Department of Renal Medicine, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Medicine, Faculty of Health, Aarhus University, Aarhus, Denmark.
Medical Research Laboratory, Department of Clinical Medicine, Faculty of Health, Aarhus University, Aarhus, Denmark.
J Ren Nutr. 2018 May;28(3):175-182. doi: 10.1053/j.jrn.2017.11.003. Epub 2018 Feb 21.
Patients on maintenance hemodialysis (HD) are unable to compensate for an enlarged mineral load with increased excretion of calcium and phosphate in the urine. Hence, excess calcium and phosphate must be neutralized by other mechanisms to avoid toxicity. The present study examined the acute handling of a mineral load in HD patients as compared with healthy subjects.
Controlled intervention study.
Twelve HD patients and 12 matched healthy subjects.
After a weight-adjusted standardized meal, blood samples were collected for the following 9 hours for ionized calcium, phosphate, parathyroid hormone (PTH), and fibroblast growth factor-23 (FGF23). The fractional excretion of calcium and phosphate was measured in controls. The patients were not allowed to take phosphate binders 24 hours before the experiment, and the study was performed on a non-HD day.
In healthy subjects, plasma calcium and phosphate did not change significantly from baseline, whereas HD patients demonstrated a decrease in plasma phosphate from 60 to 120 minutes by maximum 10% ([6; 13%], mean [95% confidence interval], P < .001) below baseline. PTH increased in both HD patients and controls and peaked 300 minutes after the meal 11% ([4; 19%], P < .004) above baseline in both groups. No changes in FGF23 were observed in HD patients, whereas FGF23 steadily decreased in controls, reaching nadir values at the end of the study 16% ([10; 21%], P < .001) below baseline. Control subjects demonstrated an immediate postprandial increase in the fractional excretion of both calcium and phosphate CONCLUSIONS: In HD patients, the mineral load paradoxically induced a decrease in plasma phosphate, whereas ionized calcium remained unchanged although PTH increased. These findings suggest that excess calcium and phosphate may be disposed of by mineral deposition, which may include soft tissue and vascular calcification.
接受维持性血液透析（HD）的患者无法通过增加尿液中钙和磷酸盐的排泄来补偿增大的矿物质负荷。因此，必须通过其他机制中和多余的钙和磷酸盐以避免毒性。本研究比较了 HD 患者与健康受试者对矿物质负荷的急性处理。
对照干预研究。
12 名 HD 患者和 12 名匹配的健康受试者。
在经过体重调整的标准化餐后，在接下来的 9 小时内采集血液样本，用于检测离子钙、磷酸盐、甲状旁腺激素（PTH）和成纤维细胞生长因子 23（FGF23）。在对照组中测量钙和磷酸盐的分数排泄。在实验前 24 小时，患者不得服用磷酸盐结合剂，并且该研究在非 HD 日进行。
在健康受试者中，血浆钙和磷酸盐从基线开始没有显著变化，而 HD 患者在 120 分钟时血浆磷酸盐从基线下降了 10%（[6；13%]，平均值[95%置信区间]，P<0.001）。PTH 在 HD 患者和对照组中均增加，并且在餐后 300 分钟时达到峰值，比两组基线增加 11%（[4；19%]，P<0.004）。在 HD 患者中未观察到 FGF23 的变化，而 FGF23 在对照组中持续下降，在研究结束时达到最低值，比基线低 16%（[10；21%]，P<0.001）。对照组表现出钙和磷酸盐的分数排泄立即餐后增加。
在 HD 患者中，矿物质负荷反常地导致血浆磷酸盐下降，而尽管 PTH 增加，但离子钙保持不变。这些发现表明，多余的钙和磷酸盐可能通过矿物质沉积来处理，这可能包括软组织和血管钙化。
