Endocrine Abstracts

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.