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2017 ; 16
(1
): 167
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Characteristics of lipid metabolism including serum apolipoprotein M levels in
patients with primary nephrotic syndrome
#MMPMID28877724
He L
; Wu P
; Tan L
; Le B
; Du W
; Shen T
; Wu J
; Xiang Z
; Hu M
Lipids Health Dis
2017[Sep]; 16
(1
): 167
PMID28877724
show ga
BACKGROUND: Apolipoprotein M (apoM) is a 26-kD apolipoprotein that is mainly
expressed in specific cell types, such as human liver parenchymal cells and
kidney proximal renal tubular epithelial cells. ApoM can regulate the formation
of pre-?-HDL and the reverse cholesterol transport and thus plays an important
role in the metabolism of lipids and lipoproteins, meaning that it can affect the
development of lipid metabolism disorders. Significantly elevated serum apoM
levels are detected in patients with hyperlipidemia. However, few studies have
shown how apoM is expressed in primary nephrotic syndrome (PNS), which is often
accompanied with hyperlipidemia, and the underlying mechanism is poorly
understood. This study was aimed at examining the apoM levels in patients with
PNS and at determining the effects of PNS on serum apoM levels in these patients.
METHODS: This study included patients with hyperlipidemia (n = 37), the PNS with
hyperlipidemia group (n = 62), PNS without hyperlipidemia group (n = 33), and
healthy controls (n = 73). The age and body-mass index (BMI) matched among the
groups of participants. Their serum apoM concentrations were measured by an
enzyme-linked immunosorbent assay. Serum levels of conventional lipids and renal
function indices were assessed using an automatic biochemical analyzer. The data
were analyzed by means of Pearson's correlation coefficient (continuous
variables) or Student's t test (mean differences). RESULTS: The average serum
apoM concentrations were higher in the hyperlipidemia group (61.1 ± 23.2 mg/L,
P = 0.004) than in the healthy controls (31.6 ± 18.92 mg/L). The serum apoM
concentrations were lower in the PNS with hyperlipidemia group
(25.1 ± 16.31 mg/L, P = 0.007) and in the PNS without hyperlipidemia group
(21.00 ± 17.62 mg/L, P = 0.003) than in the healthy controls. The serum apoM
concentrations in the PNS with hyperlipidemia group did not differ significantly
from those in the PNS without hyperlipidemia group (P = 0.083). Moreover, serum
apoM levels positively correlated with serum high-density lipoprotein cholesterol
(HDL-C) and apoA1 levels and negatively correlated with proteinuria in PNS
patients (r = 0.458, P = 0.003; r = 0.254, P = 0.022; r = -0.414, P = 0.028).
CONCLUSION: Serum apoM concentrations are higher in patients with hyperlipidemia
than in healthy controls. Low serum apoM levels in patients with PNS are likely
caused by PNS.