Carboplatin (CBDCA), iproplatin (CHIP), and high dose cisplatin in hypertonic saline evaluated for tubular nephrotoxicity

Goren, Marshall P.; Forastiere, Arlene A.; Wright, Reba K.; Horowitz, Marc E.; Dodge, Richard K.; Kamen, Barton A.; Viar, Mary Jane; Pratt, Charles B.

doi:10.1007/bf00296257

Cited by 31 publications

(12 citation statements)

References 22 publications

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“…Other authors have reported it as an infrequent problem during treatment in children (Ettinger et al, 1994;Tscherning et al, 1994), and more frequently in adults receiving high-dose carboplatin prior to autologous bone marrow transplant (Shea et al, 1989). Goren et al reported chronic sub-clinical renal tubular damage after carboplatin treatment (Goren et al, 1987). Until now there have been no reports of chronic hypomagnesaemia after carboplatin and the relationship between CD of carboplatin and hypomagnesaemia has not been noted.…”

Section: Discussionmentioning

confidence: 99%

Dose-related nephrotoxicity of carboplatin in children

et al. 1999

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Summary This study investigated changes and the time course of these changes in renal function in children following treatment with carboplatin, and identified risk factors for nephrotoxicity. Glomerular and proximal renal tubular function were investigated before and up to 2 years after treatment in 23 children who received carboplatin. The main findings were reduced glomerular filtration rate (GFR), and increased renal tubular loss of magnesium, manifested by a low serum magnesium (S Mg). The mean fall in GFR was 22 ml min -1 1.73 m -2 (P = 0.012), and in S Mg it was 0.17 mmol l -1 (P = 0.0077). No patient had a clinically important reduction in GFR, and only one patient had symptomatic hypomagnesaemia. GFR and S Mg did not change over time after completion of treatment. Cumulative dose (CD) of carboplatin was inversely related to mean S Mg at the end of treatment (P = 0.031), and directly related to the fall in S Mg (P < 0.001). Calculated cumulative area under the plasma concentration versus time curve (AUC) of carboplatin was inversely related to S Mg after treatment (P = 0.004). Dose intensity (DI) of carboplatin was not shown to be related to S Mg following treatment. CD, AUC and DI of carboplatin were not related to GFR, nor change in GFR, after treatment. High CDs of carboplatin may be associated with evidence of renal damage qualitatively similar to but less severe than that caused by cisplatin. GFR and SMg should be carefully monitored when high CDs of carboplatin are used, or if carboplatin is combined with other nephrotoxic chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Dose-related nephrotoxicity of carboplatin in children

et al. 1999

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“…In patients treated with some antineoplastic agents, nephrotoxic side-effects are observed [2,3,6,8,9,12,14,15,19,30,32,33,35], The question is whether nephrotoxic effects occur in hospital workers who are occupationally ex posed to antineoplastic agents. Up to now, no such data have been published.…”

Section: Discussionmentioning

confidence: 99%

“…These parameters are widely used in occupational medicine for the detec tion of nephrotoxic effects in workers exposed to chem icals [16,35]. They are also applied clinically to control nephrotoxic side-effects of drugs such as aminoglyco sides [3] and antineoplastic agents like cisplatin [2,3,6,8,9,12,14,15,19,30,32,33,35].…”

Section: Introductionmentioning

confidence: 99%

Occupational exposure to antineoplastic agents and parameters for renal dysfunction

Sessink

Verplanke

Herber

et al. 1997

International Archives of Occupational and Environmental Health

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To study the nephrotoxic effects of occupa tional exposure to antineoplastic agents, the early renal effect parameters retinol-binding protein (RBP) and albumin (ALB) were determined in the urine of 11 hospital workers involved in the preparation and ad ministration of antineoplastic agents and in 23 hospital workers not involved in drug handling, who served as nonexposed controls. No significant difference was found between the exposed group and the nonexposed control group with respect to the early renal effect parameters RBP and ALB. Although it was demon strated that the hospital workers were exposed to cyclophosphamide (CP) and probably other antineoplastc agents, the results of the present study show that these exposure levels did not cause nephrotoxic effects.

