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Magnesium in chronic kidney disease Stages 3 and 4 and in dialysis patients

机译:慢性肾脏疾病第3和第4阶段以及透析患者中​​的镁

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The kidney has a vital role in magnesium homeostasis and, although the renal handling of magnesium is highly adaptable, this ability deteriorates when renal function declines significantly. In moderate chronic kidney disease (CKD), increases in the fractional excretion of magnesium largely compensate for the loss of glomerular filtration rate to maintain normal serum magnesium levels. However, in more advanced CKD (as creatinine clearance falls 30 mL/min), this compensatory mechanism becomes inadequate such that overt hypermagnesaemia develops frequently in patients with creatinine clearances 10 mL/min. Dietary calcium and magnesium may affect the intestinal uptake of each other, though results are conflicting, and likewise the role of vitamin D on intestinal magnesium absorption is somewhat uncertain. In patients undergoing dialysis, the effect of various magnesium and calcium dialysate concentrations has been investigated in haemodialysis (HD) and peritoneal dialysis (PD). Results generally show that dialysate magnesium, at 0.75 mmol/L, is likely to cause mild hypermagnesaemia, results for a magnesium dialysate concentration of 0.5 mmol/L were less consistent, whereas serum magnesium levels were mostly normal to hypomagnesaemic when 0.2 and 0.25 mmol/L were used. While dialysate magnesium concentration is a major determinant of HD or PD patients' magnesium balance, other factors such as nutrition and medications (e.g. laxatives or antacids) also play an important role. Also examined in this review is the role of magnesium on parathyroid hormone (PTH) levels in dialysis patients. Although various studies have shown that patients with higher serum magnesium tend to have lower PTH levels, many of these suffer from methodological limitations. Finally, we examine the complex and often conflicting results concerning the interplay between magnesium and bone in uraemic patients. Although the exact role of magnesium in bone metabolism is unclear, it may have both positive and negative effects, and it is uncertain what the optimal magnesium levels are in uraemic patients.
机译:肾脏在镁的体内平衡中起着至关重要的作用,尽管肾脏对镁的适应性​​很高,但是当肾功能显着下降时,这种能力就会下降。在中度慢性肾脏疾病(CKD)中,镁排泄分数的增加在很大程度上补偿了肾小球滤过率的损失,以维持正常的血清镁水平。然而,在更高级的CKD中(由于肌酐清除率下降<30 mL / min),这种补偿机制变得不足,以至于肌酐清除率<10 mL / min的患者经常出现明显的高镁血症。饮食中的钙和镁可能会影响彼此的肠道吸收,尽管结果相互矛盾,同样,维生素D对肠道镁吸收的作用也尚不确定。在接受透析的患者中,已在血液透析(HD)和腹膜透析(PD)中研究了各种浓度的镁和钙透析液的作用。结果通常显示,透析液镁浓度为0.75 mmol / L时,可能会引起轻度高镁血症;透析液镁浓度为0.5 mmol / L时,结果的一致性较差;而当镁浓度为0.2和0.25 mmol / L时,血清镁水平与低镁血症基本正常。使用L。透析液镁浓度是HD或PD患者镁平衡的主要决定因素,其他因素如营养和药物治疗(例如泻药或抗酸药)也起着重要作用。这篇综述还探讨了镁对透析患者甲状旁腺激素(PTH)水平的作用。尽管各种研究表明,血清镁含量较高的患者倾向于具有较低的PTH水平,但其中许多方法存在方法学上的局限性。最后,我们检查了有关尿毒症患者镁与骨之间相互作用的复杂且经常相互矛盾的结果。尽管镁在骨骼代谢中的确切作用尚不清楚,但它可能同时具有正面和负面影响,并且不确定尿毒症患者的最佳镁水平是多少。

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