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E-Case Number Eight
S. Mr. R.K. is a 74 year old male referred
by Opthamology for hypertensive retinopathy. He is asymptomatic and has
not seen a physician in over six years. He was never told of hypertension
in the past. He is a nonsmoking, retired engineer and past history is
entirely unremarkable.
O. Pleasant, cooperative man in NAD
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B/P 220/100 bilaterally in the seated position without postural change.
P 64 and regular
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Eyes- fundoscopic exam is remarkable for hemorrhages and exudates
bilaterally, OS worse than OD.
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Chest - clear to percussion and auscultation
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Cardiac - S4 gallop, but no S3 or mumurs
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Abdomen - benign except for a bruit in the periumbilical region
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Vascular exam - right carotid bruit, but all pulses full and symmetrical
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Rectal - prostate soft and 2-3+ enlarged
Lab: CBC normal, comprehensive chemistry panel
is remarkable for a BUN of 19 and creatinine of 1.5 with a normal potassium
of 4.5. Electrocardiogram reveals left ventricular hypertrophy but is
otherwise normal.
Treatment: The patient was begun on HCTZ and
Verapamil SR but three weeks later his blood pressure was still 190/95.
Enalapril 5mg. qd was added and one week later BUN = 28, creatinine =
1.7 and potassium was 5.0. Three weeks later blood pressure remained
elevated at 185/92. Enalapril was then increased to 10 mg. qd, and one
week later creatinine was 2.2, BUN was 42, and potassium was 5.4. Enalapril
was then stopped and a diagnostic procedure was performed.
Questions
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What diagnostic procedure was performed?
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What pertinent historical, physical exam, and management points
suggest the diagnosis.
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Why make this diagnosis
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How would you treat him medically? surgically? invasive radiology?
Answers
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Duplex ultrasonagraphy was performed. It is highly accurate when
performed at Pacific Vascular and relatively inexpensive. It revealed
a total right renal artery occlusion and a severe stenosis of the
left renal artery.
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Mr. R.K.'s abrupt onset of hypertension after age fifty, his accelerated
hypertension with severe retinopathy, refractory hypertension to three
drugs, abdominal bruit, and azotemia induced with an angiotensin-converting
enzyme inhibitor [The acute introduction of ACE inhibition causes
vasodilatation of the efferent arterioles leading to a significant
drop in GFR in the face of decreased flow in the afferent arterioles
from fixed bilateral stenosis or unilateral stenosis in one functioning
kidney] all suggest renal artery stenosis as the likely cause of his
hypertension.
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The main reason to make the diagnosis is to prevent renal failure
from ischemic nephropathy. Correcting atherosclerotic renal artery
stenosis via renal artery bypass surgery or angioplasty/stent placement
rarely treats hypertension from renal artery stenosis although it
may decrease its severity. On the other hand in young patients with
renal artery stenosis secondary to the much rarer fibromuscular dysplasia
angioplasty often completely cures hypertension.
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Mr. R.K. went on to angiography and it was found he had atherosclerosis
diffusely involving his left renal artery. He underwent aortorenal
bypass surgery. His hypertension was then controlled with two drugs.
Tragically two years later his bypass graft failed and he is now on
dialysis. If his lesion had been limited and proximal, as most are,
he would have been a candidate for angioplasty/stent placement.
References
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1. Klassen, P.S.,Diagnosis and Management of Renovascular Hypertension,
Cardiology in Review, Vol. 8,No. 1, 2000 pgs. 17-29.
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2. Safian, R.D.,Renal Artery Stenosis, NEJM, Vol. 344, No.6, pgs.
431-442.
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