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. 2016 Jun 1;17(8):853–866. doi: 10.2217/pgs-2015-0007

Figure 3. . Proposed physiologic model of the effects of SLC15A2 rs1143672.

Figure 3. 

In nonhuman models of chronic kidney disease, PEPT2 is upregulated leading to dysregulation of proper levels of calcium and phosphorus in the blood. We propose the SLC15A2*2 haplotype effect observed here statistically is induced by kidney failure. That is, kidney disease patients with the SLC15A2*2 haplotype have lower affinity and thus less uptake of peptides and ACE inhibitors in the reabsorption process of the kidney's proximal tubule compared with patients with the SLC15A2*1 haplotype. The lower affinity likely results in increased urinary loss of phosphate and a decreased risk of hyperparathyroidism secondary to hyperphosphatemia (thought to be the cause of renal osteodystrophy).