Discusses the controversy and clinical relevance of unilateral renal ischemia (Goldblatt mechanism) as a cause of sustained arterial hypertension.
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Unilateral renal ischemia warrants cautious evaluation in hypertension; leaves open the Goldblatt mechanism's causal role in sustained cases.
UNILATERAL renal hypertension, its cause and its effects have been of particular interest since it was produced in dogs by Goldblatt et al.1 in 1934. Cases of so-called "Goldblatt hypertension" have been reported, but few are accepted as due solely to unilateral renal ischemia.2 3 4 5 Such reports lead many physicians to believe that the Goldblatt mechanism is rarely a clinical cause of sustained arterial hypertension.3 , 6 However, this conclusion has recently been challenged by Page, Dustan and Poutasse,7 Howard and his co-workers,8 Yendt et al.9 and others.The surgical treatment of unilateral renal hypertension has also been controversial, as shown by the . . .
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Fruchtman et al. (1960) studied this question.
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