Endocrine Abstracts

End stage renal disease (ESRD) is characterised by decreased renal synthesis of 1,25-dihydroxyvitamin D (1,25D). Therapeutic use of 1,25D analogues for the management of renal bone disease is routine. However ESRD patients are also deficient in 25D (the immediate precursor of 1,25D). Since 2014 UK guidelines recommend diagnosis and treatment of 25D deficiency/insufficiency in people with chronic kidney disease, but make no recommendations for dosage or monitoring. This, togeth...

Reduced renal synthesis of 1,25-dihydroxyvitamin D (1,25(OH)2D) from 25-hydroxyvitamin D (25OHD) in end stage renal disease (ESRD) results in low serum 1,25(OH)2D. This appears to be due to reduced renal cell function and elevated serum fibroblast growth factor 23 (FGF23). Treatment strategies have therefore focussed on 1,25(OH)2D or its synthetic analogues, alfacalcidol or paricalcitol. However this overlooks 25-hydroxyv...

Reduced renal synthesis of 1,25-dihydroxyvitamin D (1,25(OH)2D) from 25-hydroxyvitamin D (25OHD) in end stage renal disease (ESRD) results in low serum 1,25(OH)2D. This appears to be due to reduced renal cell function and elevated serum fibroblast growth factor 23 (FGF23). Treatment strategies have therefore focussed on 1,25(OH)2D or its synthetic analogues, alfacalcidol or paricalcitol. However this overlooks 25-hydroxyv...

Accelerated medial calcification is a major cause of premature cardiovascular mortality in people with chronic kidney disease. Evidence suggests that the concentration of extracellular Ca2+ and vascular smooth muscle cells play a pivotal role in the pathogenesis of vascular calcification. Extracellular Ca2+ is detected by the calcium-sensing receptor (CaSR). The CaSR is a G protein-coupled receptor that is expressed in a range of tissues, but characteriza...