Figure 5 Potential roles of phosphate and fibroblast growth factor 23 (FGF-23) in the development of cardiovascular disease in patients with chronic kidney.

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Volume 69, Issue 1, Pages (January 2006)

Figure 1 Disruption of phosphate homeostasis in chronic kidney disease (CKD) Figure 1 | Disruption of phosphate homeostasis in chronic kidney disease (CKD).

Figure 5 A layered approach to the follow-up of patients with acute kidney disease (AKD) Figure 5 | A layered approach to the follow-up of patients with.

Figure 4 Interplay between acute kidney injury (AKI),

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Figure 5 Inter-relationships between sleep apnoea, CKD and brain injury Figure 5 | Inter-relationships between sleep apnoea, CKD and brain injury. In chronic.

Figure 3 Energy metabolism regulation, cardiovascular and bone disease in CKD Figure 3 | Energy metabolism regulation, cardiovascular and bone disease.

Figure 6 Differences in glycaemic control with the study drug

Figure 4 Expression of coagulation protease receptors in renal cells

Figure 4 Interactions between adipose, the microbiome and kidney

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Figure 1 Types of coronary artery calcification

Figure 2 Proinflammatory mechanisms in CKD

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Figure 1 Role of the kidney in glucose homeostasis

Figure 3 The fat–intestine–kidney axis

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Figure 4 BMI and mortality in patients with heart failure

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Fibroblast Growth Factor 23 and CKD Prognosis

Figure 6 The bioavailability of phosphate differs according to the protein source Figure 6 | The bioavailability of phosphate differs according to the.

Figure 7 The efficacy of phosphate-binder therapy

Figure 3 Putative actions of glucagon-like peptide 1 (GLP-1)

Figure 2 The network of chronic diseases and their mutual influences

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Figure 1 The burden of chronic kidney disease (CKD)

Figure 3 Societal costs for the care of patients with chronic kidney disease in the UK Figure 3 | Societal costs for the care of patients with chronic.

Figure 2 Glomerular pathology in mice and humans with diabetic nephropathy Figure 2 | Glomerular pathology in mice and humans with diabetic nephropathy.

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Figure 4 Model of changes in the serum levels

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Use of vitamin D in chronic kidney disease patients

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Figure 4 The relationship between the time-dependent changes in the expression of immunoglobulin, mast cell, acute kidney injury (AKI), and fibrillar collagen.

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Volume 69, Issue 1, Pages (January 2006)

Diagram of the mechanisms involved in limiting the ability of the kidney to maintain the levels of 1,25-dihydroxyvitamin D in chronic kidney disease (CKD).

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Figure 5 Potential roles of phosphate and fibroblast growth factor 23 (FGF-23) in the development of cardiovascular disease in patients with chronic kidney disease (CKD) Figure 5 | Potential roles of phosphate and fibroblast growth factor 23 (FGF-23) in the development of cardiovascular disease in patients with chronic kidney disease (CKD). Patients with CKD often have hyperphosphataemia and high circulating levels of FGF-23. High levels of FGF-23 might directly induce left ventricular hypertrophy by stimulating pathological hypertrophic gene transcription in cardiomyocytes. In parallel, hyperphosphataemia and klotho deficiency disturb endothelial cell function and augment arterial wall calcification and valvular disease. These two processes might contribute to the high burden of cardiovascular events in CKD. Reproduced with permission from Springer Nature © Scialla, J.J. & M. Wolf. Nat. Rev. Nephrol. 10, 268–278 (2014). Reproduced with permission from Springer Nature © Scialla, J.J. & M. Wolf. Nat. Rev. Nephrol. 10, 268–278 (2014). Vervloet, M. G. et al. (2016) The role of phosphate in kidney disease Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.164