We all know renovascular hypertension exists. But how does it present clinically? Are their any distinguishing features that set it apart from other causes of hypertension and from subjects with essential hypertension?
Renovascular hypertension has two principal aetiologies. By far the commonest aetiology is atherosclerotic narrowing of the proximal renal artery. This can be predominantly unilateral or bilateral.
A much less common cause is fibromuscular dysplasia, affecting young females often in the 30-50 year range. This typically affects the distal renal artery, and for some reason, tends to be predominantly right sided.
So how does renovascular disease present? There are two terms often used to describe this condition, without realising that this is in fact the underlying aetiology. The first is cardio-renal syndrome and the second is flash pulmonary oedema.
Probably the most characteristic presentation of atherosclerotic renal artery stenosis is rapidly worsening hypertension, worsening renal impairment and incremental heart failure. This is often erroneously interpreted as cardio-renal syndrome, particularly in subjects with pre-existing heart failure, but the key finding is the hypertension. Subjects with longstanding heart failure, the cohort who develop cardio-renal syndrome, often have low or low-normal BP. They should not show a trend for a recent increase in BP.
This classical presentation has been somewhat tempered in the last decade or two by the widespread use of ACE inhibitors and direct angiotensin blockers for treating both hypertension and heart failure, but when present, is strongly suggestive of severe renal artery stenosis.
Some physicians measure serum renin and aldosterone levels to make a suggestive diagnosis of renovascular hypertension, before considering imaging studies such as CT angiogram. However, this could be misleading. While renin and aldosterone levels would be expected to be high in predominantly unilateral renal artery stenosis, these hormones are normal in bilateral renal stenosis and in subjects who have renal artery stenosis in a single surviving kidney.
The other, albeit, less common presentation is flash pulmonary oedema. Far too often, clinicians invoke the rare diagnosis of phaeochromocytoma in such subjects, when the blame lies with a much more common condition. Renal artery stenosis should always be suspected in subjects who have one or more episodes of "flash" pulmonary oedema.
Renovascular hypertension has two principal aetiologies. By far the commonest aetiology is atherosclerotic narrowing of the proximal renal artery. This can be predominantly unilateral or bilateral.
A much less common cause is fibromuscular dysplasia, affecting young females often in the 30-50 year range. This typically affects the distal renal artery, and for some reason, tends to be predominantly right sided.
So how does renovascular disease present? There are two terms often used to describe this condition, without realising that this is in fact the underlying aetiology. The first is cardio-renal syndrome and the second is flash pulmonary oedema.
Probably the most characteristic presentation of atherosclerotic renal artery stenosis is rapidly worsening hypertension, worsening renal impairment and incremental heart failure. This is often erroneously interpreted as cardio-renal syndrome, particularly in subjects with pre-existing heart failure, but the key finding is the hypertension. Subjects with longstanding heart failure, the cohort who develop cardio-renal syndrome, often have low or low-normal BP. They should not show a trend for a recent increase in BP.
This classical presentation has been somewhat tempered in the last decade or two by the widespread use of ACE inhibitors and direct angiotensin blockers for treating both hypertension and heart failure, but when present, is strongly suggestive of severe renal artery stenosis.
Some physicians measure serum renin and aldosterone levels to make a suggestive diagnosis of renovascular hypertension, before considering imaging studies such as CT angiogram. However, this could be misleading. While renin and aldosterone levels would be expected to be high in predominantly unilateral renal artery stenosis, these hormones are normal in bilateral renal stenosis and in subjects who have renal artery stenosis in a single surviving kidney.
The other, albeit, less common presentation is flash pulmonary oedema. Far too often, clinicians invoke the rare diagnosis of phaeochromocytoma in such subjects, when the blame lies with a much more common condition. Renal artery stenosis should always be suspected in subjects who have one or more episodes of "flash" pulmonary oedema.
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