Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 76-year-old man had biopsy-proven acute tubular necrosis (ATN) after intravenous administration of 3 doses of 60 mg of pamidronate (Aredia) over a 2-week period. Pamidronate was given to treat hypercalcemia of unknown etiology. Other potential causes of acute renal failure were excluded with appropriate investigations. The patient's preexisting renal impairment in the context of high-doses of pamidronate might have been a potentiating factor for nephrotoxicity. The ATN encountered in this patient resolved; however, short-term hemodialysis was needed. To the best of our knowledge, this is the first reported case of short-term, high-dose pamidronate-induced ATN in the absence of concomitant nephrotoxins. Although necrotic and apoptotic cell death after bisphosphonate administration has been seen in a variety of cells, the exact mechanism of nephrotoxicity is unknown. This report presents a case of pamidronate-induced ATN and discusses the potential mechanisms of bisphosphonate-induced nephrotoxicity.
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PMID:Short-term, high-dose pamidronate-induced acute tubular necrosis: the postulated mechanisms of bisphosphonate nephrotoxicity. 1277 36

Toxic nephropathy is an important cause of reversible renal injury. This article focuses on the nephrotoxicity of several new therapeutic compounds. Selective cyclooxygenase-2 inhibitor is associated with sodium retention, hypertension, ankle edema, and acute renal failure. The incidence of renal complication is similar to conventional nonsteroidal anti-inflammatory drugs. Bisphosphonates, especially when used in high dose for prolonged duration, can cause toxic acute tubular necrosis and renal failure. Pamidronate is also associated with a specific form of collapsing focal segmental glomerulosclerosis similar to one found in patients with human immunodeficiency virus (HIV) infection. Acyclic nucleoside phosphonate, a new group of antiviral agents, can cause Fanconi-like syndrome and progressive renal impairment. On the other hand, indinavir, a potent protease inhibitor for the treatment of HIV infection, can cause crystalluria, renal stone, acute tubular obstruction and chronic interstitial nephritis. Intravenous immune globulin and hydroxyethyl starch, a new plasma expander, are associated with acute renal failure with characteristic renal histology known as osmotic nephrosis. In short, physicians should be cautious about possible renal toxicity during the use of any new therapeutic agents.
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PMID:Nephrotoxicity related to new therapeutic compounds. 1595 51