title: Increased plasma acylation-stimulating protein in pediatric proteinuric renal disease.
abstract: Hyperlipidemia has been well recognized as a striking feature of nephrotic syndrome and other renal diseases. However, the underlying pathophysiological mechanisms still have not yet been elucidated. In this study, we evaluated acylation-stimulating protein (ASP) and complement component 3 (C3) in children (n=48) with various forms of proteinuric renal disease [nephrotic syndrome, acute poststreptococcal infection glomerulonephritis (APSGN), and lupus nephritis (LN)] in comparison with age- and gender-matched controls (n=279). In children with proteinuric renal disease, various aberrations in plasma lipids were noted, including increased triglyceride, cholesterol, and low-density lipoprotein cholesterol (LDL-C) (all p<0.0001). Whereas C3 was not altered in children with nephrotic syndrome (1.05+/-0.05 g/L vs. 1.29+/-0.04 controls), the decrease was pronounced in children with LN and APSGN (0.42+/-0.11, p<0.05 and 0.30+/-0.06, p<0.001, respectively). Plasma C3 correlated positively with lipid parameters [triglyceride, cholesterol, LDL-C, apolipoprotein B (apoB), high-density lipoprotein cholesterol (HDL-C) and apoA1] and inversely with total protein, blood urea nitrogen, and creatinine. By contrast, plasma ASP was significantly elevated in all proteinuric renal diseases (101.4+/-7.1 nmol/L nephrotic syndrome, 90.9+/-14.1 LN, and 81.8+/-7.2 APSGN vs. 44.3+/-1.5 controls, p<0.05 to p<0.001), and this increase was correlated with changes in lipid parameters (triglycerides and apoA1). In summary, these results demonstrate alterations in C3 and ASP that may contribute to or compensate for dyslipidemia.
authors.affiliation: Department of Pediatrics, Tongji Hospital, HuaZhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
authors.forename: Jin Hui
authors.initials: JH
authors.lastname: Tang
authors.forename: Yu
authors.initials: Y
authors.lastname: Wen
authors.forename: Fei
authors.initials: F
authors.lastname: Wu
authors.forename: Xiao Y
authors.initials: XY
authors.lastname: Zhao
authors.forename: Mei X
authors.initials: MX
authors.lastname: Zhang
authors.forename: Jie
authors.initials: J
authors.lastname: Mi
authors.forename: Katherine
authors.initials: K
authors.lastname: Cianflone
mesh_terms: D000215:Acylation; D016022:Case-Control Studies; D002648:Child; D002681:China; D003176:Complement C3 / Q000032:analysis; D015926:Complement C3a / Q000032:analysis*; D005260:Female; D005921:Glomerulonephritis / Q000097:blood* / Q000150:complications / Q000209:etiology; D006801:Humans; D008055:Lipids / Q000097:blood; D008181:Lupus Nephritis / Q000097:blood* / Q000150:complications; D008297:Male; D009404:Nephrotic Syndrome / Q000097:blood* / Q000150:complications; D011507:Proteinuria / Q000097:blood / Q000209:etiology*; D013290:Streptococcal Infections / Q000097:blood / Q000150:complications; D015854:Up-Regulation
chemical_list: D003176:Complement C3; D008055:Lipids; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a