Kikuchi Yuichi, Kobayashi Shuzo, Hemmi Noriaki, Ikee Ryota, Hyodo Naomi, Saigusa Takamitsu, Namikoshi Tamehachi, Yamada Muneharu, Suzuki Shigenobu, Miura Soichiro
Second Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan.
Nephrol Dial Transplant. 2004 Mar;19(3):602-7. doi: 10.1093/ndt/gfg603.
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.
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).
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).
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.
