11β hydroxysteroid dehydrogenase type 2 enzyme is expressed in normotensive and hypertensive patients with renal disease

Nephrology ◽  
2008 ◽  
Vol 4 (1-2) ◽  
pp. 81-86
Author(s):  
Alicia N STEIN-OAKLEY ◽  
Julie A MAGUIRE ◽  
John DOWLING ◽  
Greg J PERRY ◽  
Zygmunt KROZOWSKI ◽  
...  
Nephrology ◽  
1998 ◽  
Vol 4 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Alicia STEIN‐OAKLEY ◽  
Julie MAGUIRE ◽  
John DOWLING ◽  
Greg PERRY ◽  
Zygmunt KROZOWSKI ◽  
...  

2008 ◽  
Vol 21 (6) ◽  
pp. 644-649 ◽  
Author(s):  
J. Henschkowski ◽  
A. E. Stuck ◽  
B. M. Frey ◽  
G. Gillmann ◽  
B. Dick ◽  
...  

2002 ◽  
Vol 102 (2) ◽  
pp. 203-211 ◽  
Author(s):  
Stan H.M. VAN UUM ◽  
Brian R. WALKER ◽  
Ad R.M.M. HERMUS ◽  
C.G.J. (Fred) SWEEP ◽  
Paul SMITS ◽  
...  

The 11β-hydroxysteroid dehydrogenase (11β-HSD) isoenzymes catalyse the interconversion of cortisol and cortisone. Type 1 11β-HSD mainly converts cortisone into active cortisol. Type 2 11β-HSD inactivates cortisol in mineralocorticoid target tissues, and its activity can be inhibited by glycyrrhetinic acid (GA). Inactivation of cortisol to cortisone is impaired in a subgroup of patients with primary hypertension. To study where this defect is located, we measured cortisol and cortisone concentrations in arterial plasma, in saliva and across the forearm at baseline and after administration of GA in normotensive and hypertensive subjects. GA (500mg) or placebo was administered orally to 20 normotensive subjects in a placebo-controlled double-blind fashion. Further, we compared the effect of GA in 20 patients with primary hypertension with that in 20 normotensive subjects. Cortisol and cortisone were measured in plasma from the brachial artery and vein and in saliva. Samples were obtained at 0, 90 and 150min. Forearm blood flow (FBF) was measured simultaneously. Forearm production of corticosteroid hormones was assessed by multiplying the arteriovenous difference in corticosteroid concentration by FBF. The cortisol/cortisone ratio in arterial plasma remained at baseline levels after placebo (4.9±1.2; mean±S.D.), while after GA the ratio increased similarly in normotensive subjects (12.3±3.4) and in hypertensive patients (12.2±3.7). A similar effect of GA on the salivary cortisol/cortisone ratio was found. In both normotensive subjects and hypertensive patients no forearm production of cortisol or cortisone could be demonstrated, either at baseline or after administration of GA. Thus, both before and after GA administration, we did not find any difference in systemic and salivary 11β-HSD type 2 activity between subjects with primary hypertension and normotensive controls. Further, both at baseline and after GA administration we were not able to demonstrate net inactivation or re-activation of cortisol and cortisone by the 11β-HSD isoenzymes in the forearm in either normotensive or primary hypertensive subjects.


2000 ◽  
Vol 58 (4) ◽  
pp. 1413-1419 ◽  
Author(s):  
Tanja Zaehner ◽  
Valmai Plueshke ◽  
Brigitte M. Frey ◽  
Felix J. Frey ◽  
Paolo Ferrari

2005 ◽  
Vol 12 (3) ◽  
pp. 151
Author(s):  
V. Fusi ◽  
C. Cuspidi ◽  
S. Meani ◽  
L. Lonati ◽  
C. Valerio ◽  
...  

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 587-594 ◽  
Author(s):  
H. Mitchell Perry ◽  
J. Philip Miller ◽  
Jane Rossiter Fornoff ◽  
Jack D. Baty ◽  
Mohinder P. Sambhi ◽  
...  

2021 ◽  
pp. 239936932098478
Author(s):  
Joana Marques ◽  
Patrícia Cotovio ◽  
Mário Góis ◽  
Helena Sousa ◽  
Fernando Nolasco

Diabetic nephropathy is a well known complication of diabetes mellitus and the leader cause of end -stage renal disease worldwide. Nonetheless, other forms of renal involvement can occur in diabetic population. Since it has prognostic and therapeutic implications, differentiating non-diabetic renal disease from diabetic nephropathy is of great importance. We report an 80-year-old man with well-controlled type 2 diabetes mellitus and hypertension, who presented with rapid deterioration of renal function, nephrotic proteinuria, microscopic hematuria and leukocyturia. The atypical clinical presentation prompted us to perform a kidney biopsy. A diagnosis of proliferative glomerulonephritis with monoclonal immunoglobulin deposits (light chain only variant) was made, with however some chronic histological aspects which made us took a conservative therapeutic attitude. We emphasize that other causes of chronic proteinuric kidney disease should be considered in patients with type 2 diabetes mellitus, based on clinical suspicion, absence of other organ damage and mostly if an atypical presentation is seen. We review the spectrum of monoclonal gammopathies of renal significance, focusing on this rare and newly describe entity.


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