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Samuel Vaisrub, MD

JAMA. 1974;227(10):1168.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Normal and, less frequently, low renin activity are the expected findings in nonmalignant essential hypertension. On the other hand, they are unexpected in hypertension secondary to renal or renovascular disease. After all, increased renin release by the underperfused kidney is the hallmark of renal hypertension, the mechanism of its development and persistence.

Unanticipated fall of renin activity levels to low or normal has been reported in the experimental animal model of unilateral renal artery stenosis after removal of the contralateral kidney.^1,2 Apparently, with the uninvolved kidney no longer available for sodium and water clearance, blood volume expands. This expansion augments renal perfusion with consequent suppression of renin. Despite the fall in renin activity, hypertension, sustained by the hypervolemia, persists, or even worsens.

A somewhat analogous situation in man is reported by Kurtzman et al in the February issue of Archives of Internal Medicine.³ The investigators describe five patients . . . [Full Text PDF of this Article]

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