Silicon nephropathy.
A patient with excessive industrial exposure to silicon and an elevated silicon content in his renal tissue was found to have a distinctive nephropathy, characterized pathologically by changes in the glomeruli and proximal tubules, and manifested clinically by albuminuria and hypertension. Proximal tubular function was intact. From a biochemical standpoint, this finding correlates with the demonstration in vitro that, in contrast to cadmium, a known cause of Fanconi syndrome, silicon does not inhibit renal cortical sodium-potassium-adenosine triphosphatase (Na-K-ATPase).
D000328:Adult; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007672:Kidney Cortex / Q000187:drug effects / Q000201:enzymology; D007677:Kidney Function Tests; D007678:Kidney Glomerulus / Q000473:pathology / Q000648:ultrastructure; D007687:Kidney Tubules, Proximal / Q000473:pathology; D008297:Male; D008854:Microscopy, Electron; D009784:Occupational Diseases / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D012824:Silicic Acid / Q000494:pharmacology; D012825:Silicon / Q000506:poisoning*
D002104:Cadmium; D012824:Silicic Acid; D012825:Silicon