Increased fasting plasma acylation-stimulating protein concentrations in nephrotic syndrome

• Published in: The journal of clinical endocrinology and metabolism 2002-02, Vol.87 (2), p.853-858
• Main Authors: OZATA, Metin, OKTENLI, Cagatay, GULEC, Mustafa, OZGURTAS, Taner, BULUCU, Fatih, CAGLAR, Kayser, BINGOL, Necati, VURAL, Abdulgaffar, OZDEMIR, I. Caglayan
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Biological and medical sciences; Blood Proteins - analysis; Body Mass Index; Complement C3a - analogs & derivatives; Fasting - blood; Glomerulonephritis; Humans; Leptin - blood; Lipids - blood; Medical sciences; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Nephrotic Syndrome - blood; Nephrotic Syndrome - pathology; Osmolar Concentration; Urinary system involvement in other diseases. Miscellaneous; Urinary tract. Prostate gland
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.87.2.853

Acylation-stimulating protein (ASP) is an adipocyte-derived protein that has recently been suggested to play an important role in the regulation of lipoprotein metabolism and triglyceride (TG) storage. ASP also appears to have a role in the regulation of energy balance. In addition to its role as a hormonal regulator of body weight and energy expenditure, leptin is now implicated as a regulatory molecule in lipid metabolism. However, little is known about the alterations in fasting plasma ASP and leptin concentrations in the nephrotic syndrome. As hyperlipidemia is one of the most striking manifestations of the nephrotic syndrome, we have investigated fasting plasma ASP and leptin levels and their relation to lipid levels in this syndrome. Twenty-five patients with untreated nephrotic syndrome and 25 age-, sex-, and body mass index-matched healthy controls were included in the study. Fasting plasma lipoproteins, TG, total cholesterol, lipoprotein(a), apolipoprotein AI (apoAI), apoB, urinary protein, plasma albumin, third component of complement (C3), ASP, and leptin levels were measured in both groups. Total cholesterol, TG, low and very low density lipoproteins, lipoprotein(a), apoB, and urinary protein levels were increased in the patient group, whereas plasma albumin, high density lipoprotein cholesterol, and apoAI levels were decreased compared with those in the control group (P < 0.001). Plasma ASP levels were significantly higher in the patient group compared with the control subjects (133.72 +/- 65.14 vs. 29.93 +/- 12.68 nmol/liter; P < 0.001), whereas leptin (2.69 +/- 2.06 vs. 3.99 +/- 2.99 ng/ml; P = 0.118) and C3 (1.01 +/- 0.25 vs. 1.06 +/- 0.23 g/liter; P = 0.662) levels were not significantly different between the two groups. Plasma leptin levels were correlated with body mass index in both nephrotic patients (r(s) = 0.86; P < 0.001) and controls (r(s) = 0.98; P < 0.001), but were not correlated with the other parameters. Fasting ASP concentrations showed no correlation with body mass index, proteinuria, plasma albumin, leptin, or any lipid parameter in either group, but C3 levels (in patient group: r(s) = 0.92; P < 0.001; in control group: r(s) = 0.68; P < 0.001). Our findings showed that plasma ASP levels were significantly elevated, whereas leptin levels were normal in the nephrotic syndrome. Increased ASP levels in the setting of dyslipidemia in the nephrotic syndrome raise the possibility of an ASP receptor defect in adipocytes, which also