Thrombospondin-1 in Patients with Diabetic Nephropathy

Thrombospondin-1 in Patients with Diabetic Nephropathy

  • نوع فایل : کتاب
  • زبان : انگلیسی
  • مؤلف : Saeed Abdelwhab & Osman Fooda & Sahar Abdelmaksoud
  • چاپ و سال / کشور: 2010

Description

Thrombospondin-1 (TSP-1), a potent antiangiogenic and proatherogenic protein, has been implicated in the development of several vascular diabetic complications. The aim of the study is to find the role of TSP-1 in diabetic nephropathy.We investigated serumTSP-1 in 30 patients with type 2 diabetes mellitus and diabetic nephropathy (group 1) with renal disease grade 1 to 3 (Kidney Disease Outcomes Quality Initiative stages of kidney disease) and 15 normal control subjects (group 2). Thorough history and clinical examination, biochemical tests including renal function tests, renal ultrasound and renal artery Doppler were done to the studied groups. In addition, carotid intima media thickness and serum TSP-1 enzyme-linked immunosorbent assay were measured. Serum TSP-1 was increased in diabetic nephropathy (193.33±43.28) ng/ml compared to controls (106.27± 38.80) ng/ml (p<0.001). TSP-1 correlates negatively with glomerular filtration rate (p<0.001) and positively with resistivity index (RI) of extrarenal vessels (p<0.001) and RI intrarenal vessels (p<0.001). There is also positive correlation between serum TSP-1 with age (p=0.004) and carotid intima media thickness (p=0.004). No correlation was found with proteinuria (p=0.37). Linear regression test in group 1 shows TSP-1 is significant independent determinant for glomerular filtration rate (p<0.001) and carotid intima media thickness (p=0.002). The present study suggests that TSP-1 plays an important role in development of complications in Patients with diabetic nephropathy. Serum level of TSP-1 is related to renal injury and vascular disease. Further studies may be necessary to determine casual relationship between TSP-1 and renal damage and to determine the role of targeting TSP-1 in managing these complications and preventing its progress.
Kidney (2010) 19:229–235 DOI 10.1007/s00596-010-0156-4 Published online: 22 May 2010
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