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Renal tubular lesions

Two studies in rats have potential implications for humans. In rats with mild to severe lithium-induced nephropathy, urine TV-acetyl-p-D-glucosaminidase was an early indicator of renal insufficiency (369). Both 6Li and 7Li caused reduced urine concentrating ability and increased urine volume and renal tubular lesions, but 6Li was more nephrotoxic (370). The authors suggested that eliminating 6Li from pharmaceutical products might reduce nephrotoxicity (although 6Li accounts for only about 7% of the lithium in such products). [Pg.145]

The authors concluded that the most likely cause of renal insufficiency was etherified starch-induced tubulopathy and hypothesized that even low amounts of etherified starch as replacement fluid in plasma exchange can cause renal tubular lesions in patients predisposed for other reasons (such as drugs or renal hypoperfusion) to renal insufficiency. In this context, albumin should be combined with replacement fluids other than etherified starch. [Pg.1290]

Guder WG, Hofman W. Markers for the diagnosis and monitoring of renal tubular lesions. Clin Nephrol 1992 38 (SuppI 1) S3-S7. [Pg.119]

GritzkaTL, Trump BF. Renal tubular lesions caused by mercuric chloride electron microscopic observations. Am J Pathol 1968 52 1225-78. [Pg.824]

Lithium and only a few other drugs have been reported to cause chronic interstitial nephritis, which is usually a progressive and irreversible lesion (Choudhury and Ahmed 2006 Silva 2004). Several renal tubular lesions have been associated with lithium therapy an impaired ability to concentrate urine (nephrogenic diabetes insipidus) has been seen in up to 87% of patients (Markowitz et al. 2000). Acute... [Pg.121]

Ganther HE, Goudie C, Sunde ML, Kopecky MJ, Wager P, Oh SH, Hoekstra WG (1972) Selenium relation to decreased toxicity of methylmercury added to diets containing tuna. Science 175 1122-1124 Goldstein GW, Betz AL (1986) The blood-brain barrier. Sci Am 255 74-83 Gritzka TL, Trump BF (1968) Renal tubular lesions caused by mercuric chloride. Am J Pathol 52 1225-1277... [Pg.181]

Male rats are sensitive to renal tubular nephropathy after exposure to hexachloroethane. The lesions observed are characteristic of hyaline droplet nephropathy. They are most likely the result of hexachloroethane or one of its metabolites binding to the excretory protein 2p-globulin, altering its kidney transport, and leading to the formation of hyaline droplets. This protein is synthesized by male rats and accounts for 26% of their urinary protein excretion (Olson et al. 1990). It is not excreted in female rats except in minimal quantities. Since some effects are also seen in kidneys of female rats and in male and female mice that do not synthesize 2p-globulin, hexachloroethane must also have milder adverse effects on the kidney through a different mechanism. [Pg.61]

Acute-, intermediate-, and chronic-duration oral exposures of male rats to doses of 10 mg/kg/day or greater were associated with renal tubular nephropathy (Gorzinski et al. 1985 NTP 1977, 1989 Weeks et al. 1979). Affected animals displayed tubular necrosis, hyaline droplets in tubular epithelial cells, regenerative tubular epithelium, interstitial nephritis, and fibrosis. The severity of the renal lesions varied with the dose and the duration of exposure. [Pg.89]

Effects Noted in Study and Corresponding Doses Doses of 0.20 mg/kg/day and greater resulted in neurotoxicity evidenced by convulsions, tremors, and degenerative lesions in the brain and systemic toxicity which included renal tubular necrosis, respiratory distress and pulmonary edema, and diffuse degenerative lesions of the heart. One animal administered diet corresponding to 0.20-0.27 mg/kg/day died after 47 days of feeding. [Pg.198]

In chronic studies, DMMP was administered by gavage in corn oil for up to 2 years at doses of 500 or 1000 mg/kg/day to rats and at doses of 1000 or 2000mg/kg/day to mice. " Survival in dosed male rats was reduced, due in part to renal toxicity. Lesions of the kidney included increased severity of spontaneous age-related nephropathy including calcification, hyperplasia of the tubular and transitional epithelium, tubular cell adenocarcinomas, and transitional cell papillomas and carcinomas. Similar lesions were not seen in female rats or in mice of either sex, although reduced survival in male mice prevented adequate analysis. The... [Pg.270]

