Serum leptin in dialysis renal osteodystrophy

Coen, G; Ballanti, P.; Fischer, Maria Stephanie; Balducci, Alessandro; Calabria, Santo; Colamarco, Luisa; Zazzo, Giacomo Di; Lifrieri, Francesca; Manni, Micaela; Sardella, Daniela; Nofroni, Italo; Bonucci, E.

doi:10.1016/j.ajkd.2003.07.005

Cited by 36 publications

(20 citation statements)

References 21 publications

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“…Bone remodeling is regulated by multiple hormones, including those involved in endocrine regulation of energy metabolism, such as leptin. 29 In chronic renal failure, serum leptin is increased and inversely correlated to histomorphometric parameters of bone turnover and PTH, 30,31 suggesting that leptin might be implicated in low bone turnover and AC. 32 In a recent study, Lee et al 33 showed that osteoblasts exert an endocrine regulation on energy metabolism.…”

Section: Discussionmentioning

confidence: 99%

Association of Bone Activity, Calcium Load, Aortic Stiffness, and Calcifications in ESRD

London¹,

Marchais²,

Guérin³

et al. 2008

Journal of the American Society of Nephrology

257

181

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An inverse relationship between arterial calcifications and bone activity has been documented in patients with ESRD. Calcium overload is associated with arterial calcification, which is associated with arterial stiffening. Whether bone activity interacts with calcium load, aortic stiffness, or arterial calcification is unknown. This study assessed the impact of bone activity on the relationships between the dosage of calcium-containing phosphate binders and aortic stiffness (measured by pulse wave velocity) or abdominal aorta calcification score. Aortic stiffness and calcification were both positively associated with calcium load and negatively associated with bone activity. A significant interaction was found between dosage of calcium-containing phosphate binders and bone activity such that calcium load had a significantly greater influence on aortic calcifications and stiffening in the presence of adynamic bone disease. Independent of any other factor, including dosage of calcium-containing phosphate binders, adynamic bone was associated with greater aortic stiffening, suggesting cross-talk between the bone and arterial walls.

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Section: Discussionmentioning

confidence: 99%

Association of Bone Activity, Calcium Load, Aortic Stiffness, and Calcifications in ESRD

London¹,

Marchais²,

Guérin³

et al. 2008

Journal of the American Society of Nephrology

257

181

View full text Add to dashboard Cite

show abstract

“…Leptin is a powerful inhibitor of bone formation in vivo [51] and favors vascular calcification [52] . In ESRD, serum leptin is increased and associated with low PTH [53] , suggesting that in ESRD leptin might reduce bone activity and promote arterial calcifications.…”

Section: Bone As the 'Culprit' Of Arterial Alterations?mentioning

confidence: 99%

Soft Bone – Hard Arteries: A Link

London¹

2011

Kidney Blood Press Res

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Chronic kidney disease is characterized by mineral and various bone disorders associated with extraosseous and cardiovascular calcifications. Experimental studies and clinical observations in the general population and in chronic kidney disease patients show an inverse relationship between the extent of cardiovascular calcifications and bone mineral density or bone metabolic activity. Arterial calcification and osteoporosis are frequently observed in the same subjects and progress in parallel in postmenopausal women, and associations between histomorphometric indices of bone activity and vascular calcifications were also observed in patients with chronic and end-stage kidney diseases. The biological linkage between vascular calcifications and bone changes is certainly a part of the aging process, but in many studies these bone-vascular associations remained significant after adjustment for age, which suggests an age-independent causal relationship. Based on clinical and experimental evidence showing an association between bone disorders and functional and structural changes of the arterial system the concept of a bone-vascular axis was established complementary to the classical kidney-bone axis. Nevertheless, the factors or mechanisms accounting for these associations are not well understood, and could result from (1) arterial disease responsible for bone abnormalities; (2) action of common dysmetabolic or ‘toxic’ factors and mechanisms acting on bones and vessels, or (3) direct or indirect influence of bone cells and metabolism on the arterial system. This short review aims to illustrate these possible mechanisms.

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“…Leptin is a powerful inhibitor of in vivo bone formation (41) and facilitates vascular calcification (42). In ESRD, serum leptin is elevated and is associated with low PTH (43), suggesting that leptin might diminish bone activity and promote arterial calcifications in this setting.…”

mentioning

confidence: 99%

Bone–Vascular Axis in Chronic Kidney Disease

London¹

2009

Clinical Journal of the American Society of Nephrology

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C hronic kidney disease (CKD) is characterized by changes in mineral metabolism associated with alterations of its hormonal regulation and various forms of bone disease. In the past, these associations focused attention on the kidney-bone axis. The last decade has seen renewed interest on interactions among mineral metabolism disorders and extraosseous and cardiovascular calcifications observed in CKD or end-stage renal disease (ESRD). Vascular calcification is an active process similar to bone formation that implicates a variety of proteins involved in bone and mineral metabolism (1,2) and is considered part of a systemic dysfunction defined as CKD-mineral and bone disorder (3). Growing evidence linking bone with different functional and structural characteristics of the arterial tree has contributed to developing the concept of the bone-vascular axis (4).The first observations suggesting the existence of the bonevascular axis were the frequent associations of osteoporosis and atherosclerotic vascular calcifications observed in postmenopausal women (5-7). Longitudinal population-based studies revealed a relationship between the progression of vascular calcifications and bone demineralization, and others were identified between bone mineral density (BMD) and aortic or central artery calcifications (6), or coronary arteries in type 2 diabetes (8). The osteopenia-osteoporosis association was also linked with arterial functional indexes, such as aortic stiffness and interactions independent of calcifications, suggesting broader biologic interplay (9,10).Relationships between bone and vascular modifications were also observed in CKD and ESRD patients. In dialysis patients, coronary artery calcification score was found to be inversely correlated with vertebral bone mass (11,12). In addition, a high systemic arterial calcification score combined with bone histomorphometry suggestive of low bone activity was observed in hemodialysis patients (13,14). Arterial stiffening and low spine BMD or calcaneal osteopenia were significantly associated in CKD and hemodialysis patients (15)(16)(17).In the present issue of the Journal, Adragao et al. (18) provide new evidence linking altered bone metabolism to coronary calcifications in patients with stage-5 CKD on hemodialysis. In their cross-sectional study performed on 38 hemodialyzed patients, they analyzed the relationships between bone biopsy parameters (bone volume/total volume, bone formation rate/ bone surface, and activation frequency) and coronary calcifications determined by multislide computer tomography. Their principal conclusion was that low bone volume is associated with more coronary calcifications, whereas histomorphometric parameters of bone turnover were independent of coronary calcifications.Their results complete those of Barreto et al. (12), who found a negative correlation between coronary calcifications and trabecular bone volume or its thickness. The absence of correlations between histomorphometric indexes of bone turnover and coronary calcifications dif...

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Serum leptin in dialysis renal osteodystrophy

Cited by 36 publications

References 21 publications

Association of Bone Activity, Calcium Load, Aortic Stiffness, and Calcifications in ESRD

Association of Bone Activity, Calcium Load, Aortic Stiffness, and Calcifications in ESRD

Soft Bone – Hard Arteries: A Link

Bone–Vascular Axis in Chronic Kidney Disease

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