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Nephron Clin Pract. 2009;112(3):c137-47. doi: 10.1159/000214208. Epub 2009 Apr 24.

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

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Department of Nephrology, Fernando da Fonseca Hospital, Lisbon, Portugal.



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.


The measured variables, serum calcitriol, calcidiol, total calcium ([Ca](s)) and phosphorus ([P](s)) 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 (i[PTH](s)) (used as independent variables) numerically filtered with a moving average and partitioned into 15-25 frequency classes. All variables exhibited unimodal frequency distributions.


There was a steep fall of i[PTH](s), [P](s), 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 i[PTH](s). Except [Ca](s), all factors exhibited their physiological correlation with i[PTH](s) when GFR was above 90 ml/min/1.73 m2 and reverted to a feedback correlation below 80 ml/min/1.73 m2.


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

[Indexed for MEDLINE]

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