Case Author(s): Stephanie P.F. Yen, M.D. and Keith Fischer, M.D. , 04/17/98 . Rating: #D2, #Q4

Diagnosis: Renovascular hypertension

Brief history:

73-year-old male with recent onset of hypertension.


Posterior radionuclide angiogram

View main image(rs) in a separate image viewer

View second image(rs). Posterior sequential images

View third image(mm). Split renal function ROI's (on left); Time-activity curves (on right)

Full history/Diagnosis is available below

Diagnosis: Renovascular hypertension

Full history:

73-year-old male with new onset of hypertension. The patient denies a history of diabetes mellitus or renal disease. He was begun on Prinivil, 40 mg qday. The patient's creatinine is reportedly within normal limits. Renal scintigraphy is requested to evaluate for renovascular hypertension. The patient's ACE inhibitor medication was not withheld for this study. The patient took his Prinivil one hour prior to beginning this examination.


7.5 mCi Tc-99m MAG3, i.v.


The patient was intially hydrated before the examination was begun. The posterior radionuclide angiogram demonstrates moderately decreased perfusion to the right kidney. Normal perfusion to the left kidney is noted. Sequential renal images show the right kidney to be slightly smaller than the left. There is normal cortical uptake and excretion of tracer by the left kidney. On the right, there mild to moderately decreased initial cortical uptake and prolonged parenchymal retention of activity. Excretion of tracer by the right kidney is delayed and minimal.

The estimated contribution of the right kidney to total renal function is 30% and that of the left kidney is 70%.

These scintigraphic findings in a patient with no reported history of renal parenchymal disease are most consistent with renin-mediated hypertension due to right renal artery stenosis.


Angiotensin-converting enzyme (ACE) inhibitor renography is often requested to evaluate for renovascular hypertension. Renovascular hypertension is the underlying etiology for hypertension in only a minority of the cases (approximately 1-4%). In patients with renovascular hypertension, the cause of renal artery stenosis is most commonly atherosclerosis. Fibromuscular dysplasia is said to be the second most common cause. ACE inhibitor renal scintigraphy is reported to have both a sensitivity and specificity of greater than 90%.

In patients with renovascular hypertension, compensatory mechanisms via the renin-angiotensin system occur. ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor. In patients with renovascular hypertension, this effect results in loss of vasoconstriction of the efferent arterioles which is necessary to maintain effective filtration pressure. Consequently, a decrease in renal function occurs which can be detected scintigraphically.

In patients with renovascular hypertension, ACE inhibitor renal scintigraphy performed with a primarily tubular agent such as Tc-99m MAG3 will classically demonstrate preservation of initial uptake and excretion of tracer. However, there is prolonged retention of parenchymal activity due to the reduced GFR. Initial cortical uptake of Tc99m MAG3 may be decreased in severe stenoses. If a glomerular filtration agent such as Tc99m DTPA is employed, poor initial cortical uptake of tracer is noted predominantly, and prolonged parenchymal retention of activity may also occur. Perfusion to the involved kidney is typically preserved with both renal tubular and glomerular filtration agents, although in severe renal artery stenosis, perfusion to the affected kidney may be diminished.

Patients who are on ACE inhibitors for blood pressure control should stop their medication for 1-3 days, depending on the actual ACE inhibitor, prior to the examination. ACE-inhibitor renal scintigraphy can be performed using a one-day, two-stage protocol, or a one-stage protocol. With a one-stage protocol, renal scintigraphy with ACE inhibition is performed first, and if normal, no baseline study need be performed and renovascular hypertension is excluded. This is usually done in patients with no previous history of renal dysfunction. With respect to the case presented, the ACE-inhibitor renal scintigraphy was so strikingly abnormal that the findings were highly suspicious for renin-mediated hypertension due to right renal artery stenosis. With a one-day, two-stage protocol, a baseline study is first performed followed by a repeat examination with ACE-inhibition.


The patient subsequently underwent renal arteriography, which demonstrated an 80-90% stenosis in the proximal right renal artery, approximately 1 cm from the ostium, and a 50-60% ostial stenosis of the left renal artery. The right renal artery stenosis was then angioplastied with a 6 mm balloon. A follow-up arteriogram demonstrated a residual 50-60% stenosis and a focal dissection in the artery, for which two Palmaz stents were subsequently placed. A follow-up arteriogram following stent deployment revealed no residual stenosis or dissection.

Following right renal artery angioplasty and stent placement, the patient's blood pressure initially decreased to the normal range, but then intermittently increased. The patient returned for a follow-up ACE-inhibior renal scintigraphy study to evaluate for recurrent renovascular hypertension. The study (not shown) demonstrated significant interval improvement in right renal flow, uptake, and excretion of tracer as well as improved relative renal function since the previous study, indicating successful restoration of blood flow to the right kidney following renal artery angioplasty and stent placement. The split renal function was now more equal, with the right kidney contributing 41% and the left kidney 59% to total renal function. There was no evidence to suggest renin-mediated hypertension.

Reference: Mettler FA and Guiberteau MJ. Essentials of Nuclear Medicine Imaging. 4th ed. 1998. WB Saunders Company. Philadelphia, 349-354.

View followup image(an). Renal arteriogram (anterior view) on left; Post angioplasty of and placement of stents in right renal artery on right

Differential Diagnosis List

Acute tubular necrosis in the appropriate clinical setting can present with scintigraphic findings similar to those seen with renin-mediated hyper tension due to renal artery stenosis. Patients who are poorly hydrated may also demonstrate prolonged parenchymal retention and decreased excretion of tracer. Finally, hypotension following administration of ACE inhibitor may result in a false-positive interpretation for renovascular hypertension.

ACR Codes and Keywords:

References and General Discussion of Renal Scintigraphy (Anatomic field:Genitourinary System, Category:Other generalized systemic disorder)

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Case number: rs017

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