Final Diagnosis -- Renal Artery Stenosis (chronic hypertension)


FINAL DIAGNOSIS: RIGHT RENAL ARTERY STENOSIS

Contributor's notes:

Systemic hypertension is a major health problem in the United States affecting millions of people. Over 90% of patients with high blood pressure have primary or "essential" hypertension. Secondary causes may be renal (glomerulonephritis, renin-producing tumors), vascular (polyarteritis nodosa), endocrine (Cushing's disease, thyrotoxicosis, pheochromocytoma, oral contraception use) or neurogenic (increased intracranial pressure) in origin. Renovascular hypertension accounts for approximately 2% of tot al cases.

In the current case, this patient's hypertension appears to be related to her right renal artery stenosis, and hence, involves the renin-angiotensin-aldosterone system. The pathophysiology is as follows:

Renal artery stenosis causes decreased blood flow into one of the kidneys:

This results in a lowered blood pressure within the cortex of that kidney. The cells of the juxta-glomerular apparatus which line the afferent arteriole leading into the glomerulus, react to the decreased blood pressure by secreting renin. Renin is a protease that splits the plasma protein angiotensinogen into angiotensin I. On the surface of endothelial cells is angiotensin converting enzyme which converts angiotensin I to angiotensin II.

It is angiotensin II which is the active factor that raises blood pressure. It does this directly by inducing smooth muscle contraction, and also stimulates the adrenal cortex to secrete aldosterone. Aldosterone (mineralocorticoid) acts on the kidney by promoting the reabsorption of sodium, and the secretion of potassium. Sodium retention leads to hypervolemia.

In the current case, the finding of significantly increased plasma renin levels unilaterally, as well as the ultrasound finding of right renal atrophy is diagnostic. Causes of renal artery stenosis include atherosclerosis, arteritis and fibromuscular dysplasia.

Renovascular hypertension typically responds well to treatment with ACE inhibitors for obvious reasons. Surgery, in the form of angioplasty or nephrectomy, may be curative.

References:

Robbins, Kotran and Kumar, Robbins Pathologic Basis of Disease, 4th Edition, Saunders, pp 1062-1065, 1989

Suzanne Oparil, Arterial Hypertension, chapter in Cecil Textbook of Medicine, edited by Wyngaarden, Smith and Bennett, 19th Edition, Saunders, pp 253-269, 1992

Jordan Cohen, Vascular Disorders of the Kidney chapter in Cecil Textbook of Medicine, edited by Wyngaarden, Smith and Bennett, 19th Edition, Saunders, pp 598-599, 1992

Tyrrel and Baxter, Disorders of the Adrenal Cortex chapter in Cecil Textbook of Medicine, edited by Wyngaarden, Smith and Bennett, 19th Edition, Saunders, pp 1271-1291, 1992

Contributed by Eric Schubert, MD


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