Abstract
The aim of this paper is to review current knowledge about how calorie intake influences mineral metabolism focussing on four aspects of major interest for the renal patient: (a) phosphate (P) handling, (b) fibroblast growth factor 23 (FGF23) and calcitriol synthesis and secretion, (c) metabolic bone disease, and (d) vascular calcification (VC). Caloric intake has been shown to modulate P balance in experimental models: high caloric intake promotes P retention, while caloric restriction decreases plasma P concentrations. Synthesis and secretion of the phosphaturic hormone FGF23 is directly influenced by energy intake; a direct correlation between caloric intake and FGF23 plasma concentrations has been shown in animals and humans. Moreover, in vitro, energy availability has been demonstrated to regulate FGF23 synthesis through mechanisms in which the molecular target of rapamycin (mTOR) signalling pathway is involved. Plasma calcitriol concentrations are inversely proportional to caloric intake due to modulation by FGF23 of the enzymes implicated in vitamin D metabolism. The effect of caloric intake on bone is controversial. High caloric intake has been reported to increase bone mass, but the associated changes in adipokines and cytokines may as well be deleterious for bone. Low caloric intake tends to reduce bone mass but also may provide indirect (through modulation of inflammation and insulin regulation) beneficial effects on bone. Finally, while VC has been shown to be exacerbated by diets with high caloric content, the opposite has not been demonstrated with low calorie intake. In conclusion, although prospective studies in humans are needed, when planning caloric intake for a renal patient, it is important to take into consideration the associated changes in mineral metabolism.
Highlights
Caloric intake is known to influence the development and progression of renal disease.In general, diets rich in calories are deleterious for the kidneys
Obesity may influence the progression of chronic kidney disease (CKD) due to its effects on renal hemodynamics that result in hyperfiltration, increased glomerular pressure, and podocyte damage [5,6]
Most experimental studies with animals and the few studies that have investigated the relationship between caloric restriction (CR) and mineral metabolism tend to use a reduction in the total amount of food that averages around 30% of daily intake [11]
Summary
Caloric intake is known to influence the development and progression of renal disease. Diets with high fat content have been reported to cause renal damage in non-obese animals that did not develop type 2 diabetes, suggesting a direct effect of high fat/high calorie intake on the kidney [1]. In addition to promoting direct kidney damage, high caloric intake affects renal disease indirectly (through the development of obesity and type 2 diabetes). Obesity may influence the progression of chronic kidney disease (CKD) due to its effects on renal hemodynamics that result in hyperfiltration, increased glomerular pressure, and podocyte damage [5,6]. Measures to prevent a deleterious effect of high caloric intake on CKD should be installed early in the progression of the disease. (a) P handling, (b) FGF23 and calcitriol synthesis and secretion, (c) metabolic bone disease, and (d) VC
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