The susceptibility of the kidneys to fluoride toxicity can largely be attributed to its anatomy and function. As the filtrate moves along the complex tubular structure of each nephron, it is concentrated in the proximal and distal tubules and collecting duct. It has been frequently observed that the children suffering from renal impairments also have some symptoms of dental and skeletal fluorosis. The findings suggest that fluoride somehow interferes with renal anatomy and physiology, which may lead to renal pathogenesis. The aim of this study was to evaluate the fluoride-associated nephrotoxicity. A total of 156 patients with childhood nephrotic syndrome were screened and it was observed that 32 of them had significantly high levels ( p ≤ 0.05) of fluoride in urine (4.01 ± 1.83 ppm) and serum (0.1 ± 0.013 ppm). On the basis of urinary fluoride concentration, patients were divided into two groups, namely group 1 (G-1) ( n = 32) containing normal urine fluoride (0.61 ± 0.17 ppm) and group 2 (G-2) ( n = 32) having high urine fluoride concentration (4.01 ± 1.83 ppm). Age-matched healthy subjects ( n = 33) having normal levels of urinary fluoride (0.56 ± 0.15 ppm) were included in the study as control (group 0 (G-0)). Kidney biopsies were taken from G-1 and G-2 only, who were subjected to ultrastructural (transmission electron microscopy) and apoptotic (terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling) analysis. Various subcellular ultrastructural changes including nuclear disintegration, chromosome condensation, cytoplasmic ground substance lysis, and endoplasmic reticulum blebbing were observed. Increased levels of apoptosis were observed in high fluoride group (G-2) compared to normal fluoride group (G-1). Various degrees of fluoride-associated damages to the architecture of tubular epithelia, such as cell swelling and lysis, cytoplasmic vacuolation, nuclear condensation, apoptosis, and necrosis, were observed.

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After 45 days of complete diversion colostomy in male Wistar rats, morphometry of soma and nuclei of NADPH diaphorase positive cells of the myenteric plexus was evaluated. There was a significant (P < 0.0001) diminution in the area, perimeter and volume-weighted mean volume of soma and nuclei of nitrergic myenteric neurones in the defunctionalized colon. In addition, there was a significant reduction in the neuronal density of the myenteric neurones, and increased distance between the ganglia. In addition, there was myenteric glial atrophy. Atrophy of colonic myenteric neurones was accompanied by significant reduction (P < 0.001) in the volume fraction of the muscularis externa, the prime targets of these neurones. The disturbances in the microecology of the colon may jeopardize the finely orchestrated functioning of the components of the Enteric nervous system (ENS) leading to colonic dysfunction. Our observations, by extrapolation, may explain the bowel dysmotility in humans after restoration of colonic continuity after colostomy.