scholarly journals Osteoporosis in Patients with Chronic Kidney Diseases: A Systemic Review

2020 ◽  
Vol 21 (18) ◽  
pp. 6846 ◽  
Author(s):  
Chia-Yu Hsu ◽  
Li-Ru Chen ◽  
Kuo-Hu Chen
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
Fracture Risk ◽  
Renal Osteodystrophy ◽  
Bone Structure ◽  
Kidney Diseases ◽  
Treatment Strategies ◽  
Vitamin D Supplementation ◽  
Systemic Review ◽  
Lifestyle Modifications

Chronic kidney disease (CKD) is associated with the development of mineral bone disorder (MBD), osteoporosis, and fragility fractures. Among CKD patients, adynamic bone disease or low bone turnover is the most common type of renal osteodystrophy. The consequences of CKD-MBD include increased fracture risk, greater morbidity, and mortality. Thus, the goal is to prevent the occurrences of fractures by means of alleviating CKD-induced MBD and treating subsequent osteoporosis. Changes in mineral and humoral metabolism as well as bone structure develop early in the course of CKD. CKD-MBD includes abnormalities of calcium, phosphorus, PTH, and/or vitamin D; abnormalities in bone turnover, mineralization, volume, linear growth, or strength; and/or vascular or other soft tissue calcification. In patients with CKD-MBD, using either DXA or FRAX to screen fracture risk should be considered. Biomarkers such as bALP and iPTH may assist to assess bone turnover. Before initiating an antiresorptive or anabolic agent to treat osteoporosis in CKD patients, lifestyle modifications, such as exercise, calcium, and vitamin D supplementation, smoking cessation, and avoidance of excessive alcohol intake are important. Managing hyperphosphatemia and SHPT are also crucial. Understanding the complex pathogenesis of CKD-MBD is crucial in improving one’s short- and long-term outcomes. Treatment strategies for CKD-associated osteoporosis should be patient-centered to determine the type of renal osteodystrophy. This review focuses on the mechanism, evaluation and management of patients with CKD-MBD. However, further studies are needed to explore more details regarding the underlying pathophysiology and to assess the safety and efficacy of agents for treating CKD-MBD.

Vitamin D Supplementation and Fracture Risk

2011 ◽  
Vol 171 (3) ◽  
pp. 265 ◽  
Author(s):  
Heike A. Bischoff-Ferrari ◽  
Bess Dawson-Hughes ◽  
Susan J. Whiting
Keyword(s):  
Vitamin D ◽  
Fracture Risk ◽  
Vitamin D Supplementation

Renal osteodystrophy

2013 ◽  
pp. 1274-1282
Author(s):  
Thomas Bardin ◽  
Tilman Drüeke
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
Serum Calcium ◽  
Renal Osteodystrophy ◽  
Serum Phosphorus ◽  
Osteitis Fibrosa ◽  
Alkaline Phosphatases ◽  
Calcium Phosphorus ◽  
Turnover Markers ◽  
25 Oh Vitamin D

Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

Vitamin D supplementation and fracture risk: Evidence for a U-shaped effect

Maturitas ◽  
2020 ◽  
Vol 141 ◽  
pp. 63-70
Author(s):  
Panagiotis Anagnostis ◽  
Julia K. Bosdou ◽  
Eustathios Kenanidis ◽  
Michael Potoupnis ◽  
Eleftherios Tsiridis ◽  
...  
Keyword(s):  
Vitamin D ◽  
Fracture Risk ◽  
Vitamin D Supplementation

scholarly journals Bilateral Looser zones or pseudofractures in the anteromedial tibia as a component of medial tibial stress syndrome in athletes

2020 ◽  
Author(s):  
Julian Stürznickel ◽  
Nico Maximilian Jandl ◽  
Maximilian M. Delsmann ◽  
Emil von Vopelius ◽  
Florian Barvencik ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
High Stress ◽  
Vitamin D Supplementation ◽  
Lower Limbs ◽  
Medial Tibial Stress Syndrome ◽  
Mineral Density ◽  
Stress Syndrome ◽  
Vitamin D Levels ◽  
Common Diagnosis

Abstract Purpose Medial tibial stress syndrome (MTSS) represents a common diagnosis in individuals exposed to repetitive high-stress loads affecting the lower limb, e.g., high-performance athletes. However, the diagnostic approach and therapeutic regimens are not well established. Methods Nine patients, diagnosed as MTSS, were analyzed by a comprehensive skeletal analysis including laboratory bone turnover parameters, dual-energy X-Ray absorptiometry (DXA), and high-resolution peripheral quantitative computed tomography (HR-pQCT). Results In 4/9 patients, bilateral pseudofractures were detected in the mid-shaft tibia. These patients had significantly lower levels of 25-hydroxycholecalciferol compared to patients with MTSS but similar levels of bone turnover parameters. Interestingly, the skeletal assessment revealed significantly higher bone mineral density (BMD) Z-scores at the hip (1.3 ± 0.6 vs. − 0.7 ± 0.5, p = 0.013) in patients with pseudofractures and a trend towards higher bone microarchitecture parameters measured by HR-pQCT at the distal tibia. Vitamin D supplementation restored the calcium-homeostasis in all patients. Combined with weight-bearing as tolerated, pseudofractures healed in all patients and return to competition was achieved. Conclusion In conclusion, deficient vitamin D levels may lead to pseudofractures due to localized deterioration of mineralization, representing a pivotal component of MTSS in athletes with increased repetitive mechanical loading of the lower limbs. Moreover, the manifestation of pseudofractures is not a consequence of an altered BMD nor microarchitecture but appears in patients with exercise-induced BMD increase in combination with reduced 25-OH-D levels. The screening of MTSS patients for pseudofractures is crucial for the initiation of an appropriate treatment such as vitamin D supplementation to prevent a prolonged course of healing or recurrence. Level of evidence III.

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