van Guldener C, Donker A J, Jakobs C, Teerlink T, de Meer K, Stehouwer C D
Department of Nephrology, Vrije Universiteit, Amsterdam, The Netherlands.
Kidney Int. 1998 Jul;54(1):166-9. doi: 10.1046/j.1523-1755.1998.00983.x.
The pathophysiological mechanism of hyperhomocysteinemia in chronic renal failure in humans is unknown. The loss of a putative renal homocysteine extraction in chronic renal failure has been hypothesized as significant homocysteine uptake has been demonstrated in the normal rat kidney. We studied homocysteine extraction in the normal human kidney.
We measured plasma total (free and protein-bound) and free homocysteine (tHcy and fHcy, respectively) in arterial and renal venous blood sampled from the aorta and right-side renal vein during cardiac catheterization in 20 fasting patients with normal renal function. Renal homocysteine extraction was calculated as the arteriovenous difference divided by the arterial levels times 100%.
No significant renal extraction was demonstrated either for tHcy: 0.9% (SD 5.8; 95% CI -1.8 to +3.6) or for fHcy: -0.2% (11.0; -5.4 to +4.9).
We conclude that no significant net renal uptake of homocysteine occurs in fasting humans with normal renal function. The loss of such uptake, therefore, cannot cause hyperhomocysteinemia in patients with renal failure.
人类慢性肾衰竭中高同型半胱氨酸血症的病理生理机制尚不清楚。由于已证实在正常大鼠肾脏中存在显著的同型半胱氨酸摄取,因此有人推测慢性肾衰竭中假定的肾脏同型半胱氨酸摄取功能丧失。我们研究了正常人类肾脏中的同型半胱氨酸摄取情况。
我们在20名肾功能正常的空腹患者进行心导管插入术期间,测量了从主动脉和右侧肾静脉采集的动脉血和肾静脉血中的血浆总同型半胱氨酸(游离和与蛋白结合的,分别为tHcy和fHcy)。肾同型半胱氨酸摄取量计算为动静脉差值除以动脉水平再乘以100%。
无论是tHcy(0.9%,标准差5.8;95%可信区间-1.8至+3.6)还是fHcy(-0.2%,11.0;-5.4至+4.9),均未显示出显著的肾脏摄取。
我们得出结论,在肾功能正常的空腹人类中,未发生显著的同型半胱氨酸净肾脏摄取。因此,这种摄取功能的丧失不会导致肾衰竭患者出现高同型半胱氨酸血症。