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11β hydroxysteroid dehydrogenase type 2 enzyme is expressed in normotensive and hypertensive patients with renal disease
Author(s) -
STEINOAKLEY Alicia,
MAGUIRE Julie,
DOWLING John,
PERRY Greg,
KROZOWSKI Zygmunt,
THOMSON Napier
Publication year - 1998
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1046/j.1440-1797.1998.d01-19.x
Subject(s) - medicine , endocrinology , nephrosclerosis , mineralocorticoid receptor , kidney , aldosterone , mineralocorticoid
The enzyme 11β hydroxysteroid dehydrogenase type 2 (11βHSD2) converts glucocorticoids to their 11‐keto metabolites, permitting binding of aldosterone to the non‐selective mineralocorticoid receptor. Recent studies have suggested that 11βHSD deficiency may be implicated in essential hypertension and renal disease. Using an antibody against a peptide deduced from the cDNA sequence, the renal expression of 11βHSD2 was examined in patients with advanced stages of renal disease and associated hypertension, patients with primary hypertension resulting in renal damage, and patients with preserved or mildly damaged renal architecture without concomitant hypertension. Despite variable degrees of tubulointerstitial damage, 11βHSD2 was expressed in distal convoluted tubules and collecting ducts in all patient groups. Collapsed tubules retained strong immunoreactivity, but decreased staining was apparent in dilated tubules. There was weak staining of the thick ascending limb of Henle. Variable glomerular expression of 11βHSD2 was observed. Our results therefore suggest that absence of renal 11βHSD2 is not a prominent feature of hypertensive nephrosclerosis, or primary renal disease associated with hypertension.