{'fraction_non_alphanumeric': 0.021248915871639202, 'fraction_numerical': 0.01777970511708586, 'mean_word_length': 5.071052631578947, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The pursuit of truth and beauty.

DOI:10.1097/01.mnh.0000447025.97464.ea Years ago, understanding mineral metabolism was not difficult. Bone was simply a repository of calcium and phosphorus built by osteoblasts and broken down by osteoclasts. The intestine absorbed these ions and the kidney excreted the excess. There were only a few hormones to consider and each behaved in a logical manner, stimulating divalent ion conservation or excretion as appropriate. As long as ion concentration and skeletal integrity were reasonable, all was well. However, the more we studied mineral metabolism the more we learned that this is a very complex system that not only regulates divalent ions and bone homeostasis but also is integral to disordered cardiovascular biology and ultimately mortality. Led by curiosity, intuition and the work of predecessors, the scientists who were asked to write in this issue of Current Opinion have led efforts to understand mineral metabolism especially when the main excretory channel for ion elimination and the source for 1,25(OH)2D, namely the kidney, fails. The goal, as always, is to uncover truth, which can lead to effective treatment and the betterment of patients’ lives. Ming Chang Hu, Makoto Kuro-o and Orson Moe start the issue with a lucid presentation of aKlotho and vascular calcification. It is known that chronic kidney disease (CKD) is a state of aKlotho deficiency. They present the newest data on the role of aKlotho in preventing vascular calcification and urge understanding of its effects on overall vascular biology rather than on single isolated cells. We predict that the comprehensive figure from their article will be used by many lecturers to help explain the role of aKlotho deficiency in vascular calcification. The next two articles in this issue move from aKlotho to fibroblast growth factor 23 (FGF23). Marta Christov describes the elevation of FGF23 in patients with acute kidney injury and its correlation with mortality. The elevation appears related to increased production and decreased clearance of FGF23 and does not appear to be a function of changes in parathyroid hormone or 1,25(OH)2D. Seiji Fukumoto then discusses the exciting new work on FGF23 neutralizing antibodies. X-linked hypophosphatemic rickets and related diseases cause