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Endocrine Abstracts (2020) 70 AEP51 | DOI: 10.1530/endoabs.70.AEP51

1Hospital universitario Clínico San Carlos, Endocrinología, Madrid, Spain; 2Hospital universitario Fundación Jimenez Díaz, Endocrinología, Madrid, Spain


Isolated acquired hypoaldosteronism (HA) is considered to be a cause of hypovolemic hyponatremia (HH) with urinary sodium loss (UNaL) and hyperkalemia/upper-limit serum potassium (SK). However, some authors question the presentation of hyponatremia of these characteristics in the absence of Addison’s disease (AD).We present a series of patients with HA.

Methods: Aretrospective study of 70 cases of HH with UNaL (UNa > 25 mmol/l) and SK ≥ 5 mmol/l or in upper limits (≥ 4.8 mmol/l) with inadequately low urinary potassium (UK), in absence of oliguria. Patients were assessed for hyponatremia by the Endocrinology Department of a tertiary hospital, from 2012–2019. All presented a low central venous pressure (indicated by the internal jugular vein pulse). AD was ruled out as follows: basal cortisol > 15 µg/dl, or basal cortisol between 10-15 µg/dl with ACTH < 40 pg/ml or use of pharmacological doses of glucocorticoids (GC) during the episode. Reference aldosterone (RIA) values: 90-200 pg/ml.

Results: 44/70 (62.9%) were women, mean age: 75.5 years (SD: 12.7). Mean values at diagnosis:serum Sodium 128.5 mmol/l (SD: 5.80), SK 5.5 mmol/l (SD: 0.4), UK 28.8 mmol/l (SD: 11.3), bicarbonate 21.5 mmol/l (SD: 3.2), trans-tubular potassium gradient 4.2 (SD: 1.2). 66/70 (94.3%) presented hyperkalemia with a mean zenith SK of 5.8 mmol/l (SD: 0.5), 67.9% presented metabolic acidosis (MA) with normal anion GAP, 66% hyperkalemia with MA. Morning serum cortisol was available in 54 cases, mean cortisol without GC: 17.2 µg/dl (SD: 5.2). AD was diagnosed in 3/70 cases (4.3 %), AD was ruled out in 43/70 cases (61.4%). 24/70 cases were “indeterminate”, requiring further testing and follow-up, during which no additional cases of AD were diagnosed. In 29/43 patients with AD ruled out, serum aldosterone was measured during the episode, permitting differential diagnosis of HA. 16 cases were secondary to aldosterone deficit, with low aldosterone levels: median aldosterone 52 pg/ml [IQR: 21.5–82.5]. 7 cases were due to mineralocorticoid resistance, with elevated aldosterone levels: median aldosterone 258 pg/ml [IQR:223–293]. 6 cases presented a combination of aldosterone deficit and resistance, with inadequately “normal” aldosterone levels for hyperkalemia: median aldosterone 153.5 pg/ml [IQR: 129.35–177.65].

Conclusion: Isolated acquired hypoaldosteronism, due to aldosterone deficit and/or mineralocorticoid resistance, can induce hypovolemic hyponatremia. Furthermore, it is a more frequent cause of hypovolemic hyponatremia with urinary sodium loss and hyperkalemia than is Addison’s Disease, in patients studied for hyponatremia.

Volume 70

22nd European Congress of Endocrinology

Online
05 Sep 2020 - 09 Sep 2020

European Society of Endocrinology 

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