Histological and Ultrastructure Study of Toxic Effect of Sodium Fluoride on the Renal Cortex of Adult Albino Rats and the Possible Role of Calcium Therapy

Aim of the Study: to evaluate the toxic effects of sodium fluoride on renal cortex of adult albino rat and to investigate the possible protective effects of calcium during fluoride exposure, if it is protective or not? Material and Methods: 18 adult albino rats were used for this study. These animals were equally divided into three groups as follows: Control group: animals were received tap water and balanced diet, NaF treated group: animals were administrated sodium fluoride (NaF) at dose, (30 mg /kg/day) and NaF and Ca treated group: animals were treated with NaF (the same dose as mentioned before) and calcium chloride (Cacl) (20 mg /kg/day) orally by gastric feeding tube for 6 weeks. At the end of the experimental period, the rats were sacrificed and the kidney was rapidly removed and was utilized for light and electron microscopic examinations. Also blood samples from each group were collected for performing renal function tests by estimations the levels of serum urea and creatinine (mg/dl) and analyzed statistically using ANOVA (analysis of variance) test. The Results: by light microscope, in the NaF treated group, there was significant morphological damage to the renal cortex by exposure to NaF including; different forms of glomerular degeneration (marked lobulation, marked hypertrophy or shrinkage with expanded Bowman’s capsule) and massive degeneration of renal convoluted tubules with their epithelium (marked dilatation of some tubular lumens, sloughing of tubular epithelial cells, cell swelling, vacuolar degeneration and lysis of their cytoplasm with loss of their organelles). However, in the NaF and Ca treated group, Calcium failed to restore the renal damage induced by NaF exposure and still there were extensive degenerative changes on the renal cortex. However, by electron microscope, the most important morphological features of fluoride nephrotoxicity were a degeneration of kidney's filtration barrier, constriction and congestion of Glomerular capillaries, Mesangial hypercellularity, Mesangial matrix expansion and necrosis of podocyte. There also were different degree of degeneration of the tubular epithelial cells ranging from moderate to massive cellular destruction (reduction of the cellular and nuclear sizes, apoptosis, complete loss of the microvillar brush border, massive loss of most of cytoplasmic organelles and distortion of the cell basement membrane). However, the NaF and Ca treated group showed more excessive degenerative changes in Glomerulus more than that of NaF treated group manifested by marked swelling of the whole endothelial lining of the Glomerular capillary wall and injurious appearance of the podocyte with effacement of their foot processes, while, showed similar degenerative changes in proximal epithelial cells like that observed in NaF treated group. The Biochemical results showed significant difference between the three groups (P<0.05). Serum urea and creatinine levels were increased in NaF treated group (31.4±8.2 and 0.8±0.2 respectively), as compared to the control group (16.4±6.4 and 0.6±0.2 respectively). While in NaF and Ca treated group, the levels of Serum urea and creatinine were more greatly increased (52.6±11.6 and 1.4±0.3 respectively), if compared to the two previous groups. Conclusion: This work showed that sodium fluoride administration induced morphological degenerative changes and impairment on the renal cortex. Calcium administration not only failed to restore renal damage induced by NaF exposure but also enhanced the flouride-induced toxicity.