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Clin Nephrol. 1991 Dec;36(6):274-80.

Do limited changes in phosphate intake modulate 1,25(OH)2D3 levels in early renal failure?

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Department of Internal Medicine, University of Heidelberg, Germany.


A high dietary phosphate load relative to GFR is thought to explain, at least in part, diminished renal 1-alpha hydroxylase activity in early renal failure (RF). To assess the role of dietary phosphate/GFR ratio in more detail, we examined the response of 1,25(OH)2D3 concentration to a controlled isolated reduction of dietary phosphate intake for up to 10 days with no change of Ca, Na and energy intake. We studied 7 healthy controls (2 male, 5 female, median age 45 years) and 6 non-nephrotic patients with early renal failure (RF) (3 males, 3 females, median age 55 years; median Cin 60.5ml/min/1.73 m2; 41-69). During an initial 3-day period of controlled diet with usual phosphate intake no difference of UVPi (median 27.6 mmol/day, 18.9-43.8) was found between controls and RF. A diet with 15 mmol Pi/day (confirmed by duplicate meal analysis) significantly reduced median UVPi (controls: 27.7 to 11.9 mmol/d; RF 27.4 to 14.1 mmol/d) with no change of median UVCa. Median day to day variation of 1,25(OH)2D3 levels (by RIA) in controls was 15.4%. Lowering dietary phosphate intake did not significantly change median 1,25(OH)2D3 levels in controls (45.7 vs. 38.3 pg/ml) and patients with RF, respectively (23.5 vs. 19.1 pg/ml). No changes of intact iPTH values were found. The experiment had a 68% power to detect a 15% change and a 99% power to detect a 30% change at a significance level of p less than 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)

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