Galectin-3-positive cell infiltration in human diabetic nephropathy

Academic Article


  • Background. Galectin-3 has several functions, such as cell proliferation, regulation of apoptosis and interaction of cell adhesion, and has a high binding affinity for advanced glycation end products. In animal models with diabetic nephropathy (DMN) or acute renal failure, galectin-3 is known to be upregulated. However, galectin-3 expression has not been investigated in human kidney diseases. Methods. Using immunohistochemistry we examined galectin-3 expression in renal biopsy specimens obtained from 37 patients with nephropathy: DMN (n=9), IgA nephropathy (n=9), crescentic glomerulonephritis (n=8), membranous nephropathy (n=6) and minimal change nephrotic syndrome (n=5). Results. In normal human kidney, galectin-3 was found in distal tubuli, but not in glomeruli. However, galectin-3-positive cell infiltration was observed in glomeruli of 12 patients. Galectin-3-positive cells, also stained with CD68, were significantly more numerous in glomeruli of DMN than in glomeruli of other nephropathies. The ratio of galectin-3-positive cells to the total number of macrophages in tubules was also significantly increased in DMN. There was a significant correlation between the number of galectin-3-positive cells in glomeruli and urinary protein excretion in all patients (r=0.616, P<0.001). In diabetic patients, the number of galectin-3-positive cells in glomeruli closely correlated with the regression rate of renal function (r=-0.930, P<0.005). Conclusion. These findings suggest that galectin-3-positive cell infiltration may play an important role in the progression of DMN, and the degree of its expression may be predictive of poor prognosis of DMN. © ERA-EDTA 2004; all rights reserved.
  • Published In

    Digital Object Identifier (doi)

    Pubmed Id

  • 25854268
  • Author List

  • Kikuchi Y; Kobayashi S; Hemmi N; Ikee R; Hyodo N; Saigusa T; Namikoshi T; Yamada M; Suzuki S; Miura S
  • Start Page

  • 602
  • End Page

  • 607
  • Volume

  • 19
  • Issue

  • 3