30 or > 50; if new or previously stable hypertension rapidly worsens within 6 months; or if hypertension is initially very severe, associated with worsening renal function, or highly refractory to drug treatment.
Renal hypertension (or renovascular hypertension) is high blood pressure caused by the narrowing of your arteries that carry blood to your kidneys. It is also sometimes called renal artery stenosis.
I15. 0 Renovascular hypertension - ICD-10-CM Diagnosis Codes.
DiagnosisA doppler ultrasound of the renal arteries.A renal angiogram to see a silhouette of the renal artery.A 3D CT renal angiogram to see the cause of renal artery stenosis; to see the extent of the disease; to see if the aorta is blocked.
SymptomsHigh blood pressure that's hard to control.A whooshing sound as blood flows through a narrowed vessel (bruit), which your doctor hears through a stethoscope placed over your kidneys.Elevated protein levels in the urine or other signs of a problem with kidney function.More items...•
For patients with normal renal function but a high clinical index of suspicion for renovascular disease, contrast-enhanced magnetic resonance angiography and computed tomographic angiography are the most accurate imaging tests.
The body senses less blood reaching the kidneys and misinterprets that as the body having low blood pressure. This signals the release of hormones from the kidney that lead to an increase in blood pressure. Over time, renal artery stenosis can lead to kidney failure.
Imaging tests commonly done to diagnose renal artery stenosis include:Doppler ultrasound. High-frequency sound waves help your doctor see the arteries and kidneys and check their function. ... CT scan. ... Magnetic resonance angiography (MRA). ... Renal arteriography.
Atherosclerosis occurs in many areas of the body and is the most common cause of renal artery stenosis. Fibromuscular dysplasia. In fibromuscular dysplasia, the muscle in the artery wall doesn't grow as it should. This often begins in childhood.
Renal artery stenosis usually does not cause any specific symptoms. Sometimes, the first sign of renal artery stenosis is high blood pressure that is extremely hard to control, along with worsening of previously well-controlled high blood pressure, or elevated blood pressure that affects other organs in the body.
The body senses less blood reaching the kidneys and misinterprets that as the body having low blood pressure. This signals the release of hormones from the kidney that lead to an increase in blood pressure. Over time, renal artery stenosis can lead to kidney failure.
As a result, the kidneys may stop removing wastes and extra fluid from your blood. The extra fluid in your blood vessels may build up and raise blood pressure even more. High blood pressure can also be a complication 2. of CKD.
Presented part at the Clinical-Pathological conference chaired by Anna F. Dominiczak and Rhian Touyz during the virtual event for Hypertension 2020 Scientific Sessions, September, 11, 2020. Abhilash Koratala and Rajesh Mohandas presented the case and led the discussion.
Dr Koratala: As you mentioned, we do not know why the first angiogram was read as FMD because it did not show any lesions that were characteristic of FMD based on the report. Based on the location of the lesion (ostial), angiographic images (lack of characteristic beading), and IVUS images (lack of webs), atherosclerotic disease was deemed more likely than FMD.
The current recommendation is that these patients should be followed at 1 month post-procedure, 6 months, and 1 year and annually thereafter for blood pressure control, with renal function testing and surveillance Doppler ultrasound. Doppler ultrasound is the recommended imaging technique to screen for in-stent restenosis. However, the ultrasound criteria for native renal artery stenosis overestimate the degree of angiographic in-stent restenosis due to loss of compliance of the artery after stent placement. Therefore, it might be prudent to obtain a postprocedural Doppler ultrasound to establish a new baseline peak systolic velocity.
The mean systolic blood pressure was 151 mm Hg , and the mean diastolic was 88 mm Hg. When she was awake, the systolic and diastolic values were 157 and 91 mm Hg, respectively, and when she was asleep, the readings were 134 and 80. There was an optimal nocturnal dip in blood pressure, 14% systolic, and 11% diastolic. When she was awake, the overall blood pressure load was >80% in both systolic and diastolic readings (threshold, >130/80 mm Hg).
