NO NET RENAL EXTRACTION OF HOMOCYSTEINE IN FASTING HUMANS

Background. The pathophysiological mechanism of hyperhomocysteinemia i n chronic renal failure in humans is unknown. The loss of a putative r enal homocysteine extraction in chronic renal failure has been hypothe sized as significant homocysteine uptake has been demonstrated in the normal rat kidney. We studied homocysteine extraction in the normal hu man kidney. Methods. We measured plasma total (free and protein-bound) and free homocysteine (tHcy and fHcy; respectively) in arterial and r enal venous blood sampled from the aorta and right-side renal vein dur ing cardiac catheterization in 20 fasting patients with normal renal f unction. Renal homocysteine extraction was calculated as the arteriove nous difference divided by the arterial level times 100%. Results. No significant renal extraction was demonstrated either for tHcy: 0.9% (S D 5.8; 95% CT -1.8 to +3.6) or for fHcy: -0.2% (11.0; -5.4 to +4.9). C onclusions. We conclude that no significant net renal uptake of homocy steine occurs in fasting humans with normal renal function. The loss o f such uptake, therefore, cannot cause hyperhomocysteinemia in patient s with renal failure.