INTRODUCTION: Hyperlipidemia may cause glomerulosclerosis in children with nephrotic syndrome (NS).
OBJECTIVE: Our goal was to observe the role of soluble leptin receptor (sOBR) and leptin in serum and urine on the mechanism of hyperlipidemia in children with NS.
METHODS: Twenty-three children with untreated NS and 15 age-, gender-, and BMI-matched healthy controls were enrolled onto the study. Leptin and sOBR in serum and urine were measured by enzyme-linked immunosorbent assay, and plasma lipid and insulin levels were detected by automatic biochemistry analyzer and radioimmunoassay, respectively. sOBR messenger RNA and membrane protein expression in peripheral blood mononuclear cells were detected by reverse-transcription polymerase chain reaction and immunocytochemistry.
RESULTS: Low-density lipoprotein, total cholesterol, triglyceride, and apolipoprotein A levels were increased. sOBR messenger RNA and membrane protein expression by peripheral blood mononuclear cells were significantly lower in the patient group compared with controls. The ratio of serum leptin versus sOBR (free leptin index) was significantly higher in the NS group. Urinary leptin in the patient group was higher than that in the control group. The free leptin index showed no correlation with BMI or total cholesterol, triglyceride, or apolipoprotein B levels in both groups but did show a correlation with plasma albumin, low-density lipoprotein, high-density lipoprotein, apolipoprotein A, and insulin levels in the patient group.
CONCLUSIONS: The reduced sOBR level, which enhanced the biologically active form of leptin in children with NS, might be correlated partly with serum lipid parameters, albumin, and insulin. Increased free leptin in serum might be a complementary mechanism against hyperlipidemia in children with NS.
Submitted by Xi Qiang Yang
- Copyright © 2008 by the American Academy of Pediatrics