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Nat. Rev. Nephrol. doi: /nrneph

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Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.60 Figure 2 Pathological consequences of high alkaline phosphatase (ALP) levels Figure 2 | Pathological consequences of high alkaline phosphatase (ALP) levels. a | Cardiovascular dysfunction, chronic kidney disease, genetic factors and bone disease result in increased circulating expression of alkaline phosphatase, tissue-nonspecific isozyme (TNALP)[Au:OK?]. This increasd expression of TNALP is associated with increased mortality and cardiovascular events via mechanisms that involve vascular calcification, endothelial dysfunction, and inflammation. Interventional strategies to reduce TNALP activity include direct ALP inhibitors; epigenetic inhibitors of TNALP expression such as bromodomain and extra-terminal motif (BET) inhibitors; calcimimetic molecules; and vitamin D analogues. b | Elevation of the levels of intestinal-type alkaline phosphatase (IALP) and TNALP owing to sepsis and/or acute inflammation can lead to endotoxin and nucleotide detoxification, cytokine inactivation and reduced oxidative stress, which protect the kidney from inflammatory damage. Similarly, systemic administration of IALP, placental-type alkaline phosphatase (PALP) or chimeric IALP/PALP can exert nephroprotective and anti-inflammatory effects in sepsis and after cardiac surgery. Haarhaus, M. et al. (2017) Alkaline phosphatase: a novel treatment target for cardiovascular disease in CKD Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.60