title: Insulin resistance in children with primary nephrotic syndrome and normal renal function.
abstract: BACKGROUND
  Insulin resistance (IR) is an independent risk factor for atherosclerosis or cardiovascular events and renal function impairment. The aim of this study was to investigate IR in children with primary nephrotic syndrome (NS).
  
  
  METHODS
  One-hundred and nineteen primary NS patients with normal renal function and 125 normal controls were studied. Fasting blood glucose, fasting serum insulin, and fasting serum C-peptide were measured. The Homa index of insulin resistance (HOMA-IR), Islet B cell function, and insulin sensitivity index were calculated. Correlations were assessed between HOMA-IR, fasting serum C-peptide, blood pressure, blood lipids, renal function, coagulation, clinical disease type, pathology and the early therapeutic effectiveness of high-dose glucocorticoids.
  
  
  RESULTS
  There was no evidence of IR in the primary NS group. Although levels of fasting blood glucose, fasting serum insulin and fasting serum C-peptide were all within the normal ranges, fasting serum C-peptide was significantly higher compared to the controls. There was no disorder of carbohydrate metabolism in different hormone therapy efficacy and pathological diagnosis. Although IR was not detected, a significant increase in blood pressure, uric acid, blood lipids and coagulability was observed in the primary NS group.
  
  
  CONCLUSIONS
  A correlation observed between HOMA-IR, age, blood pressure, serum creatinine (Cr) and triglyceride may suggest that insulin sensitivity will emerge as renal disease progresses. Fasting serum C-peptide levels were increased in the primary NS group, suggesting that fasting serum C-peptide may be a protective factor.
authors.affiliation: Department of Nephrology, Nanjing Children's Hospital, Nanjing Medical University, 72 Guangzhou Road, Nanjing, 210029, Jiangsu Province, People's Republic of China.
authors.forename: Jiaping
authors.initials: J
authors.lastname: Jin
authors.forename: Bo
authors.initials: B
authors.lastname: Jin
authors.forename: Songming
authors.initials: S
authors.lastname: Huang
authors.forename: Yanggang
authors.initials: Y
authors.lastname: Yuan
authors.forename: Guixia
authors.initials: G
authors.lastname: Ding
authors.forename: Huaying
authors.initials: H
authors.lastname: Bao
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Yuan
authors.initials: Y
authors.lastname: Han
authors.forename: Fei
authors.initials: F
authors.lastname: Zhao
authors.forename: Aihua
authors.initials: A
authors.lastname: Zhang
mesh_terms: D000293:Adolescent; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D002096:C-Peptide / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D002681:China; D003430:Cross-Sectional Studies; D018450:Disease Progression; D005215:Fasting / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D005938:Glucocorticoids / Q000008:administration & dosage; D006801:Humans; D007223:Infant; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D016014:Linear Models; D008055:Lipids / Q000097:blood; D008297:Male; D015999:Multivariate Analysis; D009404:Nephrotic Syndrome / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D002096:C-Peptide; D005938:Glucocorticoids; D007328:Insulin; D008055:Lipids