Inferring disease mechanisms from epidemiological data in chronic kidney disease: calcium and phosphorus metabolism.

BACKGROUND/AIMS: By applying numerical filtering to epidemiological data of 2,512 chronic kidney disease patients, we aimed to identify some of the underlying mechanisms of the calcium/phosphorus metabolism perturbations.

METHODS

The measured variables, serum calcitriol, calcidiol, total calcium (Ca) and phosphorus (P) and the urinary excretions of calcium and phosphorus, were paired in the same patients with the glomerular filtration rate (GFR) or the serum concentrations of parathormone (iPTH) (used as independent variables) numerically filtered with a moving average and partitioned into 15-25 frequency classes. All variables exhibited unimodal frequency distributions.

RESULTS

There was a steep fall of iPTH, P, and urinary excretion fractions of Ca and P up to a value of GFR in the range of 25-45 ml/min/1.73 m2. The increase in the phosphorus urinary excretion preceded the steep increase in iPTH. Except Ca, all factors exhibited their physiological correlation with iPTH when GFR was above 90 ml/min/1.73 m2 and reverted to a feedback correlation below 80 ml/min/1.73 m2.

CONCLUSION

The perturbation of mineral metabolism in chronic kidney disease results in the maintenance of a normal range of Ca and P acting as the controlled factors at the cost of large variations of iPTH, and calcium and phosphate urinary excretions behaving as controlling factors.