Acquired Primary Hypoaldosteronism Due to an Isolated Zona Glomerulosa Defect

Williams, Fred A.; Schambelan, Morris; Biglieri, Edward G.; Carey, Robert M.

doi:10.1056/nejm198312293092606

Cited by 22 publications

(5 citation statements)

References 27 publications

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“…This entity has been observed in patients with chronic renal insufficiency associated with diabetes mellitus or interstitial nephropathies [1, 3, 4, 5]. Selective hypoaldosteronism also results from isolated defects in zona glomerulosa function (hyperreninemic hypoaldosteronism) [6], and this condition has been identified in patients with critical illness [7, 8], diabetic nephropathy [4, 9], deficiency of angiotensin-converting enzyme [10], insensitivity of the zona glomerulosa to angiotensin II [11], carcinoma metastatic to the adrenal glands [12], and heparin administration [13]. …”

Section: Introductionmentioning

confidence: 99%

Selective Hypoaldosteronism due to Combined Defects of the Conversion from Inactive Renin to Active Renin and the Aldosterone Biosynthesis from Corticosterone

Muto

Akai²,

Ono³

et al. 2001

Nephron

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A 24-year-old Japanese woman with IgA nephropathy exhibited a decreased serum aldosterone level with normal plasma renin activity after toxemia of pregnancy. Our studies revealed selective hypoaldosteronism with normal adrenoglucocorticoid functions. Levels of serum corticosterone and deoxycorticosterone were normal. Resting plasma renin activity was normal, and plasma levels of total and inactive renin were increased. Rapid ACTH administration failed to stimulate any secretion of aldosterone, whereas it adequately increased serum cortisol, deoxycorticosterone, and corticosterone concentrations. Responses of both plasma renin activity and serum aldosterone level to the furosemide-posture challenge were blunted. Angiotensin II also failed to stimulate any secretion of aldosterone despite a progressive rise in blood pressure and an appropriate increase in serum corticosterone. These results suggest that combined defects of the conversion from inactive renin to active renin and aldosterone biosynthesis are the causes of selective hypoaldosteronism in our patient.

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Section: Introductionmentioning

confidence: 99%

Selective Hypoaldosteronism due to Combined Defects of the Conversion from Inactive Renin to Active Renin and the Aldosterone Biosynthesis from Corticosterone

Muto

Akai²,

Ono³

et al. 2001

Nephron

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“…In deed, several previous studies have indicated that such an adrenal biosynthetic defect causes the syndrome of hy poaldosteronism [20][21][22][23]. Tuck et al [21] have shown that in 5 diabetic patients with hypoaldosteronism, the plasma aldosterone response to dietary salt restriction, ACTH and angiotensin II administration is markedly attenuated while the 18-hydroxycorticosterone response was normal.…”

Section: Discussionmentioning

confidence: 97%

Effect of Dopaminergic Blockade on Plasma Aldosterone in Acquired Hypoaldosteronism

Krishna

Chusid²,

Hoeldtke³

1987

Nephron

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The pathogenesis of acquired hypoaldosteronism, a frequent cause of hyperkalemia in patients with chronic renal failure, is poorly understood. The present studies were undertaken to investigate the role of dopamine in suppressing mineralocorticoid secretion in this syndrome. We studied the plasma aldosterone response to dopaminergic blockade with metoclopramide in 11 patients with chronic renal failure (5 of whom were hyperkalemic) and 7 normal controls. Following repetitive doses of metoclopramide, the normokalemic chronic renal failure patients showed an exaggerated aldosterone response (peak aldosterone 50 ± 5 ng/dl or 1,385 ± 138 pmol/l) compared to normal controls (24 + 4 ng/dl or 665 ± 110 pmol/l). In the hyperkalemic chronic renal failure patients, however, metoclopramide failed to induce a significant increase in plasma aldosterone (peak aldosterone 13 ± 3 ng/dl or 360 ± 83 pmol/l). By contrast, metoclopramide stimulated prolactin secretion in both normokalemic and hyperkalemic chronic renal failure patients. The plasma renin activity and serum potassium values were unchanged in all 3 groups. Our data show that dopaminergic blockade with metoclopramide fails to stimulate aldosterone secretion in patients with acquired hypoaldosteronism. Thus this syndrome does not result from enhanced dopaminergic inhibition of aldosterone, but rather from an independent abnormality in aldosterone biosynthesis.

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“…45], (3) In these patients there is a defect in the conversion of pro renin or 'big-renin' into active renin, leading to an accu mulation of the former in the plasma [3,26], (4) The expansion in cell volume that this kind of patient may display could be a factor in determining the hyporeni nemic state [46], (5) In recent years, considerable impor tance has been given to prostaglandins (PGs) as media tors in renin synthesis. Certain HH patients present a decreased urinary PGE: and prostacyclin excretion [47][48][49][50][51], (6) In some patients with HH, a concurrent primary defect in adrenal aldosterone synthesis has been reported [26,52], Although, from a theoretical point of view, all these factors could be related to a deficit in renin, the possible extent of the influence of each remains to be established.…”

Section: Discussionmentioning

confidence: 99%

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

Villoria

Núñez²,

Miralles³

et al. 1988

Am J Nephrol

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Plasma renin activity, plasma aldosterone levels and renal tubular capacity to excrete hydrogen ions were studied in 13 patients suffering from diabetes mellitus with a creatinine clearance of less than 40 ml/min. The results were compared with those obtained in a control group, in a group of nondiabetic subjects with chronic renal failure (CRF) and in a group of diabetic patients without CRF. Twelve of the thirteen diabetic patients with CRF had data characteristic of hyporeninemic hypoaldosteronism associated with type IV renal tubular acidosis. On comparing the results with those of the other two groups of patients, it was observed that the manifestations of the latter two groups considered separately were different from those of the problem group, although in the diabetic patients with normal glomerular filtration rate (GFR) hyporeninism but not hypoaldosteronism was present accompanied by a lower net acid excretion (p < 0.001) due to a lower excretion of NH₄ (p < 0.05) and titratable acid (p < 0.001) when the patients were challenged with an NH₄C1 overload. We believe that a conjunction of diabetes and renal failure is necessary for the diabetic patients with a decrease in GFR to show hyporeninemic hypoaldosteronism and type IV tubular acidosis.

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Acquired Primary Hypoaldosteronism Due to an Isolated Zona Glomerulosa Defect

Cited by 22 publications

References 27 publications

Selective Hypoaldosteronism due to Combined Defects of the Conversion from Inactive Renin to Active Renin and the Aldosterone Biosynthesis from Corticosterone

Selective Hypoaldosteronism due to Combined Defects of the Conversion from Inactive Renin to Active Renin and the Aldosterone Biosynthesis from Corticosterone

Effect of Dopaminergic Blockade on Plasma Aldosterone in Acquired Hypoaldosteronism

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

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