Hyperplasia of the Juxtaglomerular Complex with Hyperaldosteronism and Hypokalemic Alkalosis.

Gill, John R.; Bartter, F. C.; Pronove, Pacita; MacCardle, Ross C.

doi:10.7326/0003-4819-58-4-740_1

Cited by 475 publications

(2 citation statements)

References 26 publications

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“…When the prostaglandin synthetase inhibitor was stopped, there was a brisk return of prostaglandin E excretion to 77±9% and 108±11% of control on the 1st and 2nd days, respectively, and urinary sodium excretion on these 2 of treatment (P < 0.05). With this natriuresis, weight, urinary potassium, serum potassium, aldosterone excretion, and PRA returned to control values.…”

Section: Metabolic Effects Of Prostaglandin Synthetase Inhibitionmentioning

confidence: 96%

“…Patients with this syndrome have normal blood pressture, despite their hyperreninemia, and aldosteronism; their pressor response to intravenously administered angiotensin II or inorepinephrine is sul)normal (1,2). Voltume expanision with either saline or albumin does not change their blood pressure and does not suppress plasimia renin activity (PRA)' and aldosterone to normal values (3).…”

Section: Introductionmentioning

confidence: 99%

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The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Vinci¹,

Gill²,

Bowden³

et al. 1978

J. Clin. Invest.

120

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A B S T R A C T The kallikrein-kinin system was characterized in seven patients with Bartter's syndrome on constant metabolic regimens before, during, and after treatment with prostaglandin synthetase inhibitors. Patients with Bartter's syndrome had high values for plasma bradykinin, plasma renin activity (PRA), urinary kallikrein, urinary immunoreactive prostaglandin E excretion, and urinary aldosterone; urinary kinins were subnormal and plasma prekallikrein was normal. Treatment with indomethacin or ibuprofen which decreased urinary immunoreactive prostaglandin E excretion by 67%, decreased mean PRA (patients recumbent) from 17.3+5.3 (S.E.M.) ng/ml per h to 3.3±1.1 ng/ml per h, mean plasma bradykinini (patients recumbent) from 15.4±4.4 ng/ml to 3.9±0.9 ng/ml, mean urinary kallikrein excretion from 24.8±3.2 tosyl-arginine-methyl ester units (TU)/ day to 12.4±2.0 TU/day, but increased mean urinary kinin excretion from 3.8±1.3 ,ug/day to 8.5±2.5 ,ug/day. Plasma prekallikrein remained unchanged at 1.4 TU/ml. Thus, with prostaglandin synthetase inhibition, values for uriniary kallikrein and kinin and plasma bradykinin returned to normal pari passu with changes in PRA, in aldosterone, and in prostaglandin E. The

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Section: Metabolic Effects Of Prostaglandin Synthetase Inhibitionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Vinci¹,

Gill²,

Bowden³

et al. 1978

J. Clin. Invest.

120

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Potassium Losing Pyelonephritis

Gerstein¹

1969

Arch Intern Med

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Bartter's Syndrome

White¹

1972

Arch Intern Med

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Two brothers had evidence of Bartter's syndrome. Rapid intravenous infusions of saline reverted angiotensin insensitivity and elevated plasma renin activity to normal levels, suggesting that secondary stimulation of the renin-angiotensin-aldosterone system by a decreased extracellular volume (ECFV) may be a major defect in these patients. The data indicate that chronic ECFV depletion exists as a consequence of impaired distal sodium reabsorption. However, inexorable sodium loss does not occur, presumably due to enhanced proximal sodium reabsorption. The patients also exhibited renal wasting of potassium, in part independent of the effects of aldosterone. Bartter's syndrome appears to be the result of renal tubular defects in the handling of sodium and potassium. Evidence presented suggests this defect lies beyond the proximal part of the nephron.Bartter' s syndrome1 encompasses a group of patients with a unique form of hyperaldosteronism. These patients, many of whom have been seen as children, frequently present with growth retardation, polyuria, and weakness, and have been de¬ scribed in a recent review.2 They have been observed to be normotensive and without edema, hypokalemic, in¬ sensitive to the pressor effect of in¬ fused angiotensin (angiotensin insensitivity) and to have increased plasma renin activity (PRA), in¬ creased aldosterone production, and hyperplasia of the juxtaglomerular apparatus of the kidney. Unlike pa¬ tients with primary hyperaldosteronism who are hypertensive, these patients have normal blood pressure, and in several instances postural hypotension.3 4 A further contrast to primary hyperaldosteronism is the presence of high PRA and angioten¬ sin insensitivity.5 Their normal blood pressure also serves to distinguish Bartter's syndrome patients from those patients with renal artery ste¬ nosis or malignant hypertension who otherwise have a similar increase of PRA and angiotensin insensitivity.The metabolic abnormalities of Bart¬ ter's syndrome are similar to those of the familial hypomagnesemic disease described by Gitelman, et al." Bart¬ ter's syndrome patients very closely resemble, by clinical and laboratory examination, patients with secondary hyperaldosteronism from blood loss, salt deprivation, diuretics, or gas¬ trointestinal fluid loss, and, except for the absence of edema, those patients with secondary hyperaldosteronism associated with hypoalbuminemic states or congestive heart failure. The degree of hypokalemia is generally more severe in Bartter's syndrome than in the usual form of secondary hyperaldosteronism. Despite these similarities, attempts to identify a salt-losing defect to produce volume contraction and secondary aldosteronism or attempts to correct the ab¬ normalities of the renin-angiotensinaldosterone system by restoring a

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Hyperplasia of the Juxtaglomerular Complex with Hyperaldosteronism and Hypokalemic Alkalosis.

Cited by 475 publications

References 26 publications

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Potassium Losing Pyelonephritis

Bartter's Syndrome

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