title: Galectin-3-positive cell infiltration in human diabetic nephropathy.
abstract: 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Second Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan. grd1615@gr.ndmc.ac.jp
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Kikuchi
authors.forename: Shuzo
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Noriaki
authors.initials: N
authors.lastname: Hemmi
authors.forename: Ryota
authors.initials: R
authors.lastname: Ikee
authors.forename: Naomi
authors.initials: N
authors.lastname: Hyodo
authors.forename: Takamitsu
authors.initials: T
authors.lastname: Saigusa
authors.forename: Tamehachi
authors.initials: T
authors.lastname: Namikoshi
authors.forename: Muneharu
authors.initials: M
authors.lastname: Yamada
authors.forename: Shigenobu
authors.initials: S
authors.lastname: Suzuki
authors.forename: Soichiro
authors.initials: S
authors.lastname: Miura
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000032:analysis*; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis*; D016022:Case-Control Studies; D002465:Cell Movement / Q000502:physiology*; D003928:Diabetic Nephropathies / Q000473:pathology*; D037502:Galectin 3 / Q000032:analysis*; D005921:Glomerulonephritis / Q000473:pathology*; D006801:Humans; D007678:Kidney Glomerulus / Q000473:pathology; D008264:Macrophages / Q000502:physiology; D008875:Middle Aged; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D037502:Galectin 3; C067980:CD68 antigen, human; D000097382:CD68 Molecule