AssessmentsRenal artery stenosis
Renal artery stenosis
USMLE® Step 1 style questions USMLE
A 58-year-old man comes to the office for a one month follow-up visit after being hospitalized for an acute myocardial infarction. The patient’s medical history includes hypertension, hyperlipidemia and coronary artery disease. The patient’s social history includes a 55 pack year smoking history, but no drug or alcohol use. The patient’s family history is significant for a myocardial infarction in his father. During the last office visit Lisinopril was added to his home medications of Metoprolol, Atorvastatin, Aspirin, and Clopidogrel. The patient’s vital signs show a temperature of 37 °C (98.6°F), pulse 62/min, respirations 16/min, blood pressure 167/93mm Hg. Physical examination shows a male of stated age. Lungs are clear to auscultation. Cardiac exam reveals a regular rate and rhythm with a normal S1 and S2, no murmurs, rubs or gallops on auscultation. Abdominal exam reveals a soft, non-tender, mildly distended abdomen with an abdominal bruit heard on auscultation. Laboratory studies show:
Which of the following is the most likely underlying cause of this patient's presentation?
With renal artery stenosis, ‘stenosis’ means narrowing, which refers to a progressive narrowing of the renal artery, which carries blood to the kidney. This means that the blood downstream of the narrowed spot that goes to the kidney is at lower pressure, which gets sensed by the kidney.
Inside the kidney, there are millions of nephrons, each of which help to filter the blood and then fine-tune the composition of blood by carefully reabsorbing and secreting electrolytes as fluid passes through various parts of the nephron.
Blood approaches the nephron via the afferent arteriole. You can remember it as ‘A’ for approach, and then forms a tangle of capillaries called the glomerulus, before exiting via the efferent arteriole - “e” for exit. That efferent arteriole goes on to split into another set of capillaries - the vasa recta - which surround the nephron, and then blood leaves via the venule.
So there are two capillary beds per nephron, usually we think of it going arteriole - capillary - venule, but in the nephron it goes arteriole - capillary - arteriole - capillary - and finally venule.
So nephrons have the general shape of the letter “U”, with the beginning and end portions getting pretty close to each other.
The reason that this matters, is that over here, lining the inside of the afferent arteriole are endothelial cells.
Wrapped around them are juxtaglomerular cells which are super special smooth muscle cells that contract down like normal smooth muscle cells, but also have the ability to release a hormone called renin in response to low blood pressure.
Over here, close to the distal convoluted tubule, there is another special group of cells that line the tubule called macula densa cells which are sodium-chloride-sensing cells that detect the sodium concentration in the tubule.
This is then detected by the macula densa cells and they send out a local prostaglandin signal that reaches the juxtaglomerular cells and causes them to release renin.
In addition the juxtaglomerular cells are able to directly sense low pressure in the afferent arteriole, and also respond to sympathetic nerve fibers to release renin.
Now, renin helps to constrict blood vessels and increases sodium reabsorption in the nephrons, which ultimately causes blood pressure to rise. Normally, as the blood pressure rises, the juxtaglomerular cells are no longer triggered to release renin, so balance is restored.
One cause of renal artery stenosis is atherosclerotic plaque buildup, which is where a mix of fat, calcium, and immune cells form a crusty rim on the inside of the artery.
Another cause, though, is renal fibromuscular dysplasia, where fibro- refers to fibrous collagen connective tissue, -muscular refers to smooth muscle in the artery wall, and -dysplasia means abnormal development.
So, renal fibromuscular dysplasia is when something goes wrong with connective tissue and smooth muscles in the walls of renal artery, resulting in a series of bulges and narrow spots that leaves the artery looking like a “string of beads” instead of a uniform cylinder.
Fibromuscular dysplasia classically develops in young women, but the exact underlying cause is still unclear.