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Bile acid binding to sevelamer HCl.
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Changes in serum P at the end of treatment were −0.82 mmol/L in the JTT-751 group and −0.78 mmol/L in the sevelamer group, establishing non-inferiority of ferric citrate to sevelamer.
Thirty-four deaths occurred during the follow-up period: 23 in subjects randomized to calcium-containing phosphate binders and 11 in subjects randomized to sevelamer.
Mortality was borderline significantly lower in subjects randomized to sevelamer (5.3/100 patient years, confidence interval (CI) (2.2 8.5) compared to those randomized to calcium-containing binders (10.6/100 patient years, CI 6.3 14.9) (P=0.05).
The patients who received alphacalcidol first responded to sevelamer carbonate treatment with a reduction in iFGF23 levels as expected in contrast to patients receiving sevelamer carbonate first.
In a group of 34 patients switched to sevelamer for previously uncontrolled hyperphosphatemia, gastrointestinal complaints were reported in 23 patients (67%) (Almirall et al. 2004).
The primary efficacy measure was to show non-inferiority of calcium acetate/magnesium carbonate to sevelamer in lowering serum phosphate levels to below K/DOQI targets after 24 weeks of treatment.
Antibodies attack antigens by binding to them.
45° upon binding to PrfA.
ZNF198 exhibited minimal binding to HDAC1 alone.
Only the Δ5KA abolishes binding to PtdIns 3,4,5 P3.
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