Vimentin expression is a predictor of renal dysfunction after kidney transplantation A expressão de vimentina é um preditor de disfunção renal após o transplante renal

Objective: To identify renal transplant patients with normal and stable renal function, long-term prognostic markers of renal function. Methods: We followed a protocol for renal biopsies in 32 patients at a median time of 180 days (min: 90 – max: 690 days) after the renal transplant. According to Banff’s classification (1997), biopsies were classified according to the presence or absence of chronic allograft nephropathy (CAN), and the sum of each chronic alteration produced the chronic score. All biopsy specimens were stained with picrosirius and observed under polarized light, and fibrotic tissue identified was quantified by histomorphometry. Using immunohistochemistry techniques, markers involved in the epithelium-mesenchymal transdifferentiation phenomenon were evaluated: vimentin (mesenchymal cell marker), alpha-SMA (myofibroblast marker), and cytokeratin (epithelial cell marker). Renal function was evaluated by serum creatinine levels at the time of biopsy, one and two years after the transplant, and current levels (36.5 ± 8.42 months after the biopsy). Statistical tests used were Mann-Whitney, Kruskal-Wallis, Spearman, and Fisher’s exact test. results: Tubular expression of vimentin correlated with creatinine level at biopsy (r = 0.390 p = 0.033), at one year (r = 0.405 p = 0.026), two years (r = 0.474 p = 0.008), and current (r = 0.415 p = 0.028). The interstitial expression of alpha-SMA correlated with creatinine at biopsy (r = 0.442 p = 0.014), at two years (r = 0.364 p = 0.047), and current (r = 0.376 p = 0.048). The interstitial expression of alpha-SMA was associated with chronic changes (r = 0.412 p = 0.029), with the expression of vimentin (r = 0.502 p = 0.004), with fibrosis estimated by picrosirius (r = 0.402 p = 0.003), and the presence of chronic allograft nephropathy (p = 0.04). Tubular expression of vimentin correlated with chronic allograft nephropathy (p = 0.001) and was the marker with the strongest association to chronic tubulointerstitial changes (r = 0.513 p = 0.003). Conclusions: The increased expression of vimentin in tubules may suggest the presence of acute or chronic tubular injury or a regenerative response of epithelial tubular cells after damage, or an occurrence of the epithelial-mesenchymal phenomenon. The greatest tubular expression of vimentin was observed in areas of greatest tubulointerstitial damage and greatest recruitment of myofibroblasts, the primary matrix-producing cells. Therefore, this study suggests that patients with stable renal function who have undergone kidney transplants and show an increased expression of vimentin in tubules progress with poorer long-term kidney function. Descriptors: Kidney transplant; Vimentin; Prognosis