Prevalence and Risk Factors for Aminoglycoside Nephrotoxicity in Intensive Care Units

Abstract

In order to assess the prevalence of and risk factors for aminoglycoside-associated nephrotoxicity in intensive care units (ICUs), we evaluated 360 consecutive patients starting aminoglycoside therapy in an ICU. The patients had a baseline calculated glomerular filtration rate (cGFR) of >30 ml/min/1.73 m 2 . Among these patients, 209 (58%) developed aminoglycoside-associated nephrotoxicity (the acute kidney injury [AKI] group, which consisted of individuals with a decrease in cGFR of >20% from the baseline cGFR), while 151 did not (non-AKI group). Both groups had similar baseline cGFRs. The AKI group developed a lower cGFR nadir (45 ؎ 27 versus 79 ؎ 39 ml/min/1.73 m 2 for the non-AKI group; P < 0.001); was older (56 ؎ 18 years versus 52 ؎ 19 years for the non-AKI group; P ‫؍‬ 0.033); had a higher prevalence of diabetes (19.6% versus 9.3% for the non-AKI group; P ‫؍‬ 0.007); was more frequently treated with other nephrotoxic drugs (51% versus 38% for the non-AKI group; P ‫؍‬ 0.024); used iodinated contrast more frequently (18% versus 8% for the non-AKI group; P ‫؍‬ 0.0054); and showed a higher prevalence of hypotension (63% versus 44% for the non-AKI group; P ‫؍‬ 0.0003), shock (56% versus 31% for the non-AKI group; P < 0.0001), and jaundice (19% versus 8% for the non-AKI group; P ‫؍‬ 0.0036). The mortality rate was 44.5% for the AKI group and 29.1% for the non-AKI group (P ‫؍‬ 0.0031). A logistic regression model identified as significant (P < 0.05) the following independent factors that affected aminoglycoside-associated nephrotoxicity: a baseline cGFR of <60 ml/min/1.73 m 2 (odds ratio [OR], 0.42), diabetes (OR, 2.13), treatment with other nephrotoxins (OR, 1.61) or iodinated contrast (OR, 2.13), and hypotension (OR, 1.83). In conclusion, AKI was frequent among ICU patients receiving an aminoglycoside, and it was associated with a high rate of mortality. The presence of diabetes or hypotension and the use of other nephrotoxic drugs and iodinated contrast were independent risk factors for the development of aminoglycoside-associated nephrotoxicity.

Acute kidney injury in the perioperative period and in intensive care units (excluding renal replacement therapies)

“…More recent studies have shown that toxicity was essentially related to high levels of residual serum concentration of the drug (more than 20 h after infusion), while the peak concentration (measured ½ h after infusion) was the parameter responsible for efficiency [143][144][145][146][147][148][149][150]. Current recommendations are based on these later trials, favouring a high peak serum concentration using high doses of aminoglycoside as boluses and close monitoring of residual serum concentrations to avoid renal toxicity.…”

Acute Kidney Injury and Increasing Nephrotoxic-Medication Exposure in Noncritically-Ill Children

“…Importantly, nephrotoxic-medication exposure is becoming more prevalent as a primary cause of AKI, comprising approximately 16% of all pediatric inpatient causes of AKI (1,5,(7)(8)(9)(10). However, both the risk of developing AKI when any nephrotoxic medication is initiated and the additive risk of AKI development with multiple nephrotoxic medications are unknown.…”

“…Acute kidney injury (AKI) in children can be a devastating event and is independently associated with poor patient outcomes (1)(2)(3)(4)(5). Additionally, long-term follow-up of pediatric patients who have sustained an AKI episode demonstrate significant renal sequelae (6).…”

Acyclovir Induced Acute Kidney Injury In Acute Meningitis Patient: A Case Report Highlights the Concurrence Of AKI Risk Factors And The Neutropenic Effect Of Ticlopidine

“…This requires critical prescribing, effective hydration and extensive monitoring of renal function. There are several risk factors which can aggravate the renal insult of nephrotoxic drugs, such as patient's age (> 65 years), female sex, impaired immunity, the duration of using the nephrotoxic drug and concurrent use of other nephrotoxic drugs [6,7,9,13]. Acyclovir induced nephrotoxicity can occur within 12-72 hours after starting the therapy [4,14].…”

“…Acute kidney injury (AKI) induced by acyclovir could be due to intratubular crystal precipitation or direct insult to renal tubular cells [4,5]. Yet, the co-administration of acyclovir with other nephrotoxic drugs, such as aminoglycosides and vancomycin, can accelerate the occurrence of AKI [6][7][8][9]. This requires careful monitoring while prescribing nephrotoxic anti-microbial therapy.…”