Hyponatremia is associated with increased risk of bone fragility and fractures. In vitro studies suggest a role of hyponatremia in stimulating osteoclast activation, whereas other studies rather revealed a possible role of acute hyponatremia in impairing osteoblast function. We aimed to assess whether and how correction of hyponatremia in hospitalized patients with the syndrome of inappropriate antidiuresis (SIAD) has an impact on bone metabolism.
Material and methods
This is a pre-defined secondary analysis of 83 hospitalized patients with SIAD undergoing a randomized treatment for 5 days. Biochemical markers of bone resorption (CTX) and bone formation (PINP) were collected in serum at baseline and after the intervention (day 5). Bone formation index (defined as PINP/CTX) was calculated. Patients with steroid therapy (n = 6), fractures (n = 10), or whose data were missing (n = 16) were excluded from the analysis.
Out of 58 patients, 27 (47%) were normonatremic at day 5. These patients showed a 47.9 points higher bone formation index (95% CI 16.779.2, P = 0.0035) compared to patients with persistent hyponatremia at day 5. This observation was independent of age, sex, BMI, smoking habits, randomization arm, as well as baseline sodium and cortisol levels. Serum CTX increased similarly in the two groups (P = 0.76), whereas serum PINP increased in patients with normal sodium after intervention (P = 0.04), but not in persistent hyponatremic patients (P = 0.38).
Normalization of hyponatremia in hospitalized patients with SIAD results in an increased bone formation rate, suggesting a stimulation of osteoblast function.
22 May 2021 - 26 May 2021