Phosphate imbalance
Physiologically, the kidney eliminates or retains phosphate and calcium in order to keep both within a narrow normal range. However, in chronic kidney failure the excretion rate decreases and the balancing function is impaired. The lack of phosphate excretion leads to a positive phosphate balance, usually resulting in an increase of serum phosphate levels unless efforts are made to prevent this development. In addition, the impaired tissue is unable to synthesize sufficient activated vitamin D which leads to a concomitant decrease of calcium uptake through the gastrointestinal tract, resulting in low serum calcium levels.
To maintain a normal calcium serum level, calcium is mobilized from internal stores: the bones. This is accomplished by an increase in a hormone known as "parathyroid hormone" which is produced by the parathyroid gland leading to realase of calcium and phosphate from the bones. If this hormone is produced excessively (a state called hyperparathyroidism) the long-term consequences are impaired bone architecture and fragility (osteodystrophy). The disorder of the body mineral equilibrium as a consequence of persistent kidney failure leads to hyperphosphataemia, hypocalcaemia and chronically elevated parathyroid hormone levels, all of them part of the so called CKD-Mineral Bone Disorder (MBD).
The treatment of hyperphosphataemia is crucial, because it worsens hyperparathyroidism, contributes to the calcification of blood vessels, and is associated with high cardiovascular mortality. Attaining a neutral phosphate balance is the goal of hyperphosphataemia management in CKD, but this is a challenge. Control of phosphate depends on its removal during dialysis, on the limitation of dietary phosphate intake, and on the application of efficient phosphate binding medication.
