Bone disease in pediatric chronic kidney disease - Test2 - elhamkhani - TriplyDB

Bone disease in pediatric chronic kidney disease

Bone disease in pediatric chronic kidney disease

http://www.wikidata.org/entity/Q26864102

about

Interventions for metabolic bone disease in children with chronic kidney disease Chronic kidney disease in children.Correction of lower limb deformities in children with renal osteodystrophy by guided growth technique.Renal formulas pretreated with medications alters the nutrient profile.Roles of Vitamins D and K, Nutrition, and Lifestyle in Low-Energy Bone Fractures in Children and Young Adults.

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Bone disease in pediatric chronic kidney disease

http://www.wikidata.org/entity/Q26864102

description

2013 nî lūn-bûn

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2013 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի ապրիլին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

@yue

2013年論文

@zh-hant

2013年論文

@zh-hk

2013年論文

@zh-mo

2013年論文

@zh-tw

2013年论文

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name

Bone disease in pediatric chronic kidney disease

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Bone disease in pediatric chronic kidney disease

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Bone disease in pediatric chronic kidney disease

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type

label

Bone disease in pediatric chronic kidney disease

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Bone disease in pediatric chronic kidney disease

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Bone disease in pediatric chronic kidney disease

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prefLabel

Bone disease in pediatric chronic kidney disease

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Bone disease in pediatric chronic kidney disease

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Bone disease in pediatric chronic kidney disease

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S00467-012-2324-4

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Pediatric Nephrology

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Bone disease in pediatric chronic kidney disease

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Katherine Wesseling-Perry

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P2860

FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis

Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO)

The parathyroid is a target organ for FGF23 in rats

Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism

Elevated fibroblast growth factor 23 is a risk factor for kidney transplant loss and mortality.

Loss-of-function ENPP1 mutations cause both generalized arterial calcification of infancy and autosomal-recessive hypophosphatemic rickets

Early control of PTH and FGF23 in normophosphatemic CKD patients: a new target in CKD-MBD therapy?

Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis

Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers.

The calcemic response to continuous parathyroid hormone (PTH)(1-34) infusion in end-stage kidney disease varies according to bone turnover: a potential role for PTH(7-84)

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s00467-012-2324-4

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569-76

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scholarly article

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1336689

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10.1007/S00467-012-2324-4

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4

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28

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2013-04-01T00:00:00Z

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1045762643

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23064662

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3594120

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