Animal data and cross-sectional human studies have established that chronic hyponatraemia predisposes to osteoporosis; the effects of acute hyponatraemia on bone turnover have not been determined. Our objective was to test the hypothesis that acute hyponatraemia leads to dynamic effects on bone turnover.A prospective observational pilot study.Bone turnover markers [C-terminal crosslinking telopeptide of type 1 collagen (CTX-1), N-propeptide of type 1 collagen (P1NP) and osteocalcin] were measured prospectively over one week in 22 eunatraemic patients with subarachnoid haemorrhage. Patients treated with glucocorticoids were excluded.Eight patients developed acute hyponatraemia, median nadir plasma sodium concentration 131 mmol/L (IQR 128-132), and 14 remained eunatraemic, nadir plasma sodium concentration 136 mmol/L (IQR 133-137). Significant main effects of hyponatraemia were found for P1NP (p=0.02) and P1NP:CTX-1 ratio (p=0.02), both fell in patients with acute hyponatraemia, with significant interaction between hyponatraemia and time from baseline for P1NP (p=0.02). Significant main effects of time from baseline (p<0.001) but not hyponatraemia (p=0.07) were found for osteocalcin. For CTX-1, significant main effects of time from baseline (p=0.001) but not hyponatraemia (p=0.65) were found. There was a positive correlation between change in P1NP:CTX-1 ratio and nadir plasma sodium concentration, r=+0.43, p=0.04. Median serum cortisol (measured on day 1, 3 and 7) was higher in the hyponatraemia group than in those who remained euntraemic, 545 nmol/L (IQR 373-778) versus 444 nmol/L (IQR 379-542) p=0.03.These data suggest that acute mild hyponatraemia is associated with a reduction in bone formation activity.