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HOW TO TREAT 29
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HOW TO TREAT 29

Shypoetess / CC BY-SA 4.0 / bit. ly / 48IhTed
Figure 2. Diagram of renal corpuscle structure.
Figure 3. Renal artery stenosis.
Figure 4. Renal artery stenosis.
consider a referral to an endocrinologist
. Accurate diagnosis of Cushing’ s syndrome( see figure 7) can be challenging. Hypercorti-
as low renin essential hypertension( LREH) and is estimated to be present in one in four patients with hypertension and two in three
6, 7, 16-18, 25-33
Source:
Normal renin hypertension
solism can be demonstrated by two or more abnormal measurements in the following screening tests: a 24-hour urinary cortisol excretion, or a midnight salivary cortisol and /
patients with LRH. LREH is more common in certain groups, such as those of African descent and older age. 36 It is likely that the underlying disease processes in LREH cul-
10 %
LRH: PA
or overnight 1mg dexamethasone suppression test. Further investigations are guided by adrenocortico-
minate in an excess of salt and an expanded volume state, leading to low / suppressed renin. 37
66 % 34 %
22 %
LRH: Undefined
tropic hormone concentrations.
It has been suggested that many
Figure 8 outlines the adrenal
patients with LREH have a forme
steroidogenesis pathway.
Low renin essential hypertension
A large proportion of patients with
LRH do not have a clear diagnosis. This condition is often referred to
fruste / atypical manifestation of the known causes of LRH, that is, milder aldosterone excess secondary to bilateral adrenal hyperplasia, non-classical apparent mineralocorticoid excess with partial loss of 11-beta-hydroxysteroid
Figure 5. Estimated prevalence and aetiology of low renin hypertension.
2 %
LRH: Monogenic causes / cortisol excess