A 75-year-old man comes to the office for follow-up of hypertension. In recent weeks, his blood pressure has consistently been 160-165/85-90 mm Hg. Medical history includes a right carotid endarterectomy for recurrent transient ischemic attacks, a myocardial infarction 2 years ago, and coronary artery bypass surgery for unstable angina 1 year ago. The patient currently takes metoprolol, clopidogrel, amlodipine, and rosuvastatin. He quit smoking 20 years ago and does not drink alcohol. The patient is compliant with his medical therapy and office visits. Ramipril is added to his medication regimen. One week later, creatinine is 2.1 mg/dL, up from a baseline of 1.1 mg/dL. Assuming the patient's baseline urinalysis is normal, a repeat urinalysis at this time would most likely reveal which of the following?

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11ec160b_3c72_7c82_9249_e55d7f2ac041_MD0001_00 This patient has widespread atherosclerosis (cerebrovascular and coronary) and significant atherosclerotic risk factors (ie, hypertension, smoking). His persistent hypertension despite multiple medications suggests renal artery stenosis (RAS) due to atherosclerotic disease involving the renal arteries. Narrowing of the renal artery causes a reduction in renal blood flow and a decreased glomerular filtration rate (GFR) due to reduced hydrostatic pressure. This stimulates renin production, which leads to angiotensin II formation. Angiotensin II causes systemic vasoconstriction with a resultant rise in blood pressure, thereby increasing renal perfusion. In the kidney, angiotensin II preferentially constricts the efferent arteriole, which increases glomerular filtration. Blockade of this response by ACE inhibitors (eg, ramipril) or angiotensin II receptor blockers (eg, losartan) causes the filtration pressure to fall, leading to a reduced GFR. In unilateral RAS, the normal kidney compensates for the decreased GFR, and overall creatinine clearance is maintained. However, patients with bilateral RAS often develop a rise in serum creatinine with initiation of ACE inhibitors. Because the glomeruli and renal tubules are otherwise normal, urinalysis is typically unremarkable (ie, no hematuria, proteinuria, or casts). (Choice A) Acute renal failure and hypertension with red blood cell casts, hematuria, sterile pyuria, and proteinuria suggest glomerulonephritis. However, glomerulonephritis is often associated with systemic conditions (eg, lupus, recent infections), not ACE inhibitor use. (Choice B) White blood cell casts, sterile pyuria, and urine eosinophils suggest acute interstitial nephritis, which often occurs after new medication introduction. However, it is often accompanied by rash, fever, and eosinophilia. (Choice C) Crystal precipitation in the urine can cause kidney injury and hematuria but typically presents with flank pain. In addition, acyclovir (not ramipril) causes needle-shaped crystal precipitation in the urine. (Choice D) Oval fat bodies and significant proteinuria are seen in nephrotic syndromes (eg, membranous nephropathy, minimal change disease), which can cause acute kidney injury and hyperlipidemia. However, patients typically have significant edema, and nephrotic syndromes are not associated with ACE inhibitor use. Educational objective: In renal artery stenosis, increased production of angiotensin II causes increased systemic blood pressure (to increase renal perfusion) and preferential constriction of the glomerular efferent arteriole (to increase glomerular filtration). Patients with bilateral renal artery stenosis are dependent on this response to maintain renal function; initiation of ACE inhibitors or angiotensin II receptor blockers can precipitate acute renal failure. However, urinalysis is typically unremarkable (ie, no hematuria, proteinuria, or casts). __________ References: Epidemiology and optimal management in patients with renal artery stenosis. (http://www.ncbi.nlm.nih.gov/pubmed/23023722)

A 75-Year-Old Man Comes to the Office for Follow-Up of Hypertension