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The story of alkaline phosphatase in the management of mineral and bone disorder (MBD) in patients with chronic kidney disease (CKD) is an interesting and educational part of the history of nephrology. Circulating alkaline phosphatase, a marker of bone turnover, was among the first bone markers used for the detection and management of ‘renal osteodystrophy’, a term previously used by clinicians and researchers since the 1970s. However, by the mid-1990s and early 2000s alkaline phosphatase fell out of favor, when commercial parathyroid hormone (PTH) assays become available. At the same time, the first Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines on CKD–MBD chose not to mention alkaline phosphatase, as target ranges were uncertain [1]. A rise in serum alkaline phosphatase, known as hyperphosphatasemia or hyperphosphatasia, is an expected finding in progressive CKD with worsening kidney function [2]. Elevated serum alkaline phosphatase concentrations in CKD patients with otherwise intact liver and biliary systems usually result from excess of the bone isoforms of the enzyme [3–5]. Specific detection of the bone isoform may not have clinical utility, since it was found not to correlate with inflammation or mortality risk [6]. The recent data suggest that a rise in alkaline phosphatase in dialysis patients is associated with worsening bone mineral density [7], and worse responsiveness to erythropoiesis stimulating agents [8].

Towards the revival of alkaline phosphatase for the management of bone disease, mortality and hip fractures