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Quoted phrase not found in phrase index: "Pseudohyperaldosteronism type 2"
Page 1
Syndromes that Mimic an Excess of Mineralocorticoids.
Sabbadin C, Armanini D. Sabbadin C, et al. High Blood Press Cardiovasc Prev. 2016 Sep;23(3):231-5. doi: 10.1007/s40292-016-0160-5. Epub 2016 Jun 1. High Blood Press Cardiovasc Prev. 2016. PMID: 27251484 Review.
Enzymatic defects of adrenal steroidogenesis (deficiency of 17alpha-hydroxylase and 11beta-hydroxylase), mutations of mineralocorticoid receptor (MR) and alterations of expression or saturation of 11-hydroxysteroid dehydrogenase type 2 (apparent mineralocorticoid ex …
Enzymatic defects of adrenal steroidogenesis (deficiency of 17alpha-hydroxylase and 11beta-hydroxylase), mutations of mineralocorticoid rece …
Exploration for the real causative agents of licorice-induced pseudoaldosteronism.
Makino T. Makino T. J Nat Med. 2021 Mar;75(2):275-283. doi: 10.1007/s11418-021-01484-3. Epub 2021 Jan 22. J Nat Med. 2021. PMID: 33481180 Free PMC article. Review.
At this time, 3MGA inhibits type 2 11beta-hydroxysteroid dehydrogenase (11betaHSD2) in tubular cells to cause pseudoaldosteronism. ...Of a total of 97 patients, 67 detected GA in the serum (median 122 nM, 5 nM-1.8 M) and 68 detected compound 3 (median 239 nM, 2 …
At this time, 3MGA inhibits type 2 11beta-hydroxysteroid dehydrogenase (11betaHSD2) in tubular cells to cause pseudoaldosteron …
Heritable forms of hypertension.
Vehaskari VM. Vehaskari VM. Pediatr Nephrol. 2009 Oct;24(10):1929-37. doi: 10.1007/s00467-007-0537-8. Epub 2007 Jul 24. Pediatr Nephrol. 2009. PMID: 17647025 Free PMC article. Review.
In one group, the mutations involve the Na-transport machinery in distal tubule cells themselves: the distal convoluted tubule (DCT) cell and the principal cell of the collecting duct. Examples include Liddle's syndrome, with an activating mutation of epithelial Na …
In one group, the mutations involve the Na-transport machinery in distal tubule cells themselves: the distal convoluted tubule (DCT) cell an …
Inherited forms of mineralocorticoid hypertension.
Hassan-Smith Z, Stewart PM. Hassan-Smith Z, et al. Curr Opin Endocrinol Diabetes Obes. 2011 Jun;18(3):177-85. doi: 10.1097/MED.0b013e3283469444. Curr Opin Endocrinol Diabetes Obes. 2011. PMID: 21494136 Review.
SUMMARY: We provide an overview and diagnostic approach to apparent mineralocorticoid excess, glucocorticoid remediable aldosteronism, familial hyperaldosteronism type 2, Liddle's syndrome, Gordon's syndrome, activating mutations of the mineralo …
SUMMARY: We provide an overview and diagnostic approach to apparent mineralocorticoid excess, glucocorticoid remediable aldosteronism, famil …
Clinical and Molecular Perspectives of Monogenic Hypertension.
Levanovich PE, Diaczok A, Rossi NF. Levanovich PE, et al. Curr Hypertens Rev. 2020;16(2):91-107. doi: 10.2174/1573402115666190409115330. Curr Hypertens Rev. 2020. PMID: 30963979 Free PMC article. Review.
Pseudohypoaldosteronism type II (PHA-II), also known as Gordon's syndrome or familial hyperkalemic hypertension, is a more variable disorder typically characterized by hypertension, high plasma potassium and metabolic acidosis. ...In Liddle's syndrome, …
Pseudohypoaldosteronism type II (PHA-II), also known as Gordon's syndrome or familial hyperkalemic hypertension, is a more var …
11Beta-hydroxylase deficiency and other syndromes of mineralocorticoid excess as a rare cause of endocrine hypertension.
Melcescu E, Phillips J, Moll G, Subauste JS, Koch CA. Melcescu E, et al. Horm Metab Res. 2012 Nov;44(12):867-78. doi: 10.1055/s-0032-1321851. Epub 2012 Aug 29. Horm Metab Res. 2012. PMID: 22932914 Review.
Apart from primary aldosteronism, mineralocorticoid excess can be caused by congenital adrenal hyperplasia (CAH) due to mutations of the 11beta-hydroxylase and 17alpha-hydroxylase genes, by inactivating mutations of the glucocorticoid receptor gene (Chrousos syndrome), end …
Apart from primary aldosteronism, mineralocorticoid excess can be caused by congenital adrenal hyperplasia (CAH) due to mutations of the 11b …
Disorders of distal nephron function.
Sebastian A, Hulter HN, Kurtz I, Maher T, Schambelan M. Sebastian A, et al. Am J Med. 1982 Feb;72(2):289-307. doi: 10.1016/0002-9343(82)90822-1. Am J Med. 1982. PMID: 6277192 Review.
The pathophysiologic features of the following disorders of distal nephron function are reviewed: (1) pseudohypoaldosteronism, a heterogenous group of disorders in which the signs and symptoms are suggestive of aldosterone deficiency, but in which aldosterone levels are supernorm …
The pathophysiologic features of the following disorders of distal nephron function are reviewed: (1) pseudohypoaldosteronism, a heterogenou …
Monogenic forms of low-renin hypertension: clinical and molecular insights.
Khandelwal P, Deinum J. Khandelwal P, et al. Pediatr Nephrol. 2022 Jul;37(7):1495-1509. doi: 10.1007/s00467-021-05246-x. Epub 2021 Aug 20. Pediatr Nephrol. 2022. PMID: 34414500
These can chiefly be classified as causing (i) excessive aldosterone synthesis (familial hyperaldosteronism), (ii) dysregulated adrenal steroid metabolism and action (apparent mineralocorticoid excess, congenital adrenal hyperplasia, activating mineralocorticoid receptor mutation …
These can chiefly be classified as causing (i) excessive aldosterone synthesis (familial hyperaldosteronism), (ii) dysregulated adrenal ster …
Genetic determination of human essential hypertension.
Matsubara M. Matsubara M. Tohoku J Exp Med. 2000 Sep;192(1):19-33. doi: 10.1620/tjem.192.19. Tohoku J Exp Med. 2000. PMID: 11128865 Free article. Review.
The presence (insertion [I]) or absence (deletion [D]) of 287bp in intron 16 of angiotensin converting enzyme gene has also been examined in RAS, and the results suggest D polymorphism as a risk factor for hypertension in men. Other components in RAS, such as renin, angiotensinog …
The presence (insertion [I]) or absence (deletion [D]) of 287bp in intron 16 of angiotensin converting enzyme gene has also been examined in …
Juvenile hypertension, the role of genetically altered steroid metabolism.
Ferrari P, Bianchetti M, Frey FJ. Ferrari P, et al. Horm Res. 2001;55(5):213-23. doi: 10.1159/000049999. Horm Res. 2001. PMID: 11740142 Review.
Recently, the molecular basis of four forms of severe hypertension transmitted on an autosomal basis has been elucidated: (a) the glucocorticoid-remediable aldosteronism (GRA), (b) the syndrome of apparent mineralocorticoid excess (AME), (c) activating mutation of the mine …
Recently, the molecular basis of four forms of severe hypertension transmitted on an autosomal basis has been elucidated: (a) the glucocorti …
17 results