Bone mineral metabolism and its relationship to kidney disease in a residential care home population: a cross-sectional study.
BACKGROUND
Institutionalized older people have a high risk of bone fractures due to osteoporosis. In addition, chronic kidney disease (CKD) is highly prevalent in older people living in residential homes. Secondary hyperparathyroidism, poor calcium intake and deficiency of 1,25-dihydroxyvitamin D may lead to decreased bone mass in people with CKD. The present cross-sectional study assessed the relationship between markers of bone mineral metabolism and kidney function in a residential care home population.


METHODS
Older subjects were recruited from residential care homes and kidney function stratified by the estimated glomerular filtration rate (GFR). Parathyroid hormone (PTH), 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were measured in 188 residents not receiving vitamin D/calcium treatment [mean age 85 (range 68- 100) years, 75% female] and in 52 residents receiving vitamin D/calcium supplementation.


RESULTS
Amongst those not receiving vitamin D/calcium, median PTH increased with declining GFR (P < 0.0001), particularly as GFR (mL/min/1.73 m(2)) fell below 45. PTH concentration was suppressed by increasing 25-hydroxyvitamin D (P < 0.0001), but not 1,25-dihydroxyvitamin D (P > 0.05) concentration. Nearly all residents (92%) had 25-hydroxyvitamin D deficiency or insufficiency and this was uninfluenced by kidney function (P > 0.05). Concentration of 1,25-dihydroxyvitamin D declined with worsening renal function (P < 0.0004) but 1,25-dihydroxyvitamin D deficiency was prevalent at all stages of kidney disease, including amongst residents receiving vitamin D/calcium supplementation.


CONCLUSIONS
Vitamin D deficiency and secondary hyperparathyroidism are common in this population irrespective of renal function. However, as GFR falls below 45, the prevalence of secondary hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency increases. Unidentified CKD appears to exacerbate secondary hyperparathyroidism in this at risk population.
Carter
Joanne L
JL
Department of Clinical Biochemistry, East Kent Hospitals NHS Trust, Canterbury, Kent, UK. joanne.carter@ekht.nhs.uk
O'Riordan
Shelagh E
SE
Eaglestone
Gillian L
GL
Delaney
Michael P
MP
Lamb
Edmund J
EJ
D000368:Aged; D000369:Aged, 80 and over; D015519:Bone Density / Q000502:physiology; D001842:Bone and Bones / Q000378:metabolism*; D002908:Chronic Disease; D003430:Cross-Sectional Studies; D019587:Dietary Supplements; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D007674:Kidney Diseases / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology*; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood; D012112:Residential Facilities; D014807:Vitamin D / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D014808:Vitamin D Deficiency / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology
D010281:Parathyroid Hormone; D014807:Vitamin D; C097949:1,25-dihydroxyvitamin D; C104450:25-hydroxyvitamin D