There are two side-effects of hyperphosphataemia:
- Inhibition of vitamin D 'activation' in the kidney: The production of Vitamin D is complex, but in its final stage, if you must know, 25-hydroxycholecalciferol is α1-hydroxylated, to form 1,25-dihydroxycholecaliferol. This latter substance more handily called 'calcitriol', or the active form of vitamin D. The above chemical reaction is inhibited by high phosphate levels. Why? Calcitriol stimulates calcium and phosphate absorption from the gut, and so it makes sense that phosphate should inhibit calcitriol synthesis, to prevent its levels from getting too high. Nonetheless, a lack of active vitamin D also therefore leads to lower calcium levels, which has its own set of attendant problems.
- Calcium precipitations: Calcium readily binds with phosphate if either one of them is too high. This compound is then deposited in vessels and tissue, where it may cause damage. It is actually possible to quantify this risk, although this is obviously only an approximation: the danger is real once the product of the serum calcium and phosphate levels (both in mmol/L) is greater than 4.4.
How do you treat hyperphosphataemia? There are several strategies, but first line therapy usually exploits phosphate's keenness to bind to cations: calcium or aluminium salts are given orally, and they bind phosphate in the gut, preventing it from being absorbed. Calcium salts are especially handy, since in renal insufficiency there will often be a concomitantly low serum calcium level [why? see here], and any left over calcium can contribute towards making up this deficit.