Carboplatin-related hematuria and acute renal failure

Agraharkar, Mahendra; Nerenstone, Stacy; Palmisano, Joseph; Kaplan, André A.

doi:10.1016/s0272-6386(98)70152-0

Cited by 17 publications

(15 citation statements)

References 12 publications

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“…[10,12] Carboplatin-induced acute renal failure generally includes damage to vasculature or structures of the kidneys, hemolytic uremic syndrome, and pre-renal perfusion deficits (see Table 1). [4,6,13,14] However, rapid progression to ESRD, as seen in this case, is highly unusual and has only been reported once before in a child. [13] The mechanisms that give rise to the chronic nephropathy are conjectural.…”

Section: Discussionmentioning

confidence: 57%

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End-Stage Renal Disease Following Carboplatin Chemotherapy for a Nasopharyngeal Carcinoma

2007

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Section: Discussionmentioning

confidence: 57%

“…[1][2][3] To date, hundreds of cycles of therapy have been given without a significant incidence of renal failure. [4][5][6] We report herein a case of definitive end-stage renal failure due to renal cortical necrosis in a patient receiving carboplatin as chemotherapy for a nasopharyngeal carcinoma.…”

Section: Introductionmentioning

confidence: 99%

End-Stage Renal Disease Following Carboplatin Chemotherapy for a Nasopharyngeal Carcinoma

2007

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“…These doses are equivalent to the clinical therapeutic doses of carboplatin in cancer patients (Bishop 1992;Bohm et al 1999;Wandt et al 1999;Maldoon et al 2000). However, administration of high and/or cumulative doses of carboplatin produced renal toxicity in humans (Agraharkar et al 1998;English et al 1999) and experimental animals (Ueda et al 1991;Martinez et al 1993). The data show that carboplatin in single high doses (192 and 256 mg/ kg) caused renal dysfunction in rats as evidenced by elevation of plasma creatinine and blood urea nitrogen levels.…”

Section: Discussionmentioning

confidence: 96%

“…dysfunction (Agraharkar et al 1998;English et al 1999). Clinically, treatment with carboplatin significantly reduced glomerular filtration rate and serum magnesium in children (English et al 1999).…”

mentioning

confidence: 99%

Dose Response of Carboplatin‐Induced Nephrotoxicity in Rats

Husain¹,

Jagannathan²,

Hasan³

et al. 2002

Pharmacology & Toxicology

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Carboplatin, a second-generation platinum-containing anticancer drug, is currently being used against a variety of cancers. High-dose carboplatin chemotherapy can cause renal tubular injury in cancer patients. However, the biochemical mechanism of carboplatin-induced renal injury has not been well studied. This study investigated the dose response of carboplatin-induced changes in endogenous antioxidants, lipid peroxidation and platinum content in rat kidney. Male Wistar rats (250-300 g) were divided into five groups and treated as follows: (1) control (saline, intraperitoneally); (2) carboplatin (64 mg/kg, intraperitoneally); (3) carboplatin (128 mg/kg, intraperitoneally); (4) carboplatin (192 mg/kg, intraperitoneally); and (5) carboplatin (256 mg/kg, intraperitoneally). The animals were sacrificed four days after treatment. The blood and kidneys were isolated and analyzed. Plasma creatinine and blood urea nitrogen levels were increased significantly in response to carboplatin in a dose-dependent manner. Renal superoxide dismutase and catalase activities were decreased significantly due to carboplatin at dosages of 128 mg/kg and above. The protein expressions of renal copper/zinc-superoxide dismutase and manganese-superoxide dismutase significantly depleted after carboplatin. Carboplatin (192 and 256 mg/kg) significantly increased lipid peroxidation (malondialdehyde concentration) in rat kidneys. Carboplatin dose-dependently increased the renal platinum concentration, with significance at dosages of 128 mg/kg and above. Carboplatin (256 mg/kg) significantly increased renal xanthine oxidase activity, while ratio of reduced to oxidized glutathione depleted significantly. The data suggested that carboplatin caused dose-dependent oxidative renal injury, as evidenced by renal antioxidant depletion, enhanced lipid peroxidation, platinum content, plasma creatinine and blood urea nitrogen levels in rats.

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“…Moreover, former reports (English et al, 1999;Yasumasu et al, 1992) shows that renal side effects are induced by carboplatin, especially when supplied in higher dosage regimens or in the presence of other risk factors like altered pretreatment GFR, cumulative dose of carboplatin or carboplatin dose intensity. Carboplatin is primarily excreted by the kidneys via tubular filtration and secretion; hence dose of carboplatin requires to be adjusted in patients with renal dysfunction (Agraharkar et al, 1998;English et al, 1999). The biochemical mechanism of nephrotoxicity induced by carboplatin has not been well understood.…”

Section: Introductionmentioning

confidence: 99%