Fructose consumption has steadily increased over the past 30 years in parallel to the growth of the obesity and metabolic syndrome epidemic. It was recently reported that fructose is a risk factor for incident kidney disease and induces an inflammatory response in the kidney.Aim of the work
This study was conducted to determine the histological changes in the renal cortex of rats with high fructose intake.Materials and methods
Thirty adult male albino rats were used and were divided equally into three groups. Animals of the control group received the standard rat chow, the fructose-fed group received a high-fructose diet for 4 weeks, and the third group received high-fructose diet as similar to the second group and then also received the standard rat chow for another 4 weeks after stoppage of fructose. Kidney specimens were processed for histological and immunohistochemical study using light and electron microscopes.Results
In this study, a statistically significant elevation in the level of serum uric acid was observed in the fructose-fed group; histologically, some malpighian corpuscles appeared enlarged, whereas others were partially or completely atrophied. However, effacement of podocyte feet processes with irregular thickening of the filtration barrier was observed. In addition, tubulointerstitial injury in the form of tubular dilatation, vacuolation, and peritubular hemorrhage with inflammatory cellular infiltration and collagen fiber deposition in interstitial tissue were also observed. Using immunostaining, excess actin fibers were detected in tubular cells that indicated exposure of these cells to stress, which had also been detected previously in cases of acute tubular failure. The third group showed no evidence of improvement as the previous changes were still present.