Kidney nephrotoxicity

Nephritis. Inflammation of the kidney. Nephropathy. Disease of the kidneys. Nephrotoxic. Toxic or destructive to kidney cells. 

Two of the natural CDs are known to be parenterally unsafe due to nephrotoxic effects [9], The etiology of the nephrotoxicity of a- and P-CD is unknown but is believed to be related to either CD uptake by kidney tubule cells resulting in disruption of intracellular function or the extraction of lipid membrane components by the CDs. The latter is suggested to be of validity since there seems to be a linear correlation between the ability of some CDs to disrupt cellular membranes and kidney nephrotoxicity [2, 6], The ability of CDs to cause red blood cell hemolysis and membrane irritation seems also to correlate with their ability to extract lipid membrane components cholesterol and phospholipids [10,11],... 

Apart from their acute and chronic toxicity, mycotoxins may possess carcinogenic, mutagenic, and teratogenic properties. They may act primarily on the liver (hepatotoxicity), kidney (nephrotoxicity), nervous (neurotoxicity), and immune systems (immunotoxicity or immunosuppression), on the uterus (uterotropism), and on the skin (dermatotoxicity), or they may act as... 

Key words Kidney, Nephrotoxicity, RPTEC/TERT1, LLC-PK1, HK-2, MDCK, Proximal tubular cells, Glomerulus, Podocytes, Epithelial, Claudin, GST, Immortalization... 

Effects of repeated ethylene glycol peroral overexposure in treated rats and mice can result in kidney, Hver, and nervous system damage. The most sensitive indicators of ethylene glycol toxicity are disturbances in acid—base balance and nephrotoxic (kidney) effects. Effects of repeated chronic peroral overexposure of diethylene glycol in treated rats result in kidney and Hver damage (48). 

In experimental animals and in vitro, DHBs show a variety of biological effects including binding of metaboHtes to various proteins. Clastogenic effects have been observed in vitro and in some in vivo studies with the three compounds. No reproductive effects have been shown by conventional studies with either hydroquinone, catechol, or resorcinol (122). Hydroquinone has been shown to induce nephrotoxicity and kidney tumors at very high doses in some strains of rat (123) catechol induces glandular stomach tumors at very high dose (124). Repeated dermal appHcation of resorcinol did not induce cancer formation (125). 

Aminophenol is a selective nephrotoxic agent and intermpts proximal tubular function (121,122). Disagreement exists concerning the nephrotoxity of the other isomers although they are not as potent as 4-aminophenol (123,124). Respiration, oxidative phosphorylation, and ATPase activity are inhibited in rat kidney mitochondria (125). The aminophenols and their derivatives are inhibitors of 5-Hpoxygenase (126) and prostaglandin synthetase... 

In addition to variable chemical stabiUty the carbapenems are susceptible to P-lactam cleavage by a dehydropeptidase en2yme (DHP-I) located on the bmsh borders of the kidney (53). Clinically, MK 0787 (18) is used with an inhibitor of this en2yme, cil a sta tin [78852-98-9] (MK 0791) (34), 16 26 2 5 dramatic effect not only on the urinary recovery of the drug, but also reduces any nephrotoxic potential (52) (see Enzyme... 

The first human kidney and bone marrow transplants using cyclosporine were reported in 1978. Oral or intravenous cyclosporine is an immunosuppressant for transplantation of these and other organs and investigations are underway for its possible use in a variety of autoimmune diseases including rheumatoid arthritis, severe psoriasis, and Crohn s disease. Dose-dependent nephrotoxicity (261—264) remains the primary limitation of the dmg and necessitates close monitoring of patients, including measurement of dmg levels in blood. Cyclosporine research has been reviewed (265—274). 

Other adverse reactions that may be seen with administration of the cephalosporins are headache, dizziness, nephrotoxicity (damage to the kidneys by a toxic substance), malaise, heartburn, and fever. Intramuscular (IM) administration often results in pain, tenderness, and inflammation at the injection site Intravenous (IV) administration has resulted in thrombophlebitis and phlebitis. 

Nephrotoxicity (damage to the kidneys) and ototoxicity (damage to the organs of hearing) may be seen with the administration of this drug. Additional adverse reactions include nausea, chills, fever, urticaria, sudden fall in blood pressure with parenteral administration, and skin rashes. 

The nurse must carefully monitor fluid intake and output because this drug may be nephrotoxic (harmful to the kidneys). In some instances, the nurse may need to perform hourly measurements of the urinary output. Periodic laboratory tests are usually ordered to monitor the patient s response to therapy and detect toxic drug reactions. 

Goering PL, Fisher BR, Chaudhary PP, Dick CA. 1992. Relationship between stress protein induction in rat kidney by mercuric chloride and nephrotoxicity. Toxicol Appl Pharmacol 113 184-191. 

Kidney Metal ion-mediated nephrotoxicity Protoporphyrin photo-oxidation... 

Amphotericin B-induced ARF occurs in as many as 40% to 65% of patients treated with the conventional desoxycholate formulation.30 Nephrotoxicity is due to renal arterial vasoconstriction and distal renal tubule cell damage. Risk factors include high doses, treatment for at least 7 days, preexisting kidney dysfunction, and concomitant use of other nephrotoxic drugs.31 Three lipid-based formulations of amphotericin B have been developed in an attempt to decrease the incidence of ARF amphotericin B lipid complex, amphotericin colloidal dispersion, and liposomal amphotericin B. The range of... 

Cyclosporine and tacrolimus are calcineurin inhibitors that are administered as part of immunosuppressive regimens in kidney, liver, heart, lung, and bone marrow transplant recipients. In addition, they are used in autoimmune disorders such as psoriasis and multiple sclerosis. The pathophysiologic mechanism for ARF is renal vascular vasoconstriction.41 It often occurs within the first 6 to 12 months of treatment, and can be reversible with dose reduction or drug discontinuation. Risk factors include high dose, elevated trough blood concentrations, increased age, and concomitant therapy with other nephrotoxic drugs.41 Cyclosporine and tacrolimus are extensively metabolized by... 

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