Urinary β2-microglobulin early indicator of high dose cisdiamminedichloroplatinum nephrotoxicity? Influence of furosemide

Gislain, C. De; Dumas, Monique; d’Athis, Philippe; Lautissier, J. L.; Escousse, A; Guerrin, J

doi:10.1007/bf00273402

Cited by 11 publications

(5 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Carboplatin is also primarily eliminated by the kidneys [30] and may compete with melphalan for renal clearance. Platinum therapy has also been known to induce renal damage [31]. In one series, half the patients developed reduced GFR during carboplatin therapy [32].…”

Section: Discussionmentioning

confidence: 99%

Melphalan pharmacokinetics in children with malignant disease: influence of body weight, renal function, carboplatin therapy and total body irradiation

Nath

Shaw

Montgomery

et al. 2005

Brit J Clinical Pharma

View full text Add to dashboard Cite

AimTo analyse the pharmacokinetics of melphalan in 52 children (0.3-18 years) and determine whether any clinical factors affect the pharmacokinetic parameters Additionally, to examine whether a test melphalan dose can predict the pharmacokinetics of a full dose, when there are 5 intervening days of carboplatin therapy. MethodsMelphalan concentrations were measured in 14 blood samples collected from each child following doses ranging from 30 to 180 mg m -2 . The pharmacokinetics were analysed with Kinetica 4.0. ResultsChildren who did not have carboplatin ( n = 27) had median melphalan clearance (CL) of 15.5 l h -1 m -2 (interquartile range: 12.4-19.9 l h -1 m -2 ) and steady state volume of distribution (Vss) of 14.9 l m -2 (interquartile range: 12.7-18.3 l m -2 ). Children who had carboplatin ( n = 25) had 34% lower median CL (10.2 l h -1 m -2 ) and 18% lower median Vss (12.2 l m -2 ) ( P < 0.001). Melphalan elimination was impaired in a separate group of three children given concomitant carboplatin and etoposide. Stepwise multiple linear regression indicated that weight, carboplatin, glomerular filtration rate (GFR) and total body irradiation (TBI) significantly affected CL, while weight and carboplatin influenced Vss. A test dose (10 mg m -2 ) tended to underpredict the area-under-the-concentration-vs. -time-curve for a full (180 mg m -2 )

show abstract

Section: Discussionmentioning

confidence: 99%

Melphalan pharmacokinetics in children with malignant disease: influence of body weight, renal function, carboplatin therapy and total body irradiation

Nath

Shaw

Montgomery

et al. 2005

Brit J Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…37 In one study, patients that had abnormal increases in urinary B2M did not subsequently develop nephrotoxicity. 38 One reason could be that increased systemic production of B2M may occur in the presence of underlying malignancy. Several studies have shown that baseline urinary B2M concentrations are elevated in cancer patients who have not received chemotherapy, compared to healthy volunteers.…”

Section: Beta-2-microglobulinmentioning

confidence: 99%

“…35 While most of these studies have focused on urinary B2M excretion, it is important to note that serum B2M does not change significantly following cisplatin therapy. 38…”

Section: Beta-2-microglobulinmentioning

confidence: 99%

“…35 While most of these studies have focused on urinary B2M excretion, it is important to note that serum B2M does not change significantly following cisplatin therapy. 38 N-acetyl-beta-D glucosaminidase N-acetyl-beta-D glucosaminidase (NAG) is a lysosomal enzyme identified in the proximal and distal tubules of rat kidneys. 42 Due to its large molecular weight (130 kDa), NAG is not normally filtered and its presence in the urine largely reflects tubular destruction (reviewed in Hong and Chia 43 ).…”

Section: Beta-2-microglobulinmentioning

confidence: 99%

See 1 more Smart Citation

Urinary protein biomarkers of kidney injury in patients receiving cisplatin chemotherapy

George

Joy²,

Aleksunes

2017

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Despite recent progress in the development of novel approaches to treat cancer, traditional antineoplastic drugs, such as cisplatin, remain a mainstay of regimens targeting solid tumors. Use of cisplatin is limited by acute kidney injury, which occurs in approximately 30% of patients. Current clinical measures, such as serum creatinine and estimated glomerular filtration rate, are inadequate in their ability to detect acute kidney injury, particularly when there is only a moderate degree of injury. Thus, there is an urgent need for improved diagnostic biomarkers to predict nephrotoxicity. There is also interest by the U.S. Food and Drug Administration to validate and implement new biomarkers to identify clinical and subclinical acute kidney injury in patients during the drug approval process. This minireview provides an overview of the current literature regarding the utility of urinary proteins (albumin, beta-2-microglobulin, N-acetyl-D-glucosaminidase, kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, and cystatin C) as biomarkers for cisplatin-induced AKI. Many of the well-studied urinary proteins (KIM-1, NGAL, B2M, albumin) as well as emerging biomarkers (calbindin, monocyte chemotactic protein-1, and trefoil factor 3) display distinct patterns of time-dependent excretion after cisplatin administration. Implementation of these biomarker proteins in the oncology clinic has been hampered by a lack of validation studies. To address these issues, large head-to-head studies are needed to fully characterize time-dependent responses and establish accurate cutoff values and ranges, particularly in cancer patients. Impact statement There is growing interest in using urinary protein biomarkers to detect acute kidney injury in oncology patients prescribed the nephrotoxic anticancer drug cisplatin. We aim to synthesize and organize the existing literature on biomarkers examined clinically in patients receiving cisplatin-containing chemotherapy regimens. This minireview highlights several proteins (kidney injury molecule-1, beta-2-microglobulin, neutrophil gelatinase-associated lipocalin, calbindin, monocyte chemotactic protein-1, trefoil factor 3) with the greatest promise for detecting cisplatin-induced acute kidney injury in humans. A comprehensive review of the existing literature may aid in the design of larger studies needed to implement the clinical use of these urinary proteins as biomarkers of kidney injury.

show abstract

“…All patients tested showed increased levels of urinary β 2 -microglobulin, a sensitive marker of renal tubular damage. 27 …”

Section: Molecular and Biochemical Findings In Asymptomatic Newbornsmentioning

confidence: 99%

Neonatal Diagnosis and Treatment of Menkes Disease

Kaler¹,

Holmes²,

Goldstein³

et al. 2008

N Engl J Med

284

291

View full text Add to dashboard Cite

show abstract

Urinary β2-microglobulin early indicator of high dose cisdiamminedichloroplatinum nephrotoxicity? Influence of furosemide

Cited by 11 publications

References 11 publications

Melphalan pharmacokinetics in children with malignant disease: influence of body weight, renal function, carboplatin therapy and total body irradiation

Melphalan pharmacokinetics in children with malignant disease: influence of body weight, renal function, carboplatin therapy and total body irradiation

Urinary protein biomarkers of kidney injury in patients receiving cisplatin chemotherapy

Neonatal Diagnosis and Treatment of Menkes Disease

Contact Info

Product

Resources

About