Alteration in the epithelial markers presents in renal tubules from a rat model of Hemolytic Uremic Syndrome (HUS).

OCHOA F, MIRABELLI C, LAGO N, IBARRA C, ZOTTA E.

Río de Janeiro, Brasil

Congreso; 7 World Congress of Nephrology.; 2007

Introduction: In Argentina, HUS is the most frequent cause of acute renal failure (ARF) in children of 5 years old, caused by Shiga toxin (Stx) producing Escherichia coli. It has been reported that 30% of the patients with HUS progress to chronic renal disease. The aim of our work was to study the responsible factors able to induce the renal chronic progression. Methods: Sprague-Dawley rats (150 g) were inoculated by intraperitoneal route with 3 mL of culture supernatant of recombinant E. coli that contain 80 ng/mL of Shiga toxin type 2 (Stx2). Light microscopy and immunohistochemical studies using anti TGF-beta1, Bax, e-cadherine, beta- catenine and alpha actin antibodies were performed. Results: After 48 hs post inoculation, rats developed ARF. Immunohistochemical studies revealed the presence of Stx2 in the basolateral membranes and cytoplasm of epithelial cells. TGF beta 1 was expressed in basolateral membranes of necrotic proximal tubules and in the isolated glomeruli. In the same regions sites of apoptosis was confirmed by Bax immunodetection. The renal necrotic tubules that expressed TGF beta 1 did not show expression of e-cadherine and beta catenine. However, beta catenine was found in cytoplasmic granules of several tubule cells. Moreover, alpha actin was localized in the apical membrane in necrotic proximal tubules. Conclusion: In conclusion, renal tubules from a rat model of HUS developed acute necrosis and expressed TGF beta 1, with lost of epithelial markers. This results suggests a change in epithelial tubular structure that could be involved in the later evolution to fibrosis, loss of the tubular function and consequent advance to the chronic renal failure.