Abstract
Bone disorders are a common complication of chronic kidney disease (CKD), obesity and gut malabsorption. Secondary hyperparathyroidism (SHPT) is defined as an appropriate increase in parathyroid hormone (PTH) secretion, driven by either reduced serum calcium or increased phosphate concentrations, due to an underlying condition. The available evidence on the effects of dietary advice on secondary hyperparathyroidism confirms the benefit of a diet characterized by decreased phosphate intake, avoiding low calcium and vitamin D consumption (recommended intakes 1000–1200 mg/day and 400–800 UI/day, respectively). In addition, low protein intake in CKD patients is associated with a better control of SHPT risk factors, although its strength in avoiding hyperphosphatemia and the resulting outcomes are debated, mostly for dialyzed patients. Ultimately, a consensus on the effect of dietary acid loads in the prevention of SHPT is still lacking. In conclusion, a reasonable approach for reducing the risk for secondary hyperparathyroidism is to individualize dietary manipulation based on existing risk factors and concomitant medical conditions. More studies are needed to evaluate long-term outcomes of a balanced diet on the management and prevention of secondary hyperparathyroidism in at-risk patients at.
Highlights
Bone and mineral metabolism is characterized by a complex interaction between minerals and hormones such as calcium, phosphate and magnesium, parathyroid hormone (PTH), fibroblast growth factor-23 (FGF23) and active vitamin D (1,25(OH)2D3)
In this article, we reviewed the available literature regarding the association between diet and all causes of secondary hyperparathyroidism
In case of a low calcium diet, the 1,25(OH)2D3-dependent transcellular intestinal uptake of calcium prevails [69]. Both vitamin D and animal-derived calcium intake have been inversely correlated with PTH [126], some other authors observed a null effect of total dietary calcium on the risk for Secondary hyperparathyroidism (SHPT) [40]
Summary
Bone and mineral metabolism is characterized by a complex interaction between minerals and hormones such as calcium, phosphate and magnesium, parathyroid hormone (PTH), fibroblast growth factor-23 (FGF23) and active vitamin D (1,25(OH)2D3). Bone disorders are a common complication of chronic kidney disease (CKD) and dietary advice plays a fundamental role in its management [1,2]. We review the physiology and pathophysiology of bone and mineral metabolism and the effect of diet in its regulation
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