title: Acute-phase markers of inflammation and glomerular structure in patients with type 2 diabetes.
abstract: Type 2 diabetes is frequently associated with an inflammatory status; the relationships between low-grade inflammation and diabetic nephropathy are still unclear. The aim of this study was to evaluate the relationships between acute-phase markers of inflammation, glomerular structure, and albumin excretion rate (AER) in type 2 diabetes. In 74 patients with type 2 diabetes (23 normoalbuminuric, 30 microalbuminuric, and 21 proteinuric) fibrinogen, serum amyloid A protein (SAA), C-reactive protein (CRP), and IL-6 were determined. AER was measured on three 24-h urine collections; GFR was measured by 51Cr EDTA plasma clearance. A kidney biopsy was performed, and mesangial fractional volume [Vv(mes/glom)] and glomerular basement membrane (GBM) width were estimated by electron microscopic morphometric analysis. CRP, fibrinogen, SAA, and IL-6 differed among groups, with proteinuric patients having the highest levels. SAA and fibrinogen correlated with AER (P < 0.03 and P < 0.001, respectively). GBM width and Vv(mes/glom) increased from normoalbuminuric to proteinuric patients [P < 0.005 normoalbuminuric and microalbuminuric versus proteinuric for GBM, P < 0.01 normoalbuminuric versus proteinuric for Vv(mes/glom)]. In patients with increased GBM width (> 396 nm), CRP, SAA, and IL-6 were higher than in patients with normal GBM width (P < 0.003, P < 0.004, and P < 0.0004, respectively). GBM width was directly correlated with fibrinogen (r = 0.33, P < 0.002) and IL-6 (r = 0.25 P < 0.05). In conclusion, this study demonstrates that acute-phase markers of inflammation are associated with nephropathy status and GBM thickening, suggesting a role for inflammation in the pathogenesis of diabetic glomerulopathy.
authors.affiliation: Department of Medical and Surgical Sciences, University of Padova Medical School, Padova, Italy.
authors.forename: Michele
authors.initials: M
authors.lastname: Dalla Vestra
authors.forename: Michele
authors.initials: M
authors.lastname: Mussap
authors.forename: Pietro
authors.initials: P
authors.lastname: Gallina
authors.forename: Marino
authors.initials: M
authors.lastname: Bruseghin
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Cernigoi
authors.forename: Alois
authors.initials: A
authors.lastname: Saller
authors.forename: Mario
authors.initials: M
authors.lastname: Plebani
authors.forename: Paola
authors.initials: P
authors.lastname: Fioretto
mesh_terms: D000208:Acute Disease; D000368:Aged; D000419:Albuminuria / Q000097:blood / Q000175:diagnosis*; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy; D003928:Diabetic Nephropathies / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D018450:Disease Progression; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011336:Probability; D011379:Prognosis; D012016:Reference Values; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D002097:C-Reactive Protein