EJMS

Abstract

Introduction: Excessive salt intake in diet was proved to produce some renal diseases. However, the duration of this excessive intake affecting the structure of the kidney and the underlying mechanisms inducing renal injury were not properly investigated. Aim of the work: This study was designed to compare the influence of high salt diet, for two different durations (two weeks and sixteen weeks), on the renal tissue in rats. Material and methods: Thirty adult Sprague Dawley male rats were equally divided into three groups; group I (control group); fed diet containing 0.3% NaCl, and high salt fed groups including: group II fed diet with 8% NaCl for 2 weeks and group III fed diet with 8% NaCl for 16 weeks. At the end of experiment, plasma level of urea and creatinine was detected. Samples from the kidneys were taken and stained with H & E, Masson’s Trichrome stain to assess collagen fibers and PAS stain to detect the amount of polysaccharides. Then, the specimens were prepared for light microscopic examination, Cox 2 and caspase-3 for immunohistochemical study and histomorphometric analysis. Results: High salt diet for 2 weeks caused only higher plasma urea and mild tubular damage compared to the control group. 16 week-high salt diet fed group exhibited significant higher plasma urea and creatinine, more prominent tubular damage and apoptosis compared to either the controls or group II, as well as extensive degeneration of the renal cortex, in the form of presence of many shrunken glomeruli with widened Bowman’s space. Also, tubular dilatation, exfoliated tubular cells and darkly stained pyknotic nuclei were observed. Large amount of collagen fibers around Bowman’s capsules and the renal tubules was determined in the 16 week-high salt diet fed group denoting renal fibrosis and faint PAS reaction around Bowman’s capsule and the renal tubules indicating reduction of the amount of polysaccharides. Moreover, the 16 week-high salt diet fed group showed strong positive Cox2 reaction in the renal tubules suggesting inflammation and degeneration of the tubular cells, in addition to strong positive caspase-3 reaction in the glomeruli denoting marked apoptosis.