Renal tubular necrosis

Renal Effects. Acute renal failure occurred in a man who washed his hair with an unknown amount of diesel fuel (Barrientos et al. 1977). In addition, he had oliguria biopsy revealed mitosis and vacuolization in renal cells, tubular dilation, and some cellular proliferation in the glomerulus. Another man developed acute tubular renal necrosis after washing his hands with an unspecified diesel fuel over several weeks (Crisp et al. 1979). Specifically, patchy degeneration and necrosis of the proximal and distal tubular epithelium with preservation of the basement membranes were noted. Also, increased blood urea nitrogen and serum creatinine levels were noted in this individual. Effects resulting from inhalation versus dermal exposure could not be distinguished in these cases. 

Renal Effects. In one individual, acute renal failure was noted from inhalation and/or dermal exposure to diesel fuel which was used as a shampoo. Biopsy detected tubular dilation, mitosis, and vacuolization in renal cells, and some cellular proliferation in the glomerulus in this individual (Barrientos et al. 1977). Another individual experienced renal failure following inhalation of diesel fuel vapor for 10 days (Reidenberg et al. 1964). Renal necrosis developed in one man after washing his hands with diesel fuel over several weeks (Crisp et al. 1979). Urinalysis was normal following inhalation of JP-5 by two individuals or ingestion of kerosene by numerous individuals (Dudin et al. 1991 Mahdi 1988 Nouri and Al-Rahim 1970 Porter 1990). 

The nephropathy induced by accumulation of this protein has not been noted in female rats, female mice (studies conducted on male mice were not located), or dogs of either sex when exposed under similar conditions to either JP-5 or marine diesel fuel vapors (Bruner 1984 Cowan and Jenkins 1981 Gaworski et al. 1984). There is no evidence of renal necrosis in humans acutely exposed to JP-5 vapor (Porter 1990). In a case report, one individual exposed to an unspecified diesel fuel for several weeks exhibited acute tubular necrosis (Crisp et al. 1979). However, renal necrosis did not occur in two other individuals acutely exposed to diesel fuel vapor (Barrientos et al. 1977 Reidenberg et al. 1964), although they did... 

Trichloroethylene is metabolized similarly and gives rise to dichlorovinyl cysteine. It has been found that S-(l,2-dichlorovinyl)-L-cysteine (DCVC) and S-(2-chloroethyl)-DL-cysteine (CEC) (Fig. 7.30) are both nephrotoxic when administered to animals causing renal proximal tubular necrosis. CEC does not require 3-lyase activation to be nephrotoxic, but can rearrange, possibly to a reactive episulfonium ion, by nucleophilic displacement of the chlorine atom. These compounds decrease the activity of the renal tubular anion and cation transport system. 

Janssen U, Thomas G, Giant T, Phillips A. Expression of inter-alpha-trypsin inhibitor and tumor necrosis factor-stimulated gene 6 in renal proximal tubular epithelial cells. Kidney... 

Flealy E, Dempsey M, Lally C, and Ryan MP. Apoptosis and necrosis mechanisms of cell death induced by cyclosporine A in a renal proximal tubular cell line. Kidney Int 54 1955-1966,1998. 

Colourless oily liquid chloroform-like odour. Sweet taste. Vapour can be ignited. Irritant to eyes and gut. CNS depressant. Sensitizes myocardium to endogenous catecholamines. Headache, ataxia, dizziness, dilated pupils, convulsions, coma, renal failure (tubular necrosis), liver damage (jaundice), extrapyramidal effects can occur. Death arrhythmia. 

Crystalline colourless solid. Found in many plants, particularly the leaves of the rhubarb plant and in the juice of wood sorrel. Salts of Sorrel, Salts of Lemon. Used as a bleach and ink stain remover. The concentrated solution is corrosive. Harmful if inhaled or absorbed through skin 15 g oral agonizing pain, nausea and vomiting with haematemesis. Lowers plasma calcium convulsions, tetany, tingling of mucous membranes. Renal damage tubular necrosis. Smallest lethal dose reported 3.8 g in a 16-year-old boy. 

The timing of the urine collections is a critical factor in detecting renal injury. Tubular necrosis is an event more likely to occur early in a study, and therefore urine samples are best taken during this early period, whereas renal papillary necrosis is more likely to occur in a later part of a study (Heywood 1981). In some acute cardiac toxic events, the cardiac biomarkers increase within a few hours of injury, so sampling needs to be timed within this window because later samples may not show elevations of these biomarkers. 

The mechanisms of kidney injury include direct tubular epithelial cell toxicity with increased tubular permeability and necrosis, as well as arterial vasoconstriction and ischemic injury (Fanos and Cataldi 2000). Overall, the combined effects of increased cell energy and oxygen requirements due to greater cell membrane permeability, and reduced cellular oxygen delivery due to renal vasoconstriction, results in renal medullary tubular epithelial cell necrosis and kidney injury. Risk factors include CKD, higher average daily doses, volume depletion, and concomitant administration of diuretics and other nephrotoxins (e.g., cyclosporine) (Deray 2002 Costa and Nucci 2001). Rapid infusions of amphotericin B have the potential... 

Garcia TM, da Costa JA, Costa RS, Ferraz AS. Acute tubular renal necrosis in kidney transplant patients treated with enalapril. RenFail (1994) 16, 419-23. 

Lash, L.H., Putt, D.A., Hueni, S.E., Krause, R.J., and Elfarra, A.A. (2003) Roles of necrosis, apoptosis, and mitochondrial dysfunction in S-(l,2-dichlorovinyl)-L-cysteine sulfoxide-induced cytotoxicity in primary cultures of human renal proximal tubular cells. J. Pharmacol. Exp. Ther. 305, 1163-1172. 

Burn injury fluid loss and increased blood viscosity with blood and muscle damage blocked microcirculation and decreased renal perfusion decreased perfusion of renal cells - ischemia necrosis tubular necrosis and decreased renal function fluid, electrolyte, and acid-base imbalance... 

The majority of the recent reports on adverse reactions to cephalosporins pertain to nephrotoxic effects (acute renal failure, tubular necrosis) after high dosages (8—24 g/day) of cephalothin, especially in elderly patients with a pre-existing renal insufficiency (44 —47 ). Acute interstitial nephritis with haematuria, eosinophilia, oliguria and azotaemia developed in a 56-year-old woman after 9 days of treatment with 16g of cephalothin per day. The pa-... 

Renal Effects. Hemorrhage of the medullary layer of the kidneys was reported in three persons who died following ingeshon of endosulfan (Terziev et al. 1974). Acute renal failure was a major contributor to the deaths of two individuals who ingested unknown amounts of endosulfan (Blanco-Coronado et al. 1992 Loetal. 1995). In both cases, postmortem examination revealed extensive tubular necrosis. In contrast, no kidney lesions were found in a man who died 4 days after ingesting approximately 260 mg endosulfan/kg (Boereboom et al. 1998). 

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