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“…CDDP induces tubular damage in most patients but we could not find signs of tubular damage after carboplatin administration as measured by the urinary excretion of tubular enzymes, because of infrequent sampling. For the evaluation of tubular damage timing of specimen collection plays an important role (Goren et al, 1987). As reported for cisplatin (Goren et al, 1986) and carboplatin , urinary enzymes can peak as late as several days after the administration of the drug.…”

Section: Patients and Therapymentioning

confidence: 99%

Acute and cumulative effects of carboplatin on renal function

Sleijfer

Smit²,

Meijer³

et al. 1989

Br J Cancer

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Summanr Carboplatin. a cisplatinum analogue, has no reported nephrotoxicity in phase I'II studies, assessed by creatinine clearance. We prospectively deterniined renal function in 10 untreated lung cancer patients with normal baseline renal function, treated with carboplatin 400mgm 2 day 1 and vincristine 2mg day 1 al., 1985). An alternative approach was the synthesis of analogues of cisplatin with the aim to find Pt-complexes with less nephrotoxicity and more or comparable antitumour activity (Burchenal et al., 1979). About 2,000 second generation Pt-compounds have been synthesised and screened for cytotoxicity. Only a few have been selected for clinical evaluation, of which carboplatin (CBDCA, JM8) probably is the most promising. In human and animal studies carboplatin has demonstrated increased haematological toxicity compared to CDDP, but it is less emetogenic and has little or no oto-or neurotoxicity and no nephrotoxicity even in the absence of forced diuresis (Lelieveld et al.. 1984: Van Glabbeke et al., 1988. In these studies the renal function was measured by monitoring serum creatinine and creatinine clearances. However, the determination of creatinine as a reflection of the glomerular filtration rate has proved to be a relatively insensitive method to monitor CDDP-induced renal damage (Meijer et al., 1983;Daugaard et al., 1988). Moreover, using 52Cr EDTA clearances, Calvert et al. (1982) were also unable to identify CBDCA as a nephrotoxic drug.In this study we prospectively determined changes in glomerular filtration rate and effective renal plasma flow by the more sensitive method developed by Donker et al. (1977) in 10 patients treated with standard dose carboplatin. The possible tubular damage was monitored by measuring the excretion of tubular enzymes. Methods Patients and therapyTen patients, one female, nine male, were studied. All had histologically proved lung cancer (eight small cell lung cancer, one squamous cell carcinoma, one endobronchial carcinoid). One All patients were treated with carboplatin 400mgm 2 day 1 and vincristine 2mg day 1 and 8 every 4 weeks. Carboplatin was dissolved in 250 ml of glucose 5% and given as a 30 mn i.v. infusion on day 1. Vincristine was given as bolus injection. No pre-or post-hydration was given.Seven responding patients received the maximum of five courses. The treatment had to be stopped in two patients after three and in one patient after two courses. because of tumour progression.Renal function studies Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured simultaneously in supine position with radioisotopes. ERPF was determined by measuring the clearance of 1311-hippuran (I x V P) and GFR by the clearance of '251-iothalamate (Ux V P) (I= counts per minute of I ml sustaining solution, V= infusion volume or urine volume in ml per minute, P =counts per minute in 2 ml of plasma and U=counts per minute in 2ml urine). After a standard pnrmary dose and sustaining infusion for 2h, 1-h clearances were determined for acute ef...

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Carboplatin (CBDCA), iproplatin (CHIP), and high dose cisplatin in hypertonic saline evaluated for tubular nephrotoxicity

Cited by 31 publications

References 22 publications

Dose-related nephrotoxicity of carboplatin in children

Dose-related nephrotoxicity of carboplatin in children

Occupational exposure to antineoplastic agents and parameters for renal dysfunction

Acute and cumulative effects of carboplatin on renal function

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