The CBP machine takes one blood pressure reading every 5 minutes for a total of 3 readings. This is done in an unmonitored office setting, so it should be closer to home blood pressures. I believe the first reported blood pressure was the regular office blood pressure. Therefore, she definitely has an element of white-coat hypertension.
Dr Mohandas: No, unfortunately, we were not able to repeat it because the patient was lost to follow-up. So, after the angioplasties, she was scheduled for a repeat renal Doppler to evaluate her renal blood flow, as well as an ambulatory blood pressure. However, she dropped out of the system, and we were not able to locate her to do that.
Dr Koratala: This is a great point. That’s what we actually did, and she did have home blood pressures, but they were pretty erratic, and we did not have a log. As you said, we do not know about adherence and dietary compliance. This was the first visit, so we reinforced the importance of lifestyle modifications. We also restarted amlodipine and spironolactone that she had taken previously and ordered ambulatory blood pressure monitoring.
Renovascular disease is caused by progressive occlusive renal artery disease presenting with a myriad of symptoms ranging from renovascular hypertension to ischemic nephropathy. Renovascular hypertension (RVH) is one of the most common causes of secondary hypertension and has been widely studied as the prototype of angiotensin-dependent hypertension.1The great majority of the cases is caused by atherosclerotic lesions followed by fibromuscular dysplasia, but a variety of causes such renal artery dissection or embolic disease can produce the same symptoms. However, they are much less common.
The pathophysiology of RVD has served as the basis for the use of radionuclide studies using captopril renography as well as renal vein renin measurements for the diagnosis and treatment of RAS. The RAAS axis has widespread effects beyond vasoconstriction and sodium retention. Angiotensin II has complex cellular interactions that lead to activation of inflammatory and fibrogenic mechanisms. These lead to vascular remodeling and tissue fibrosis within the stenotic kidney and left ventricular hypertrophy.37–39Furthermore, ARAS typically occurs in the context of systemic atherosclerosis and the inflammatory milieu that accompanies this disease. Increased sympathetic activation, endothelial dysfunction, and increased oxidative stress have been also demonstrated in clinical studies. All these factors contribute to RVH in this population.40–42
RVH in the setting of RVD can accelerate cardiovascular disease. When severe, the increase of blood pressure can be associated with volume retention and precipitate circulatory congestion associated with left ventricular dysfunction. This series of events has been designated “flash pulmonary edema” and represents a cardio-renal syndrome commonly associated with worsening renal function.47Pulmonary edema associated with RVD leads to increased hospitalizations and increased morbidity and mortality in patients with congestive heart failure.48Ultimately, progressive occlusive renal artery disease produces overt hypoxia within the kidney and irreversible worsening of kidney function designated “ischemic nephropathy” especially in the context of other risk factors such as diabetes, hypertension, and smoking.49
It is important to point out that the role of the RAAS axis in RVD depends, in part, on whether or not a contralateral nonstenotic kidney is present. Unilateral RVH in human corresponds to the animal model of 2-kidney 1-clip (2K1C) Goldblatt model or also called “renin dependent” hypertension characterized by increased peripheral resistance. The rise in blood pressure stimulates pressure natriuresis by the intact contralateral kidney, which prevents volume expansion and sodium retention. Hence the nonstenotic kidney tends to counter the elevation of systemic blood pressure, which maintains reduced perfusion of the stenotic kidney and leads to continuous renin release. Although renovascular disease remains a prototype of angiotensin dependent hypertension, these hormonal responses are usually transient. As the occlusion progresses or if there is absence of a contralateral perfused kidney, the mechanisms of sustained hypertension differ. As intravascular volume increases due to impaired sodium and water excretion by an ineffective contralateral kidney, there is progressive decrease of renin secretion over time. This phase is referred to as “volume dependent” hypertension.35Renin activity can be normal or low in this phase.
