Nat. Rev. Nephrol. doi: /nrneph

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

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Figure 1 Cardiac and renal biosynthesis and

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Figure 6 Approach to drug management in patients with acute kidney disease (AKD) Figure 6 | Approach to drug management in patients with acute kidney disease.

Figure 4 Expression of coagulation protease receptors in renal cells

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Figure 3 The fat–intestine–kidney axis

Nat. Rev. Nephrol. doi: /nrneph

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

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Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Loss of the glycocalyx leads to podocyte and kidney injury

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Nat. Rev. Nephrol. doi: /nrneph

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Nat. Rev. Nephrol. doi: /nrneph

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Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

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Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.191 Figure 5 Interactions between the gut and kidney control sodium balance Figure 5 | Interactions between the gut and kidney control sodium balance. Ingested sodium is sensed by sodium channels in G cells of the stomach, leading to the release of gastrin and L-DOPA, which are taken up by amino acid (AA) transporters in the renal tubule. Conversion of L-DOPA to dopamine occurs, and gastrin and dopamine activate their respective receptors, synergistically leading to inhibition of renal sodium transport and therefore increased natriuresis. Câmara, N. O. S. et al. (2017) Kidney disease and obesity: epidemiology, mechanisms and treatment Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.191