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Primary Aldosteronism
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
To avoid missing any patients with PA, the screening tests are set to be highly sensitive (Figure 62.1). This implies that they often give false positive results that must be identified to the aim of excluding the patient from AVS. The oral sodium loading test, the saline infusion test, the captopril challenge test and the fludrocortisone with salt loading test have been put forward as ‘confirmatory’ tests. In reality, what they actually serve for is to exclude false positive results, because at the prevalence rate commonly encountered at hypertension centres their negative predictive (exclusion) value largely exceeds their positive predictive (confirmatory) value (56,57).
Duplicated adrenal veins in primary aldosteronism misdiagnosed with ectopic aldosteronoma due to apparent bilateral aldosterone suppression
Published in Blood Pressure, 2023
Jingwen Yu, Cunxia Fan, Weiping Wei, Haiwei Liu, Tuanyu Fang, Huibiao Quan, Kaining Chen, Yuhai Zhang
The diagnosis of PA was ascertained after the captopril-challenge test. The subsequent AVS procedure conducted in our institution results revealed bilateral suppression of the aldosterone secretion (Aldosterone/Cortisol ratios from both adrenal veins were lower than those in the peripheral veins). This indicated the possibility of ectopic aldosteronoma because of the murky margin between the right-side adenoma and the liver (Table 1). Under sufficient communication and informed consent, the patient agreed to undergo a laparoscopic adrenalectomy on the right side. The resected mass illustrated duplicated right adrenal veins (Figure 2) and the cut surface was typically golden (Figure 3A). Haematoxylin and Eosin (HE) staining identified adrenal adenoma cells (Figure 3B). After surgery, the patient returned to antihypertensive monotherapy (Nifedipine) and achieved normotension, normokalemia, and a normal aldosterone-renin ratio. He reached complete biochemical and clinical remission one month later.
Clinical characteristics of concurrent primary aldosteronism and renal artery stenosis: A retrospective case–control study
Published in Clinical and Experimental Hypertension, 2021
Xu Meng, Yan-Kun Yang, Yue-Hua Li, Peng Fan, Ying Zhang, Kun-Qi Yang, Hai-Ying Wu, Xiong-Jing Jiang, Jun Cai, Xian-Liang Zhou
All patients were diagnosed with PA according to the recommendation of the Endocrine Society practice guidelines (16). Orthostatic aldosterone renin ratio (ARR) was used as the case detection test for PA (17), which was calculated by dividing PAC by PRA. A subsequent intravenous saline infusion test (SIT) or captopril challenge test (CCT) was performed as a confirmatory test if screening orthostatic ARR was >30 ng dL−1/ng mL−1 h−1 (7). A PA diagnosis was confirmed when the PAC level decreased less than 30% of the baseline level in captopril challenge test, or higher than 10 ng/dL after saline injection. The tests were repeated when results were inconclusive or difficult to interpret.
Liddle syndrome misdiagnosed as primary aldosteronism is caused by inaccurate aldosterone-rennin detection while a novel SCNN1G mutation is discovered
Published in Blood Pressure, 2022
Yaling Yang, Chenwei Wu, Duoduo Qu, Xinyue Xu, Lili Chen, Quanya Sun, Xiaolong Zhao
A 21-year-old female patient who complained of recurrent lower limb weakness for 5 years was admitted to the endocrinology ward. Two years ago, she visited a neurological clinic because of similar limb weakness. Her medical records then showed her BP was 130/70 mmHg, plasma potassium was 1.6 mmol/l (normal range, 3.5–5.3 mmol/l), aldosterone was 37.75 ng/dl (normal range, 4–31 ng/dl), renin was 0.73 ng/l (normal range 4–38 ng/dl) and aldosterone renin ratio (ARR) was 40.59 (positive for screening if >3.8). The aldosterone level was not inhibited in the captopril challenge test (data not available). She was diagnosed with primary aldosteronism and treated with spironolactone 20 mg bid and potassium chloride. However, the weakness of her limbs still emerged intermittently. She had no history of vomiting or diarrhoea, using diuretic or laxative, or using liquorice or glycyrrhetinic acid. There is no evidence of cortisol overabundance. Spironolactone had been stopped 1 month before admission and only a potassium chloride supplement was used. Her BP was 158/105 mmHg (not on anti-hypertension treatment) and hypertension was further confirmed after several repeated measurements. Plasma potassium was 3.2 mmol/l while synchronous 24 h urinary potassium was 96.2 mmol/day. Aldosterone was 20.85 ng/dl (normal range, 4–31 ng/dl), renin was 1.09 ng/l (normal range, 4–38 ng/dl) and ARR was 19.13 (positive for screening if >3.8). Saline infusion test showed aldosterone decreased from 28.78 to 22.86 ng/dl, indicating not suppressed. Enhanced CT scanning of the adrenal gland showed the medial branch of the left adrenal gland was slightly thickened, which was about 4 mm wide. Serum cortisol and plasm adrenocorticotropic hormone and 24 h urinary free cortisol were normal. Plasma-free or urinary-fractionated metanephrines were normal. Primary aldosteronism was diagnosed then. Considering other family members such as father, aunt and grandmother had hypertension and hypokalaemia, then we suspected the diagnose of glucocorticoid-remediable aldosteronism and carried out a dexamethasone inhibition test and gene test. However, the test was negative (aldosterone decreased from 38.53 ng/dL to 19.44 ng/dL after 4 mg dexamethasone was administrated in 48 h).