In:
Kidney and Blood Pressure Research, S. Karger AG, Vol. 40, No. 2 ( 2015), p. 153-165
Abstract:
〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Since the discovery of FGF23, secondary hyperparathyroidism (SHPT) in renal disease has been considered to result primarily from phosphorus retention rather than vitamin D deficiency. However, the impact of phosphorus restriction and vitamin D supplementation on SHPT is still ill defined. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We investigated the development of SHPT in a doxorubicin-induced proteinuric mouse model and tested different treatment strategies including a low phosphorus diet and substitution with native or active vitamin D in 129 S1/SvImJ wild-type mice. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Development of SHPT at day 30 was strongly related to the magnitude of induced proteinuria. In mice with a proteinuria 〈 100 mg/mg creatinine, SHPT was mild (PTH increase 2.4-fold), and serum levels of FGF23, phosphate and urea remained almost stable, whereas mice with heavy proteinuria ( 〉 100 mg/mg creatinine) developed marked SHPT (PTH increase 10.1-fold) accompanied by massive increase in FGF23 (27.0-fold increase), hyperphosphatemia (1.8-fold increase), renal failure (7.3-fold urea increase) and depletion of both 25-OH vitamin D and 1,25-OH vitamin D. Substitution with native or active vitamin D was unable to suppress SHPT, whereas a low-phosphorus diet (P 〈 sub 〉 i 〈 /sub 〉 content 0.013%) completely suppressed SHPT in mice with both mild and heavy proteinuria. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 The development of SHPT resulted from phosphate retention in this proteinuric model and could completely be suppressed with a low-phosphorus diet.
Type of Medium:
Online Resource
ISSN:
1420-4096
,
1423-0143
Language:
English
Publisher:
S. Karger AG
Publication Date:
2015
detail.hit.zdb_id:
1482922-8
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