الفهرس 
Acknowledgement
Normal Electroyte HomeostasisOnly 14 pages are availabe for public view
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Abstract
In chronic kidney disease (CKD), several abnormalities in bone and mineral metabolism develop in the majority of patients. The parathyroid plays a very important role in regulating bone and mineral metabolism; thus, control of parathyroid function is one of the main targets of the management of CKD-mineral and bone disorder (CKD-MBD)
In the parathyroids, magnesium serves this role in stimulus-secretion coupling. Hypomagnesemia inhibits PTH secretion and also causes resistance to PTH, leading to a form of hypoparathyroidism that is reversible. Hypermagnesemia also results in inhibition of PTH secretion (Edward 2012)
There have been inconsistent results studies of the relationship between Mg and PTH in.A positive linear relationship between magnesium and PTH, a finding which is consistent with some previous reports. chronic hypermagnesaemia is known to suppress the excretion of PTH in end-stage CKD, which contributes to the calcification of the soft tissues including vascular calcification (Wei et al., 2006).
Further more, in dialysis patients hypermagnesaemia is known to suppress PTH production, thus it is considered an important factor in the manufacturing of dialysis fluids (Wei et al., 2006, E3 Journal of Medical, September, 2012)
High Mg concentrations do not seem to pose a problem according to experiments. The relative potencies of Ca and Mg in inhibiting PTH secretion were previously addressed by Habener and Potts 2013, Brown et al., 2013; who reported that Ca was about three times more potent than Mg in reducing PTH secretion in vitro. (Rodríguez-Ortiz et al, 2013)
The effect of Mg on the expression of the parathyroid VDR, another key receptor in the regulation of PTH secretion, was also evaluated. The expression of VDR is upregulated by Ca and calcimimetics. Here, we show that Mg upregulates the VDR expression at mRNA and protein levels. This effect of Mg would favour the inhibition of PTHs ecretion by vitaminD.
Recent studies have shown that FGF23 regulates parathyroid function. FGF23 exerts an inhibitory effect on PTH secretion and parathyroid cell proliferation by binding to the receptor FGFR1 in the presence of its co-receptor Klotho. Klotho and FGFR are abundantly expressed in normal parathyroid cells, but in hyperplastic parathyroid glands the expression of FGFR1 and Klotho is markedly reduced, which likely makes the tissue resistant to the action of FGF23 Both FGFR1 and Klotho gene expression are upregulated by Ca. Thus, we assessed whether Mg is also able to modulate the expression of these receptors. Therefore, the increased levels of expression of FGFR1 and Klotho may be considered as an additional mechanism underlying the downregulation of PTH secretion by Mg. (Rodríguez-Ortiz et al, 2013)
Further more, the inhibitory effects of Mg on parathyroid function, mainly when Ca is moderately low, could help to control secondary hyperparathyroidism. Interestingly, Mg also would favour the efficiency of therapeutic molecules targeting the parathyroid CaR, VDR or FGF23/Klotho. (Rodríguez-Ortiz et al, 2013)
In this study We found that the high level of Mg+2 are associated with lower level of PTH in patients who are both DM & hypertensive rather than hypertensive patients only in both groups Haemdialysis patients & CKD patients. as in many recent studies. So we recommend that regular follow up is important.