Toxicity kidney

Uranium as of 12/08/03 zero as of 12/08/03 30ug/L Increased risk of cancer, kidney toxicity Erosion of natural deposits... 

Compounds that Cause Kidney Damage Several drugs and some anesthetic compounds such as methoxyflurane cause kidney damage when present at high doses. Kidney-toxic compounds found in occupational environments include mycotoxins, halogenated hydrocarbons, several metals, and solvents (see Table 5.16). 

There are undifferentiated stem cells of the blood elements in the bone marrow that differentiate and mature into erythrocytes, (red blood cells), thrombocytes (platelets), and white blood cells (leukocytes and lymphocytes). The production of erythrocytes is regulated by a hormone, erythropoietin (see the section on kidney toxicity), that is synthetized and excreted by the kidney. An increase in the number of premature erythrocytes is an indication of stimulation of erythropoiesis, i.e., increased production of erythrocytes in anemia due to continuous bleeding. 

Metabolomics studies the entire metabolism of an organism. It is possible to consider characterising the complex pattern of cellular proteins and metabolites that are excreted in urine. Pattern recognition techniques of nuclear magnetic resonance spectra have been applied to determine the dose-response using certain classical liver and kidney toxicants (Robertson et al, 2000). This could well provide a signature of the functional state of the kidney, and perturbations in the pattern as a result of exposure to a chemical could be observed. But first it would be necessary to understand how compounds with known effects on the kidney affect these processes. 

ROBERTSON D G, REILY M D, SIGLER R E et al, (2000) Metabonomics Evaluation of nuclear magnetic resonance (NMR) and pattern recognition technology for rapid in vivo screening of liver and kidney toxicants. Toxicol Sci. 57 326-37. 

No information is available on the adverse health effects of hexachloroethane in humans. Animal studies revealed that hexachloroethane primarily causes liver and kidney toxicity. Effects on the nervous system and lungs have also been reported. The mechanism by which these effects are mediated is not well characterized. Reductive metabolism by cytochrome P-450 and production of a free radical intermediate have been suggested as factors in hexachloroethane-induced hepatotoxicity (Nastainczyk et al. 1982a Thompson et al. 1984 Town and Leibman 1984). Accordingly, one possible approach may be to reduce free radical injury. To that end, oral administration of N-acetylcysteine can be used as a means of reducing free radical injury. Also, oral administration of vitamin E and vitamin C may be of value since they are free radical scavengers. 

The RfDs and TDIs are often used to establish regulatory standards. Such standards usually specify a limit on the allowable concentration of a chemical in an environmental medium. The process is not difficult to understand. The RfD and its related estimates of population thresholds is a dose, typically expressed in mg/(kg b.w. day), that is considered to be without significant risk to human populations exposed daily, for a lifetime. Consider mercury, a metal for which an RfD of 0.0003 mg/(kg b.w. day) has been established by the EPA, based on certain forms of kidney toxicity observed in rats (Table 8.4). These are not the only toxic effects of mercury, but they are the ones seen at the lowest doses. Note also that we are dealing with inorganic mercury, not the methylated form that is neurotoxic. 

The MRL was based on liver toxicity rather than kidney toxicity because the effects of 1,4-dichlorobenzene on the kidneys of male rats are associated with the occurrence of hyaline droplets from 2. -globulin and are not applicable to humans (EPA 1991i). 

Other reports have confirmed the species-and sex specificity for kidney toxicity by decalin. Relevance to human exposure has not been established. ... 

Animal studies have shown MEK to enhance the development of or increase the severity of neurotoxic effects due to methyl n-butyl ketone, ethyl butyl ketone, -hexane, and 2,5-hexanedione."MEK exposure did not, however, potentiate the neurobehavioral test decrements produced by acetone. Exposure to 200 ppm MEK or 100 ppm MEK plus 12 5 ppm acetone for 4 hours did not produce any significant effects in a variety of behavioral performance tests, whereas exposure to 250 ppm acetone caused some mild decrements. The liver and kidney toxicity of haloalkane solvents may also be potentiated by MEK. ... 

Lipid formulations of amphotericin B have been shown to reduce the severe kidney toxicity of amphotericin B and are indicated in patients with renal impairment or when unacceptable toxicity precludes the use of amphotericin B deoxycholate in effective doses. 

Severe reactions Because of the possibility of severe toxic reactions (which can be fatal), fully inform patients of the risks involved and assure constant supervision. Deaths Use methotrexate only in life-threatening neoplastic diseases, or in patients with psoriasis or rheumatoid arthritis (RA) with severe, recalcitrant, disabling disease that is not adequately responsive to other forms of therapy. Deaths have occurred with the use of methotrexate in malignancy, psoriasis, and RA. Closely monitor patients for bone marrow, liver, lung, and kidney toxicities. 

Aristolochic acid I was used in clinical trials in cancer therapy however, it was abandoned due to liver and kidney toxicity 98). It is interesting that the cytotoxicity of aristolochic acid, not only previously observed in animal cells, has also been confirmed for plant cells (99). Aristoloside (10), isolated from A. manshuriensis, possessed antitumor activity (31). 

In addition to altered oxygen-binding characteristics, free haemoglobin in plasma disassociates rapidly into afi dimers, which are in turn rapidly oxidized and cleared by the kidneys. Indeed, high plasma concentrations can result in kidney toxicity. Development of a... 

Delayed respiratory distress, fibrosis, and atelectasis Gastrointestinal, liver, and kidney toxicity Formation of reactive oxygen species Block tricarboxylic acid cycle (fluoroacetates)... 

Nitroprusside is metabolicaUy degraded by the liver, yielding thiocyanate. Because thiocyanate is excreted by the kidney, toxicities due to this compound are most likely in patients with impaired renal function. 

Soderlund, E.J., Nelson, S.D. Dybing, E. (1981) In vitro and in vivo covalent binding of the kidney toxicant and carcinogen tris(2,3-dibromopropyl)-phosphate. Toxicology, 21,291-304... 

Van der Water B. Kidney toxicity. In Mulder GJ, Dencker L, eds. Pharmaceutical Toxicology. London Pharmaceutical Press, 2006. 

Lead is a toxic metal to which there is wide exposure. Exposure is via inhalation (main source, leaded petrol) and ingestion (water, old paint). Multi-organ toxicity occurs with the kidneys, central and peripheral nervous system, testes, red cells, bones, and gastrointestinal tract all damaged. After initial distribution into red blood cells, it is eventually deposited in bone. The main biochemical effect is interference with heme synthesis at several points. Kidney toxicity may be due to lead-protein complexes and inhibition of mitochondrial function. Damage to nerves leads to peripheral neuropathy. 

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