ライフサイエンスコーパス: phosphaturia

1 blast growth factor-23 secretion, increasing phosphaturia.

2 r these associations differ by the degree of phosphaturia.

3 hosphate homeostasis primarily by increasing phosphaturia.

4 Phosphaturia after intestinal phosphate administration o

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

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

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

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

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

10 Finally, triple knockout mice present phosphaturia and hypophosphatemia, suggesting exacerbate

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

12 and the co-receptor alpha-Klotho to promote phosphaturia and reduce circulating 1,25D levels.

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

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

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

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

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

18 3 concentration increased after the onset of phosphaturia, followed by a decrease in plasma 1,25(OH)2

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

20 ger than WT littermates, and have heightened phosphaturia from downregulation of two key NaPi cotrans

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

22 mulation and improved metabolic acidosis and phosphaturia in the animals by normalizing the expressio

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

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

25 Phosphaturia is not elicited when phosphate is instilled

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

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

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

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

30 strate that FGF23 is not capable of inducing phosphaturia via FGFR4 and that FGFR4 does not promote o

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

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

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

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

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

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