Renovascular disease is a major cause of hypertension and it accounts for 1 to 5% of all cases of hypertension in the general population and 5.4% of secondary hypertension cases in young adults.9–11RVD is more prevalent in the older population of >65 years of age when significant RAS (> than 60% of occlusion by Doppler ultrasound) may be nearly 7%.12However, the real incidence and prevalence varies due to the variability of RAS definition and the type of the populations being studied. The prevalence may reach 40% in highly selected referral populations.13,14In 90% of the cases, RVD is caused by atherosclerotic renal artery stenosis (ARAS) (Figure 1) followed by fibromuscular dysplasia (9%). The remainder are due to miscellaneous causes as described in Table 1.15,16
Activation of the RAAS axis in this population magnifies blood pressure fluctuations especially if the patient is not on optimal medical therapy. Additional reabsorption of salt and water in the setting of increased RAAS activity commonly leads to volume overload and pulmonary congestion. The combination of volume excess and increased RAAS activation can accelerate target organ manifestations, including direct vascular injury, left ventricular hypertrophy, and renal dysfunction. These manifestations are seen more commonly in RVD than in patients with essential hypertension, if compared to age-matched population with same degree of blood pressure control.46
Atherosclerotic RVD of some degree is found in up to 12–45% of the cases of patients undergoing vascular studies of patients with peripheral vascular disease and 14–40% of the cases of patients undergoing coronary angiography.13,19,20
Presented part at the Clinical-Pathological conference chaired by Anna F. Dominiczak and Rhian Touyz during the virtual event for Hypertension 2020 Scientific Sessions, September, 11, 2020. Abhilash Koratala and Rajesh Mohandas presented the case and led the discussion.
Dr Koratala: As you mentioned, we do not know why the first angiogram was read as FMD because it did not show any lesions that were characteristic of FMD based on the report. Based on the location of the lesion (ostial), angiographic images (lack of characteristic beading), and IVUS images (lack of webs), atherosclerotic disease was deemed more likely than FMD.
The current recommendation is that these patients should be followed at 1 month post-procedure, 6 months, and 1 year and annually thereafter for blood pressure control, with renal function testing and surveillance Doppler ultrasound. Doppler ultrasound is the recommended imaging technique to screen for in-stent restenosis. However, the ultrasound criteria for native renal artery stenosis overestimate the degree of angiographic in-stent restenosis due to loss of compliance of the artery after stent placement. Therefore, it might be prudent to obtain a postprocedural Doppler ultrasound to establish a new baseline peak systolic velocity.
The mean systolic blood pressure was 151 mm Hg , and the mean diastolic was 88 mm Hg. When she was awake, the systolic and diastolic values were 157 and 91 mm Hg, respectively, and when she was asleep, the readings were 134 and 80. There was an optimal nocturnal dip in blood pressure, 14% systolic, and 11% diastolic. When she was awake, the overall blood pressure load was >80% in both systolic and diastolic readings (threshold, >130/80 mm Hg).
The CBP machine takes one blood pressure reading every 5 minutes for a total of 3 readings. This is done in an unmonitored office setting, so it should be closer to home blood pressures. I believe the first reported blood pressure was the regular office blood pressure. Therefore, she definitely has an element of white-coat hypertension.
Dr Mohandas: No, unfortunately, we were not able to repeat it because the patient was lost to follow-up. So, after the angioplasties, she was scheduled for a repeat renal Doppler to evaluate her renal blood flow, as well as an ambulatory blood pressure. However, she dropped out of the system, and we were not able to locate her to do that.
Dr Koratala: This is a great point. That’s what we actually did, and she did have home blood pressures, but they were pretty erratic, and we did not have a log. As you said, we do not know about adherence and dietary compliance. This was the first visit, so we reinforced the importance of lifestyle modifications. We also restarted amlodipine and spironolactone that she had taken previously and ordered ambulatory blood pressure monitoring.