ライフサイエンスコーパス: phosphaturia

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1 r these associations differ by the degree of phosphaturia.

2 blast growth factor-23 secretion, increasing phosphaturia.

3 Phosphaturia after intestinal phosphate administration o

4 velop a Fanconi-like syndrome of glucosuria, phosphaturia, aminoaciduria, low molecular weight protei

5 tric Pi loading elicited similar but delayed phosphaturia and endocrine responses but did not affect

6 se it is a circulating protein that promotes phosphaturia and hypophosphatemia and blunts compensator

7 vel factor(s), phosphatonin(s), which causes phosphaturia and hypophosphatemia by cAMP-independent pa

8 Recombinant FGF-23 induces phosphaturia and hypophosphatemia in vivo, suggesting th

9 e infusion of rat recombinant FGF23 enhanced phosphaturia and increased renal FGFR1 expression; howev

10 esulted in low molecular weight proteinuria, phosphaturia, and acidemia.

11 tho had preserved levels of Klotho, enhanced phosphaturia, better renal function, and much less calci

12 of several candidate phosphatonins, promotes phosphaturia, but whether it also affects intestinal pho

13 y, high FGF23 levels increase FGFR1, whereas phosphaturia decreases Klotho expression through the act

14 Denervation of the kidney does not attenuate phosphaturia elicited after intestinal phosphate adminis

15 3 concentration increased after the onset of phosphaturia, followed by a decrease in plasma 1,25(OH)2

16 ntravenous infusion caused hypophosphatemia, phosphaturia from decreased proximal phosphate reabsorpt

17 eem to be an acute postprandial regulator of phosphaturia in CKD or in health, but inappropriate post

18 Recent data identifying a novel mechanism of phosphaturia in X-linked hypophosphatemic rickets, autos

19 osphate levels; is associated with increased phosphaturia independent of parathyroid hormone (PTH); a

20 Phosphaturia is not elicited when phosphate is instilled

21 ressive increases in levels of FGF23 enhance phosphaturia on a per-nephron basis and inhibit calcitri

22 liorates vascular calcification by enhancing phosphaturia, preserving glomerular filtration, and dire

23 Fibroblast growth factor-23 (FGF23) induces phosphaturia through its effects on renal tubules.

24 ravenous or intestinal Pi bolus causes rapid phosphaturia through mechanisms requiring PTH and downre

25 ation of FGF23 by anti-FGF23 administration, phosphaturia was still abundant, Klotho expression remai

26 Since natriuresis as well as phosphaturia were observed in all animals, the sodium ef

27 e expression of renal Klotho is modulated by phosphaturia, whereas the FGFR1 expression is regulated

28 however, only intravenous Pi loading caused phosphaturia, which was blunted and transient compared w

29 it enhanced sympathetic nervous activity and phosphaturia with decreased bone density.

30 and creatinine clearance and an increase in phosphaturia within 10 minutes.

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