Background
Vascular calcification is a recognised source of morbidity among mid-age and elderly subjects. Its development follows classical mineralisation pathways, inhibited by acidosis.

Aims
To examine the argument for using acetazolamide to retard vascular calcification.

Results
The final mechanism of tissue mineralization involves three processes, all of which are highly pH dependent. Calcium interacts with phosphate in its trivalent form, but this step is inhibited by pyrophosphate, the substrate for alkaline phosphatase. Separately, matrix vesicles create nucleation sites and indirectly disrupt vascular smooth muscle cells. Metabolic acidosis acts at every point to delay mineralization. The diuretic acetazolamide creates a sustained mild acidosis and phosphate loss and, though usually ineffective in the experimental model, has been used with success in certain clinical conditions.

Conclusion
We suggest that acetazolamide, well studied and tolerated, could be trialled in selected subjects to offset the progression of vascular calcification, through its dual action of lowering tissue pH and phosphate concentration.