1978
DOI: 10.1159/000181411
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Juxtaglomerular Cell Tumor

Abstract: A 15-year-old female with primary reninism presented with benign hypertension, normokalemia, normal aortagram and normal intravenous pyelogram. The diagnosis was suggested only by a remarkably elevated plasma renin activity (PRA). Selective catheterization of renal vein branches was necessary to make the diagnosis of a tumor. A local resection of the tumor resulted in normalization of blood pressure and PRA. Prior to the definitive surgery, oral propranolol was effective in lowering PRA and blood pressure.

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Cited by 23 publications
(6 citation statements)
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“…As far as active renin was concerned, orthostatism increased PRA, to suggest that, even in our patient as in others [6,7,10,14,18,19], renin secretion from the tumor was probably under some degree of sympathetic control. This pattern of response, however, is not the rule in primary hyperreninism, because PRA unresponsiveness to postural stimulation has also been reported [12,19], On the other hand, acute converting enzyme inhibition by captopril did not cause the expected increment in PRA, in spite of an evident hypotensive and aldosterone-inhi biting effect, both signs of systemically effective convert ing enzyme inhibition.…”
Section: Discussionsupporting
confidence: 43%
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“…As far as active renin was concerned, orthostatism increased PRA, to suggest that, even in our patient as in others [6,7,10,14,18,19], renin secretion from the tumor was probably under some degree of sympathetic control. This pattern of response, however, is not the rule in primary hyperreninism, because PRA unresponsiveness to postural stimulation has also been reported [12,19], On the other hand, acute converting enzyme inhibition by captopril did not cause the expected increment in PRA, in spite of an evident hypotensive and aldosterone-inhi biting effect, both signs of systemically effective convert ing enzyme inhibition.…”
Section: Discussionsupporting
confidence: 43%
“…However, a correct preoperative diagnosis of the disease needed to go through the crucial step of the demonstration of unilateral renin secretion from the in volved kidney, in absence of renal vascular lesions. In our experience, as of others [5,13,14,19], this proved rather hard to obtain. One plausible explanation for it is that renin lateralization may be difficult to demonstrate when renal blood flow is normal -as it was probably in our patient -in contrast with that seen in renal artery stenosis, where the reduction in renal blood flow makes it easier to obtain positive results.…”
Section: Discussionmentioning
confidence: 57%
“…These two situations can be distinguished clinically by stimulatory tests: in renovascular hypertension plasma renin is elevated by upright posture or sodium restriction in the diet and ACE inhibitors dramatically increase plasma renin activity (captopril test (Muller et al, 1986)), while in renin-producing tumors controversial results (both preservation or loss of the renin response) have been reported (Conn et al, 1972;Hollifield et al, 1975;Anderson et al, 1989;Connor et al, 1978;Baruch et al, 1984;Gordon et al, 1990). In addition, infusion of angiotensin II or the use of saralasin, an angiotensin II antagonist have given controversial results.…”
Section: Discussionmentioning
confidence: 99%
“…A Mib I antibody revealed proliferative activity in less than 5% of the tumor cells. Electron microscopy failed to show the typical rhomboid shaped electron dense granules of juxtaglomerular cells partly due to insufficient tissue preservation (Robertson et al, 1967;Conn et al, 1972;Hollifield et al, 1975;Connor et al, 1978;Lopez et al, 1991).…”
Section: Localization Proceduresmentioning
confidence: 99%
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