Excessive exposure to several metallic elements is known to produce a variety of nephrotoxic syndromes such as glomerulonephritis, nephrotic syndrome, interstitial nephritis, structural and functional abnormalities of proximal tubule resembling the Fanconi's syndrome and acute tubular necrosis. Although the pulmonary toxicities of silicon are relatively well documented as a cause of silicoproteinosis and lung fibrosis after acute and chronic exposure to free silica(SiO2), but is little known about the nephrotoxicity of this trace element. Clinical manifestations of silicon nephropathy are similar to other heavy metal nephropathy as proteinuria, hematuria, active urinary sediments and renal failure. Diagnosis of silicon nephropathy is based on distinct exposure history to silica, variable degree of renal dysfunction and characteristic histologic findings such as cytoplasmic vacuoles and dense membrane-enclosed cytoplasmic bodies which is resembling lysosomes in proximal tubular cells. A 26-year-old man with ingestion of silicon compound(SiO2-NaOCO3) developed acute renal failure due to acute tubular necrosis. And he was recovered with conservative management to acute renal failure. So we report this case with a brief review of literature.
Acute Kidney Injury* ; Adult ; Cytoplasm ; Diagnosis ; Eating* ; Fibrosis ; Glomerulonephritis ; Hematuria ; Humans ; Lung ; Lysosomes ; Necrosis ; Nephritis, Interstitial ; Nephrotic Syndrome ; Proteinuria ; Renal Insufficiency ; Silicon Dioxide ; Silicon* ; Vacuoles