Lemann J, Pleuss J A, Gray R W, Hoffmann R G
Department of Medicine, Medical College of Wisconsin, Milwaukee.
Kidney Int. 1991 May;39(5):973-83. doi: 10.1038/ki.1991.123.
This study was undertaken to evaluate the effects of dietary K intake, independent of whether the accompanying anion is Cl- or HCO3-, on urinary Ca excretion in healthy adults. The effects of KCl, KHCO3, NaCl and NaHCO3 supplements, 90 mmol/day for four days, were compared in ten subjects fed normal constant diets. Using synthetic diets, the effects of dietary KCl-deprivation for five days followed by recovery were assessed in four subjects and of KHCO3-deprivation for five days followed by recovery were assessed in four subjects. On the fourth day of salt administration, daily urinary Ca excretion and fasting UCa V/GFR were lower during the administration of KCl than during NaCl supplements (delta = -1.11 +/- 0.28 SEM mmol/day; P less than 0.005 and -0.0077 +/- 0.0022 mmol/liter GFR; P less than 0.01), and lower during KHCO3 than during control (-1.26 +/- 0.29 mmol/day; P less than 0.005 and -0.0069 +/- 0.0019 mmol/liter GFR; P = 0.005). Both dietary KCl and KHCO3 deprivation (mean reduction in dietary K intake -67 +/- 8 mmol/day) were accompanied by an increase in daily urinary Ca excretion and fasting UCaV/GFR that averaged on the fifth day +1.31 +/- 0.25 mmol/day (P less than 0.005) and +0.0069 +/- 0.0012 mmol/liter GFR (P less than 0.005) above control. Both daily urinary Ca excretion and fasting UCaV/GFR returned toward or to control at the end of recovery. These observations indicate that: 1) KHCO3 decreases fasting and 24-hour urinary Ca excretion; 2) KCl nor NaHCO3, unlike NaCl, do not increase fasting or 24-hour Ca excretion and 3) K deprivation increases both fasting and 24-hour urinary Ca excretion whether the accompanying anion is Cl- or HCO3-. The mechanisms for this effect of K may be mediated by: 1) alterations in ECF volume, since transient increases in urinary Na and Cl excretion and weight loss accompanied KCl or KHCO3 administration, while persistent reductions in urinary Na and Cl excretion and a trend for weight gain accompanied K deprivation; 2) K mediated alterations in renal tubular phosphate transport and renal synthesis of 1.25-(OH)2-vitamin D, since KCl or KHCO3 administration tended to be accompanied by a rise in fasting serum PO4 and TmPO4 and a fall in fasting UPO4 V/GFR, a fall in serum 1,25-(OH)2-D and a decrease in fasting UCa V/GFR, while dietary KCl or KHCO3 deprivation were accompanied by a reverse sequence.
本研究旨在评估膳食钾摄入量（独立于伴随阴离子是氯离子还是碳酸氢根离子）对健康成年人尿钙排泄的影响。在10名食用正常常量饮食的受试者中，比较了连续4天每天补充90 mmol氯化钾、碳酸氢钾、氯化钠和碳酸氢钠的效果。使用合成饮食，对4名受试者评估了5天低钾饮食（氯化钾）后恢复的效果，对4名受试者评估了5天低钾饮食（碳酸氢钾）后恢复的效果。在给予盐的第4天，氯化钾给药期间的每日尿钙排泄量和空腹尿钙排泄率（UCaV/GFR）低于氯化钠补充期间（差值 = -1.11 ± 0.28 SEM mmol/天；P < 0.005和 -0.0077 ± 0.0022 mmol/升GFR；P < 0.01），碳酸氢钾给药期间低于对照组（-1.26 ± 0.29 mmol/天；P < 0.005和 -0.0069 ± 0.0019 mmol/升GFR；P = 0.005）。膳食氯化钾和碳酸氢钾缺乏（膳食钾摄入量平均减少-67 ± 8 mmol/天）均伴随着每日尿钙排泄量和空腹UCaV/GFR增加，在第5天平均比对照组高+1.31 ± 0.25 mmol/天（P < 0.005）和+0.0069 ± 0.0012 mmol/升GFR（P < 0.005）。恢复结束时，每日尿钙排泄量和空腹UCaV/GFR均恢复到或接近对照组水平。这些观察结果表明：1）碳酸氢钾可降低空腹和24小时尿钙排泄量；2）与氯化钠不同，氯化钾和碳酸氢钠均不会增加空腹或24小时钙排泄量；3）无论伴随阴离子是氯离子还是碳酸氢根离子，钾缺乏均会增加空腹和24小时尿钙排泄量。钾产生这种作用的机制可能由以下因素介导：1）细胞外液量的改变，因为氯化钾或碳酸氢钾给药伴随着尿钠和氯排泄量短暂增加以及体重减轻，而钾缺乏则伴随着尿钠和氯排泄量持续减少以及体重增加趋势；2）钾介导的肾小管磷酸盐转运和1,25-(OH)₂-维生素D肾合成的改变，因为氯化钾或碳酸氢钾给药往往伴随着空腹血清磷酸盐和TmPO₄升高以及空腹UPO₄V/GFR降低、血清1,25-(OH)₂-D降低和空腹UCaV/GFR降低，而膳食氯化钾或碳酸氢钾缺乏则伴随着相反的变化顺序。
