Bone resorption and acute renal failure in the hypercalcaemic critically ill

Introduction

We have reported increased bone resorption without elevated bone formation in both hypercalcaemic and normocalcaemic critically ill patients. The extent to which acute renal failure (ARF) is a factor in the development of hypercalcaemia in this group is unknown.

Aims

To investigate the contribution of (ARF) to hypercalcaemia in the critically ill.

Methods

Twenty-three hypercalaemic (Gp 1) were compared to six normocalcaemic (Gp 2) mechanically ventilated, critically ill adults. Urinary pyridinoline (Pyr), deoxypyridinoline (Dpyr) and plasma carboxyterminal cross-linked telopeptide of type 1 collagen (ICTP) were measured as markers of bone resorption. Plasma carboxyterminal propeptide of type 1 procollagen (P1CP), bone specific alkaline phosphatase (BAP) and osteocalcin were measured as markers of bone formation. ARF was defined as the need for renal replacement therapy. For analysis the Mann–Whitney U and Fisher's exact tests were used (significance = P < 0.05).

Results

Medians (ranges) for indices of bone resorption and formation together with the prevalence of acute renal failure are presented in the Table.

Table

Increased bone resorption without an increase in bone formation was demonstrated in both groups, with no significant difference between the groups. ARF was significantly more prevalent in Gp 1.

Conclusion

Increased bone resorption leads to efflux of calcium from bone into the plasma pool in hypercalcaemic and normocalcaemic critically ill patients. Our results suggest that ARF may be a contributory factor to the development of hypercalcaemia.