Article

Nephrotoxicity From Chemotherapeutic Agents: Clinical Manifestations, Pathobiology, and Prevention/Therapy

Section of Nephrology, Department of Medicine, Yale University School of Medicine, New Haven, CT, USA.
Seminars in Nephrology (Impact Factor: 2.94). 11/2010; 30(6):570-81. DOI: 10.1016/j.semnephrol.2010.09.005
Source: PubMed

ABSTRACT Nephrotoxicity remains a vexing complication of chemotherapeutic agents. A number of kidney lesions can result from these drugs, including primarily tubular-limited dysfunction, glomerular injury with proteinuria, full-blown acute kidney injury, and long-term chronic kidney injury. In most cases, these kidney lesions develop from innate toxicity of these medications, but underlying host risk factors and the renal handling of these drugs clearly increase the likelihood of nephrotoxicity. This article reviews some of the classic nephrotoxic chemotherapeutic agents and focuses on examples of the clinical and histopathologic kidney lesions they cause as well as measures that may prevent or treat drug-induced nephrotoxicity.

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    • "Although some methods have been tried in preventing cisplatin-induced nephrotoxicity, none of them has been widely accepted yet (Asna et al., 2005). Therefore, during the use of cisplatin, the changes in the renal function should be closely monitored for early diagnosis of the renal damage (Perazella et al., 2010). "
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    ABSTRACT: Background: For early detection of renal damage during the usage of cisplatin based chemotherapy, changes in renal function should be monitored carefully. In recent years, neutrophil gelatinase-associated lipocalin, a small polypeptide molecule, has shown promise as a marker of acute renal failure. The aim of this present study was to assess possible risk prediction of cisplatin-induced nephrotoxicity using serum NGAL. Materials and Methods: A total of 34 consecutive patients with documented serum creatinine at least 24 hours before every cycle of cisplatin-based chemotherapy were included in the study. Demographic and medical data including age, performance status, tumor characteristics and comorbid diseases were collected from medical charts. Renal function was evaluated at least 48 hours before the treatment and at the end of the treatment based on the Modification of Diet in Renal Disease (MDRD) formula. Before and after cisplatin infusion serum NGAL levels were measured for the first and 3rd cycles of chemotherapy. Results: The median age of the study population was 54 (32-70) years. Fifteen patients (41.1%) were treated on an adjuvant basis, whereas 19 patients (58.9%) were treated for metastatic disease. There was no correlation of serum NGAL levels with serum creatinine (r=0.20, p=0.26) and MDRD (r=-0.12, p=0.50) and creatinine clearance-Cockcroft-Gault (r=-0.22, p=0.22) after cisplatin infusion at the end of the 3rd cycle of chemotherapy. Conclusions: In our study, serum NGAL levels were not correlated with the cisplatin induced nephrotoxicity. Further prospective studies are needed to conclude that serum NGAL level is not a good surrogate marker to predict early cisplatin induced nephrotoxicity.
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