Pseudohypoaldosteronism (PHA) is a condition that mimics hypoaldosteronism.[1] However, the condition is due to a failure of response to aldosterone, and levels of aldosterone are actually elevated, due to a lack of feedback inhibition.
This syndrome was first described by Cheek and Perry in 1958.[2] Later pediatric endocrinologist Aaron Hanukoglu reported that there are two independent forms of PHA with different inheritance patterns: Renal form with autosomal dominant inheritance exhibiting salt loss mainly from the kidneys, and multi-system form with autosomal recessive form exhibiting salt loss from kidney, lung, and sweat and salivary glands.[3]
Treatment of severe forms of PHA requires relatively large amounts of sodium chloride.
These conditions also involve hyperkalemia.[4]
Types include:
References
External links
See also
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| Pancreas/ glucose metabolism |
Hypofunction | |
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| Hyperfunction | |
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| Hypothalamic/ pituitary axes |
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| Height | |
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| Multiple | |
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noco (d)/cong/tumr, sysi/epon
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proc, drug (A10/H1/H2/H3/H5)
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| Abdominal |
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| Pelvic |
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| Any/all | |
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noco/acba/cong/tumr, sysi/epon, urte
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proc/itvp, drug (G4B), blte, urte
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| (1) Basic domains | |
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| (2) Zinc finger DNA-binding domains | |
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| (3) Helix-turn-helix domains | |
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| (4) β-Scaffold factors with minor groove contacts | |
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| (0) Other transcription factors | |
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| Ungrouped | |
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| Transcription coregulators | |
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See also transcription factors
- B structural
- perx
- skel
- cili
- mito
- nucl
- sclr
- DNA/RNA/protein synthesis
- membrane
- transduction
- trfk
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