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In fact, it is not unusual for the magnesium balance to be normal or even decreased in uraemic patients owing to decreased dietary intake of magnesium combined with the impaired intestinal magnesium absorption characteristic of CKD [36]. The role of ankyrin magnesium in bone mineralization and in the pathogenesis of renal bone disease has been a matter of some debate in recent years and a hypothesis has been advanced in the past to the effect that magnesium is directly involved in the development of osteomalacia and/or renal osteodystrophy [9, 85, 87�C89]. This is on the one hand because of magnesium��s known effect on the CaSR and thus on PTH levels, (mentioned earlier in this review) and on the other hand because of its ability to prevent mineralization and/or calcification. Only Quisinostat purchase two small clinical studies involving therapeutic interventions with magnesium (both in Selleckchem GSK 3 inhibitor reason for these contradictory results could be the possible confounding by the use of aluminum. A larger, more recent cross-sectional observational study which focused on trace metal alterations in renal patients and possible associations with bone diseases [91] did not find a higher absolute bone magnesium content in these patients, though an increased magnesium-to-calcium ratio was found compared with controls. In particular, no association was observed between bone magnesium content and adynamic bone disease. At present, the role of magnesium in influencing bone metabolism remains unclear. There are many other factors such as vitamin D status, PTH level, calcium and phosphate concentration, and metabolic acidosis, which contribute to bone metabolism and function [92]. Recently investigated molecules such as FGF-23 or Klotho [93] factors such as vitamin K [94] and matrix Gla protein for which magnesium serves as a cofactor and/or modulator [95] may also play important roles in regulating bone turnover and mineralization.