The relationship between circulating Fibroblast growth factor 23 and bone metabolism factors in Korean hemodialysis patients
Department of Nephrology, Kyung Hee University School of Medicine, Dongdaemun-Gu, Seoul, 130-701, Korea. Clinical and Experimental Nephrology
(Impact Factor: 2.02).
04/2010; 14(3):239-43. DOI: 10.1007/s10157-010-0272-5
Fibroblast growth factor 23 (FGF-23) is a circulating factor that acts as a phosphaturic factor in the kidneys. It is also involved in several disorders of phosphate regulation and bone metabolism. We hypothesized that increased FGF-23 levels in patients with endstage renal disease (ESRD) on maintenance hemodialysis would be associated with increased bone demineralization, and we analyzed the relationship between FGF-23 levels and bone mineral density (BMD).
The serum level of FGF-23 was measured in this cross-sectional study, whose subjects consisted of 54 patients with ESRD on maintenance hemodialysis. Clinical parameters associated with hemodialysis and bone metabolism were measured. The relationship between serum FGF-23 and BMD and the factors affecting the serum level of FGF-23 were analyzed.
Serum FGF-23 levels were significantly higher in ESRD patients on maintenance hemodialysis than in normal persons (2961.4 vs. 30 pg/ml). Multiple regression analysis showed that increasing FGF-23 levels were associated with serum phosphate (r = 0.684, P < 0.001), but not with BMD or other bone metabolism factors. Factors affecting log(10)FGF-23 included the serum calcium phosphate product (beta = 0.603) and K (t)/V (integrated fractional clearance expressed per dialysis, beta = -0.244). These results were also seen in an analysis of the correlations based on T score or gender.
FGF-23 levels were positively associated with serum phosphate levels but were not correlated with BMD. The only factors affecting log(10)FGF-23 were the serum calcium phosphate product and K (t)/V. These findings suggest that FGF-23 may have no direct effect on bone mineralization, and further studies are warranted to examine the effects of FGF-23 on vitamin D metabolism.
Available from: David C Klonoff
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ABSTRACT: Bone disease is caused not only by increased bone turnover accompanying secondary hyperparathyroidism but also by factors such as bone metabolic disorder accompanying kidney disease and postmenopausal or age-related osteoporosis in hemodialysis patients. In this study, we investigated the effects of raloxifene on bone turnover markers and bone mineral density (BMD) in female hemodialysis patients to determine involvement of estrogen deficiency in bone disease.
The subjects were 47 female patients on maintenance hemodialysis. Raloxifene hydrochloride (60 mg) was administered to 21 patients for 1 year, and these patients were compared with a control group of 26 patients. Serum levels of N-terminal cross-linking telopeptide of type I collagen (NTx), bone alkaline phosphatase, and intact parathyroid hormone were measured, and BMD was determined by quantitative heel ultrasound as the speed of sound (SOS) in the calcaneus over this period.
NTx decreased after treatment with raloxifene for 1 year, but significantly increased in the control group. SOS increased after treatment with raloxifene for 1 year, but significantly decreased in the control group. Treatment with raloxifene resulted in a significant decrease of NTx and a significant increase of SOS in subgroups of patients aged <60 and ≥ 60 years.
Treatment with raloxifene can suppress a rise in NTx and increase bone mineral density in patients around the time of menopause and in postmenopausal patients of advanced age. A reduction in bone mineral density caused by estrogen deficiency may be involved in the development of bone disease in female hemodialysis patients.
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ABSTRACT: Fractures are common in patients with chronic kidney disease (CKD) and associated with substantially high morbidity and mortality. Bone mass measurements are commonly used to assess fracture risk in the general population, but the utility of these measurements in patients with CKD, and specifically among those on hemodialysis, is unclear. This review will outline the epidemiology and etiology of fractures in patients with CKD with a particular emphasis on men and women on hemodialysis. As well, we will summarize the published data, which describes the association between risk factors for fracture (including bone mass measurements, biochemical markers of mineral metabolism, and muscle strength) and fractures in patients with CKD. Patients with CKD suffer from fractures due to impairments in bone quantity, bone quality, and abnormalities of neuromuscular function. There is a paucity of evidence on the associations between bone quality, bone turnover markers, neuromuscular function, and fractures in patients with CKD. Furthermore, the complex etiology of fractures combined with the technical limitations of bone mineral density testing, both by dual energy X-ray absorptiometry (DXA) and by peripheral quantitative tomography (pQCT), limits the clinical utility of bone mass measurements for fracture prediction in CKD; this is particularly true among patients with stages 4 and 5 CKD. Further prospective studies to identify noninvasive measures of bone strength that can be used for fracture risk assessment are needed.
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