Nielsen A H, Knudsen F, Danielsen H, Pedersen E B, Fjeldborg P, Madsen M, Brøchner-Mortensen J, Kornerup H J
Eur J Clin Invest. 1987 Feb;17(1):37-42. doi: 10.1111/j.1365-2362.1987.tb01223.x.
In fourteen hypertensive and fourteen normotensive renal transplant recipients, and in a group of thirteen healthy controls, changes in natriuresis, glomerular filtration rate (GFR), and tubular reabsorption of sodium were determined in relation to intravenous infusion of 2 mmol isotonic sodium chloride per kg body weight. An exaggerated natriuresis was demonstrated in the hypertensive renal transplant recipients. This new finding indicates that the augmented natriuresis following plasma volume expansion, which is a characteristic finding in subjects with arterial hypertension, is not mediated by the renal nerves. Investigation of the tubular reabsorption rates of sodium by simultaneous determination of the renal clearance of 51Cr-EDTA and lithium showed that in the hypertensives the changes in tubular handling of sodium were different from those registered in the normotensive subjects. The increased sodium excretion in the hypertensive renal transplant recipients was caused by an increased output of sodium from the proximal tubules which was not fully compensated for by an increased distal reabsorption. Whether this increased delivery of sodium to the distal segments was caused by changes in GFR or in the proximal tubular reabsorption of sodium could not be clarified in the present study and warrants further investigations.
在14名高血压肾移植受者、14名血压正常的肾移植受者以及一组13名健康对照者中，通过静脉输注每千克体重2毫摩尔等渗氯化钠溶液，测定了钠排泄、肾小球滤过率（GFR）以及肾小管对钠的重吸收的变化。结果显示，高血压肾移植受者存在过度的钠排泄。这一新发现表明，血浆容量扩张后增强的钠排泄（这是动脉高血压患者的一个典型表现）并非由肾神经介导。通过同时测定51Cr - EDTA和锂的肾清除率来研究肾小管对钠的重吸收率，结果表明，高血压患者肾小管对钠的处理变化与血压正常者不同。高血压肾移植受者钠排泄增加是由于近端小管钠输出增加，而远端重吸收增加并未完全代偿。在本研究中，无法明确这种钠向远端节段输送增加是由GFR变化还是近端小管对钠的重吸收变化引起的，这值得进一步研究。
