Physicians' Academy for Cardiovascular Education

Chronic Kidney Disease & Mineral Bone Disorder:

Slides (presentation) - Feb. 20, 2012

Chronic Kidney Disease & Mineral Bone Disorder:
What are the drivers of disease?

Presentation prepared by
Prof John Cunningham
UCL Centre for Nephrology
The Royal Free Hospital and UCL Medical School, London

Presented at PACE Renal Master Class in Madrid, February 17-18, 2012


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Mechanisms in chronic kidney disease
Chronic Kidney Disease & Mineral Bone Disorder
Where is the initial “push” as GFR declines? At what are the early adaptive responses aimed?
Where is the initial “push” as GFR declines? At what are the early adaptive responses aimed?
Phosphate: the achilles heel of
Relationship Between GFR and TRP
Effect of Dietary Phosphate Restriction on PTH
“Trade-off”
Phosphate is a poor marker for SHPT in early CKD
Fibroblast Growth Factor-23 in Early Chronic Kidney Disease
Progression of SHPT: parathyroid hyperplasia
Impaired calcium sensing in SHPT
Calcimimetic Compounds Increase theSensitivity of the CaR to Calcium
PTH-Ca curve obtained before and after calcimimetic therapy
1,25-dihydroxyvitamin D not only a hormone
1,25(OH)2D3 and 25(OH)D3 deficiency and SHPT SEEK study
25-hydroxyvitamin D3 suppresses PTH synthesis
PT Injection with 22-oxacalcitriol
Slide 21
Regulation of calcitriol production by phosphate
Regulation of calcitriol production by phosphate
Phosphate restriction/supplementation in paediatric CKD
Adaptive responses are often more striking than the initial perturbation
Adaptive responses are often more striking than the initial perturbation

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