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Lipoprotein(a) levels in relation to albumin concentration in childhood nephrotic syndrome

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have been found in patients with end-stage renal disMethods. To investigate a model of nephrotic syndrome in eases, whereas after kidney transplantation, Lp(a) levels the absence of renal failure, we studied a group of 84 children seem to decrease [7‐9]. To explain the increase of Lp(a) in different clinical stages of the disease for a period of five plasma levels in end-stage renal diseases, it has been years. We evaluated the direct relationships between lipoproteins, including Lp(a), and/or plasma albumin and proteinuria. suggested that the kidney might play a role in Lp(a) Results. Lp(a) levels were significantly higher in the subjects metabolism as a catabolic site or by producing some with the active disease compared with patients in remission, factors affecting the Lp(a) liver synthesis [10, 11]. and were also significantly different when subjects were ranked Abnormalities of apoB-containing lipoproteins are by albumin quartiles. Multiple regression analysis revealed that common features of nephrotic syndrome [12‐14]. MetaLp(a) levels were inversely correlated with apo(a) isoform size and plasma albumin levels but not with the proteinuria/creati- bolic studies have shown that LDL-apoB overproduction nine clearance ratio. Among subjects in complete remission, and/or decreased clearance are the main causes of hyperLp(a) levels were different in patients with albumin levels lipidemia in nephrotic syndrome [15‐18]. However, below or above the fifth percentile. After the improvement of whether or not hypoalbuminemia, decreased oncotic the clinical stage of the disease, the D% variation of albumin levels was related to the D% of apoB and LDL cholesterol pressure, and/or proteinuria are the major determinants (LDL-C), but not with the D% variation of Lp(a), whereas the of the increased synthesis of apoB-containing particles D% variation of LDL-C was, in turn, related to the D %o f is still being debated [14‐16, 19‐23]. In adult patients Lp(a) levels. with nephrotic syndrome, Lp(a) levels are commonly Conclusions. These results suggest that in the childhood ne- high, decreasing after remission to the control levels, phrotic syndrome, the increased Lp(a) levels are mainly related to hypoalbuminemia, probably through a mechanism involving regardless of the type of therapy and the apo(a) phenoapoB overproduction, which leads to an increased number of type [18‐25]. The attempt to link the Lp(a) level to paLDL particles to be converted into Lp(a). rameters monitoring the stage of the disease has led to contrasting results. Although some investigators were able to show an association of Lp(a) with low plasma Lipoprotein(a) [Lp(a)] is a plasma lipoprotein con- levels of albumin or degree of proteinuria, others did sisting of a low-density lipoprotein (LDL) particle linked not confirm this significant relationship [18, 19, 24, 25]. Childhood nephrotic syndrome is an ideal model to study the relationships between plasma lipoproteins, including