No deaths were observed in rats at concentrations up to 800 ppm or in mice up to 400 ppm in an NTP study lasting 13 weeks (6 hours/day, 5 days/week). Nasal cavity lesions and reduced body weight were seen in rats exposed at 800 ppm. In mice, renal tubular necrosis was found at 800 ppm, a dose that was lethal. Inflammation of the nasal turbinates was observed in female mice at 100 ppm and above and in male mice at 2 00 ppm and above. In an earlier study, slight growth retardation was observed in rats and mice exposed at 600 ppm for 13 weeks inflammatory and degenerative changes in the nasal mucosa were observed in both species. Myeloid hyperplasia in bone marrow occurred in male rats only. No effects were noted at 75 or 150ppm. [Pg.297]

In the only alleged case of chronic human poisoning, an exterminator repeatedly exposed over a period of 10 years presented with severe and progressive lesions of the renal tubular... [Pg.635]

In the chronic gavage study by NTP (1986), dosed male rats had increased incidences of renal tubular cell hyperplasia, epithelial cell hyperplasia of the renal pelvis, and tubular mineralization. The male rats also had increased incidences of renal tubular cell tumors. The hyperplasia of the tubular cells, therefore, may represent a preneoplastic response (see discussion of cancer below). These proliferative kidney lesions were not observed in male or female mice or in female rats. The mechanism for the induction of proliferative kidney lesions may also be related to a2p-globulin-induced nephropathy (see discussion of cancer below), again raising the question of the relevance of the proliferative kidney lesions in male rats to humans. This issue is presently the subject of scientific investigation. [Pg.50]

Several heavy metals, particularly lead, are known to cause major adverse effects to the mammalian kidney, resulting in kidney function impairment. Adverse effects to the mammalian kidney caused by lead include lesions on the proximal tubule and Henle s loop, and the presence of lead inclusion bodies. The metal also is known to cause aminoaciduria, phosphaturia, glycosuria, and renal tubular acidosis. Workers associated with lead-smelting industries also have shown kidney cancer. [Pg.400]

Large doses of acetaminophen can cause renal and hepatic toxicity in rats and mice. Toxicity is characterized by renal tubular necrosis in the proximal tubules (Schnellmann, 2001). Acetaminophen toxicity has also been reported in humans. Generally, toxicosis is a result of large overdoses which result in proximal tubular necrosis. Aspirin, ibuprofen, and acetaminophen are the important analgesics, which are reported to cause toxicosis in veterinary medicine. Renal lesions including renal tubular necrosis and papillary necrosis have been reported in dogs. [Pg.566]

Gross lesions are absent and microscopic findings include degeneration and necrosis of proximal renal tubular epithelium with intact basement membrane, regeneration of the tubular epithelium and mineralization. The tubules contain granular and protein casts. In some animals, fibrinous arteritis of the large colon was also observed (Eubig et al, 2005 Morrow et al, 2005). [Pg.572]

Renal 0.8 2.9 (micoscopic focal lesions in renal tubular ... [Pg.54]

F (proteinuria minimal microscopic lesions in renal tubular epithelium)... [Pg.157]


See other pages where Renal tubular lesions is mentioned: [Pg.1289]    [Pg.884]    [Pg.702]    [Pg.1289]    [Pg.884]    [Pg.702]    [Pg.46]    [Pg.106]    [Pg.121]    [Pg.39]    [Pg.246]    [Pg.370]    [Pg.684]    [Pg.604]    [Pg.28]    [Pg.237]    [Pg.331]    [Pg.23]    [Pg.75]    [Pg.146]    [Pg.565]    [Pg.565]    [Pg.566]    [Pg.568]    [Pg.568]    [Pg.569]    [Pg.210]    [Pg.238]    [Pg.418]    [Pg.421]    [Pg.428]    [Pg.3284]    [Pg.461]   
See also in sourсe #XX -- [ Pg.702 , Pg.780 ]




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