Necrosis proximal convoluted tubules

Additional studies of decalin exposure in rats have characterized the specific sequence of renal alterations first the variable occurrence of light-microscopically evident proximal convoluted tubule epithelial cell necrosis, presumably a reflection of cellular injury associated with excessive protein accumulation (hyaline droplets) then the occurrence of granular casts at the junction of the inner and outer bands of the outer zone of the medulla and finally, chronic nephrosis, occurring secondary to tubular obstruction by granular casts. It is not... 

Renal 29 (necrosis, vascular degeneration of proximal convoluted tubules, increased BUN, excessive diuresis, oliguria, anuria, decreased creatinine clearance) ... 

The molecular structure of 5-ASA is very close of that of salicylic acid, phenacetin and aminophenol, drugs with a well-documented nephrotoxic potential (Figure 6). In rats, it is demonstrated that after a single intravenous injection of 5-ASA, at doses of 1.4, 2.8, 5.7 mM per kg body weight (high pharmacological doses), necrosis of the proximal convoluted tubules and papillary necrosis developed [107]. 

Mouse L pictor Laborious movement and ataxia Single-cell necrosis in file heart. Autophagic vacuoles in proximal convoluted tubules of file kidney. Glommili normal. Vacuolation and fat d osition in midzonal hepatocytes. Autophagic vacuoles in pancreatic acinar cells. Vacuolation in intestinal epithelium [93]... 

Histopathology of the liver showed centrilobular necrosis with a sharp demarcation. Death occurred rapidly, due to hypoglycemia. In these cases, centrilobular hepatocytes appeared swollen and showed karyolysis. In cases where death occurred only after a few days from liver failure, hepatocytes were necrotic. Fat vacuoles were seen in some hepatocytes, and the liver had minimal inflammatory infiltration. In cases of kidney failure, renal histology showed necrosis of the proximal convoluted tubules and loop of Henle. In these cases, the liver showed centrilobular collapse of the reticulum framework and cholestasis. 

This system was also used to demonstrate 3-Cys-A adducts in the mouse kidney and lung. Three hours after 400 mg/kg acetaminophen, adduct was present in most proximal and some distal convoluted tubules in the kidney (Figure 7). In the lung, adducts were restricted to epithelial cells lining the bronchi and bronchioles, sites previously reported to be the target of acetaminophen-induced necrosis ( ) and the location of the ethanol-inducible P-450 ( ) (Figure 8). 

After administration of mercuric chloride to mice, cell necrosis was found to be severest in the S2 and proximal S3 [228] segments of the proximal tubules corresponding to the preferential accumulation of mercury, engaging the convoluted part of the proximal tubular segment [229]. Very large mercury-containing lysosomes developed in the distal S3 segment. 

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