Risk factors for colistin-associated nephrotoxicity

Rattanaumpawan, Pinyo; Ungprasert, Puangpaka; Thamlikitkul, Visanu

doi:10.1016/j.jinf.2010.11.013

Cited by 63 publications

(71 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Ascorbic acid at 4 g/day was chosen for this study because such a dosage was reported to be safe without increased urinary oxalate (44,45) and a similar dose was found to be effective in a previous clinical study for preventing nephrotoxicity after contrast medium injection (46). In this study, the overall incidence of nephrotoxicity, determined according to the widely used RIFLE criteria (39), was 50 to 60%, and it was not significantly different from that observed in the patients at Siriraj Hospital in 2007 (47). The incidence of AKI in the colistin-ascorbic acid group (53.8%) was not significantly different from that in the colistin group (60.0%).…”

Section: Discussionmentioning

confidence: 73%

Preliminary Clinical Study of the Effect of Ascorbic Acid on Colistin-Associated Nephrotoxicity

Sirijatuphat

Limmahakhun

Sirivatanauksorn

et al. 2015

Antimicrob Agents Chemother

Self Cite

View full text Add to dashboard Cite

c Nephrotoxicity is a dose-limiting factor of colistin, a last-line therapy for multidrug-resistant Gram-negative bacterial infections. An earlier animal study revealed a protective effect of ascorbic acid against colistin-induced nephrotoxicity. The present randomized controlled study was conducted in 28 patients and aimed to investigate the potential nephroprotective effect of intravenous ascorbic acid (2 g every 12 h) against colistin-associated nephrotoxicity in patients requiring intravenous colistin. Thirteen patients received colistin plus ascorbic acid, whereas 15 received colistin alone. Nephrotoxicity was defined by the RIFLE classification system. Additionally, urinary neutrophil gelatinase-associated lipocalin (NGAL) and N-acetyl-beta-D-glucosaminidase (NAG) were measured as markers of renal damage, and plasma colistin concentrations were quantified. The baseline characteristics, clinical features, and concomitant treatments of the patients in the two groups were comparable. The incidences of nephrotoxicity were 53.8% (7/13) and 60.0% (9/15) in the colistin-ascorbic acid group and the colistin group, respectively (P ‫؍‬ 0.956; relative risk [RR], 0.9; 95% confidence interval, 0.47 to 1.72). In both groups, the urinary excretion rates of NGAL and NAG on day 3 or 5 of colistin treatment and at the end of colistin treatment were significantly higher than those at the respective baselines (P < 0.05). However, the urinary excretion rates of these biomarkers at the various times during colistin treatment did not differ significantly between the groups (P > 0.05). The plasma colistin concentrations in the two groups were not significantly different (P > 0.28). The clinical and microbiological outcomes and mortality of the patients in the two groups were not significantly different. This preliminary study suggests that ascorbic acid does not offer a nephroprotective effect for patients receiving intravenous colistin. (This study has been registered at ClinicalTrials.gov under registration no. NCT01501968.) I nfections caused by carbapenem-resistant Gram-negative bacteria, such as Acinetobacter baumannii, have become a serious problem globally, including in Thailand (1-3). Colistin (i.e., polymyxin E) and polymyxin B have been reintroduced over the past decade for therapy of multidrug-resistant (MDR) Gram-negative bacterial infections, especially those caused by carbapenem-resistant Gram-negative pathogens (4). Colistin is administered parenterally as colistimethate sodium (CMS), an inactive prodrug that is converted to colistin, the entity that possesses both antibacterial activity and the potential to cause toxicity (5, 6). The efficacy of colistin for treatment of infections by MDR Gram-negative bacteria is modest, and nephrotoxicity is the major dose-limiting factor in the clinical use of colistin (7, 8). The incidence of colistinassociated nephrotoxicity ranges from approximately 10% to 55%, and it appears to be related to the total dose of CMS, the duration of therapy, and the plasma colistin concentrat...

show abstract

Section: Discussionmentioning

confidence: 73%

Preliminary Clinical Study of the Effect of Ascorbic Acid on Colistin-Associated Nephrotoxicity

Sirijatuphat

Limmahakhun

Sirivatanauksorn

et al. 2015

Antimicrob Agents Chemother

Self Cite

View full text Add to dashboard Cite

show abstract

“…In some studies, concomitant NSAID or vancomycin use, hypertension, and older age were identified as independent risk factors for colistin-induced AKI (6,14,24,25), whereas these findings were not corroborated in several other studies, including ours (10,13,17,19,25,26).…”

Section: Discussionmentioning

confidence: 61%

Risk Factors for Colistin-Associated Acute Kidney Injury: A Multicenter Study from Turkey

Gül

Kuşçu²,

Aydemir

et al. 2016

Jpn J Infect Dis

View full text Add to dashboard Cite

“…La dosis utilizada se ha relacionado en forma directamente proporcional con la incidencia de este evento adverso. Para algunos autores se asocia con la dosis total acumulada 72,73 y para otros con la dosis diaria administrada 74,75,81 . Se ha descrito para pacientes que reciben CMS por más de dos semanas 3,7 veces más riesgo de nefrotoxicidad 73 y, por esta razón, se debe evitar cursos prolongados de tratamiento con polimixinas cuando el contexto clínico lo permita.…”

Section: Toxicidadunclassified