Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We determined the serum amyloid A protein (SAA) levels in patients with non-insulin-dependent diabetes mellitus (NIDDM), and investigated the possible association between SAA and the complications of NIDDM. The concentrations of SAA were measured in the plasma of 105 patients with NIDDM (52 men and 53 women, age mean +/- SD, 61 +/- 13 years) and 91 healthy subjects (37 men and 54 women, aged 57 +/- 11 years). SAA concentrations were assayed by enzyme-linked immunosorbent assay. SAA concentrations in the patients with NIDDM were significantly higher than those in healthy subjects (2.1 +/- 1.3 vs. 1.2 +/- 0.5 mg/L). There were no obvious relationships between SAA levels and duration of diabetes, type of therapy, or control of blood sugar in the patients with NIDDM. However, SAA levels in patients with NIDDM increased significantly, with increase of urinary albumin excretion (p = 0.027). The increase of SAA in the patients with NIDDM did not influence the serum concentrations of lipid or lipoprotein. The SAA concentration in NIDDM was unrelated to the type of treatment, but seemed to be related to the development of diabetic nephropathy.
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PMID:Serum amyloid A protein in patients with non-insulin-dependent diabetes mellitus. 753 7

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.
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PMID:Acute-phase markers of inflammation and glomerular structure in patients with type 2 diabetes. 1593 41