September 1, 1997Journal of Lipid Research108 citationsOpen Access
View Full PaperRenovascular arteriovenous differences in Lpa plasma concentrations suggest removal of Lpa from the renal circulation
Key Result
Passage through the renal circulation significantly reduced Lp[a] plasma concentrations compared to the ascending aorta (18.7 vs 20.1 mg/dL, P<0.001), suggesting renal uptake of Lp[a].
Study Design
Type
Cross-Sectional (n=100)
Structured PICO
Does the human kidney remove Lp[a] from the circulation in patients undergoing coronary angiography?
P
Population
100 patients undergoing coronary angiography or coronary angioplasty.
E
Exposure
Simultaneous measurement of Lp[a] plasma concentrations in the ascending aorta and renal vein
C
Comparator
Ascending aorta vs. renal vein Lp[a] levels
O
Outcome
Arteriovenous difference in Lp[a] plasma concentrationssurrogate
This study demonstrates for the first time that the human kidney plays an active role in the catabolism of Lp[a], which may explain elevated Lp[a] concentrations in patients with chronic renal insufficiency.
Main Result
Mean Difference: -1.4
Absolute Event Rate: 18.7% vs 20.1%
p-value: p=< 0.001
Limitations
- Cannot assign the kidney a regulatory role for Lp[a] plasma levels in humans with normal renal function
- The underlying mechanisms of renal uptake are unknown at the moment
Abstract
High plasma concentrations of lipoproteina (Lpa) are considered a genetically determined risk factor for atherosclerosis. Lpa is produced by the liver. The site(s) and mechanism(s) of catabolism are presently unclear. Lpa is elevated secondary to end-stage renal disease which suggests a direct or indirect role of the kidney in the metabolism of Lpa. We therefore investigated, by a simple in vivo approach, whether Lpa is removed by the human kidney. Lpa plasma concentrations were measured simultaneously by various methods in the ascending aorta and renal vein of 100 patients undergoing coronary angiography or coronary angioplasty. Lpa levels differed significantly between the two vessels even after correcting for hemoconcentration (20.1 +/- 21.6 mg/dL versus 18.7 +/- 20.3 mg/dL, P < 0.001). This corresponds to a mean arteriovenous difference of -1.4 mg/ dL or -9% of the arterial concentration. No Lpa or intact apoa could be detected in urine from healthy probands. Although we cannot assign the kidney a regulatory role for Lpa plasma levels in humans with normal renal function, we conclude from our data that substantial amounts of this atherogenic lipoprotein are taken up by the kidney. The underlying mechanisms are unknown at the moment. This study therefore demonstrates for the first time that the human kidney plays an active role in the catabolism of Lpa. This may explain the elevated Lpa concentrations found in patients with chronic renal insufficiency.