A 64-year-old man comes to the office after learning at the dentist's office that he has elevated blood pressure. The patient is a combat veteran and has always been "fit as a bull." He has undergone various minor surgical procedures for wartime injuries. He reports many years of tobacco and alcohol use but currently uses neither. On careful questioning, he describes chest pain on exertion. Blood pressure is 155/90 mm Hg and pulse is 76/min. Physical examination is significant for decreased pulse amplitude over the right femoral artery and a systolic bruit over the left carotid artery. Resting ECG is unremarkable, and serum creatinine is 1.1 mg/dL. Urinalysis is negative for protein. Treatment for hypertension is initiated with ramipril. On a follow-up visit 3 weeks later, blood pressure is 142/85 mm Hg but serum creatinine has increased to 2 mg/dL. This laboratory finding is best explained by an effect of the drug on which of the following structures (as indicated in the image)?

Question

A 64-year-old man comes to the office after learning at the dentist's office that he has elevated blood pressure.  The patient is a combat veteran and has always been "fit as a bull."  He has undergone various minor surgical procedures for wartime injuries.  He reports many years of tobacco and alcohol use but currently uses neither.  On careful questioning, he describes chest pain on exertion.  Blood pressure is 155/90 mm Hg and pulse is 76/min.  Physical examination is significant for decreased pulse amplitude over the right femoral artery and a systolic bruit over the left carotid artery.  Resting ECG is unremarkable, and serum creatinine is 1.1 mg/dL.  Urinalysis is negative for protein.  Treatment for hypertension is initiated with ramipril.  On a follow-up visit 3 weeks later, blood pressure is 142/85 mm Hg but serum creatinine has increased to 2 mg/dL.  This laboratory finding is best explained by an effect of the drug on which of the following structures (as indicated in the image)?

Quizplus · Accepted Answer

11ec160b_3c66_6f7e_9249_c115bc84d3ca_MD0001_00 This patient with angina, reduced femoral pulsation, and a carotid bruit has diffuse atherosclerosis. Patients with severe atherosclerosis or atherosclerotic risk factors (eg, hypertension, hyperlipidemia, smoking) are more likely to develop atherosclerotic renal artery stenosis (RAS). Conditions that reduce renal perfusion (eg, hypovolemia, congestive heart failure, RAS [as in this patient]) lower glomerular filtration pressure and the glomerular filtration rate (GFR), stimulating the renin-angiotensin-aldosterone system. This results in increased levels of angiotensin II, a potent vasoconstrictor that causes systemic hypertension and preferentially constricts the efferent arteriole to restore GFR. ACE inhibitors lower angiotensin II levels, causing systemic vasodilation and reduced blood pressure. However, they also cause efferent arteriolar dilation and lower intraglomerular pressure, preventing the kidney from maintaining GFR in the setting of reduced renal perfusion. Many patients experience up to a 30% increase in serum creatinine within 2-5 days of starting ACE inhibitors. Patients with bilateral RAS (who are heavily dependent on angiotensin II to maintain GFR) can experience a precipitous fall in GFR and develop acute renal failure. (Choice A) Locally produced vasodilators (prostaglandins and nitric oxide) in the afferent arteriole counteract the vasoconstrictive effects of angiotensin II; as a result ACE inhibitors do not significantly affect the afferent arterioles. However, nonsteroidal anti-inflammatory drugs (eg, ibuprofen) and calcineurin inhibitors (eg, cyclosporine) inhibit prostaglandin formation, resulting in constriction of the afferent arterioles and a reduction in intraglomerular pressure. (Choices C and D) Aminoglycosides, vancomycin, certain antiretrovirals (eg, cidofovir), and foscarnet can damage the renal tubular cells, resulting in acute tubular necrosis. However, ACE inhibitors are not directly toxic to the renal tubules and have no effect on the descending or ascending loop of Henle. (Choice E) ACE inhibitors block the release of aldosterone, resulting in decreased Na⁺ reabsorption and K⁺ secretion in the distal and collecting tubules. Although this effect is responsible for the hyperkalemia often seen with ACE inhibitor therapy, it would not cause the rise in creatinine. Educational objective: ACE inhibitors reduce angiotensin II levels and cause efferent arteriole dilation, thereby decreasing the glomerular filtration pressure and filtration rate. This can precipitate acute renal failure in patients with reduced intrarenal perfusion pressure at baseline (eg, renal artery stenosis, congestive heart failure, hypovolemia).

A 64-Year-Old Man Comes to the Office After Learning at the Dentist's