Vimentin expression is a predictor of renal dysfunction after kidney transplantation

renal function, long-term prognostic markers of renal function. Methods:We followed a protocol for renal biopsies in 32 patients at a mediantime of 180 days (min: 90 – max: 690 days) after the renal transplant.According to Banff’s classification (1997), biopsies were classifiedaccording to the presence or absence of chronic allograft nephropathy(CAN), and the sum of each chronic alteration produced the chronicscore. All biopsy specimens were stained with picrosirius and observedunder polarized light, and fibrotic tissue identified was quantifiedby histomorphometry. Using immunohistochemistry techniques,markers involved in the epithelium-mesenchymal transdifferentiationphenomenon were evaluated: vimentin (mesenchymal cell marker),alpha-SMA (myofibroblast marker), and cytokeratin (epithelial cellmarker). Renal function was evaluated by serum creatinine levels atthe time of biopsy, one and two years after the transplant, and currentlevels (36.5 ± 8.42 months after the biopsy). Statistical tests usedwere Mann-Whitney, Kruskal-Wallis, Spearman, and Fisher’s exact test.Results: Tubular expression of vimentin correlated with creatinine levelat 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 atbiopsy (r = 0.442 p = 0.014), at two years (r = 0.364 p = 0.047), andcurrent (r = 0.376 p = 0.048). The interstitial expression of alpha-SMAwas associated with chronic changes (r = 0.412 p = 0.029), with theexpression of vimentin (r = 0.502 p = 0.004), with fibrosis estimated bypicrosirius (r = 0.402 p = 0.003), and the presence of chronic allograftnephropathy (p = 0.04). Tubular expression of vimentin correlated withchronic allograft nephropathy (p = 0.001) and was the marker with thestrongest association to chronic tubulointerstitial changes (r = 0.513p = 0.003). Conclusions: The increased expression of vimentin intubules may suggest the presence of acute or chronic tubular injury ora regenerative response of epithelial tubular cells after damage, or anoccurrence of the epithelial-mesenchymal phenomenon. The greatesttubular expression of vimentin was observed in areas of greatesttubulointerstitial damage and greatest recruitment of myofibroblasts,the primary matrix-producing cells. Therefore, this study suggeststhat patients with stable renal function who have undergone kidneytransplants and show an increased expression of v