Relationship of non-LDL-bound apo(a), urinary apo(a) fragments and plasma Lp(a) in patients with impaired renal function

Background. Plasma lipoprotein (a) [Lp(a)] has been shown to be a risk factor for atherosclerosis in numerous studies. However, the catabolism of this lipoprotein is not very clear. We andothers have shown that Lp(a) is excretedinto urine in the form of fragments. Lp(a) has also been shown to exist in a low-density non-lipoprotein (LDL)-bound form. Since Lp(a) is increased in all forms of kidney disease with reduced excretory kidney function and decreased excretion of apo(a) fragments couldbe partially responsible for this increase, we investigatedthe relationship of non-LDL-boundapo(a), urinary apo(a) fragments andplasma Lp(a) in patients with impairedrenal function. Methods. Plasma Lp(a), non-LDL-boundapo(a) and urinary apo(a) fragments were measuredin 55 kid ney disease patients (28 males and 27 females) and matchedcontrols. Results. Plasma Lp(a) andnon-LDL-boundapo(a) were increasedin patients, whereas urinary apo(a) was decreased, especially in patients with a creatinine clearance < 70 ml/min. There was a significant correlation between plasma Lp(a) andnon-LDLboundapo(a) in patients andcontrols. Conclusion. We conclude that decreased urinary apo(a) excretion couldbe one possible mechanism of increasedplasma Lp(a) andnon-LDL-bound apo(a) in patients with decreased kidney function.