Drug-associated acute kidney injury: who’s at risk?

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Abstract

<p class="first" id="P1">The contribution of nephrotoxic medications to the development of acute kidney injury (AKI) is becoming better understood with the rise in incidence of AKI in children. Treatment of AKI is not yet available, so prevention continues to be the most effective approach. There is an opportunity to mitigate severity and prevent the occurrence of AKI if children at increased risk are identified early and nephrotoxins are used judiciously. Early detection of AKI is limited by the dependence on serum creatinine as an indicator. Promising new biomarkers may offer early detection of AKI prior to the rise in serum creatinine. Early detection of AKI is evolving and offers opportunities for better management of nephrotoxins. However, identification of patients at increased risk will remain an important first step both to focus the use of biomarker testing and to aid in its interpretation. </p>

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Classifying AKI by Urine Output versus Serum Creatinine Level.

John A. Kellum, Florentina E Sileanu, Raghavan Murugan … (2015)

Severity of AKI is determined by the magnitude of increase in serum creatinine level or decrease in urine output. However, patients manifesting both oliguria and azotemia and those in which these impairments are persistent are more likely to have worse disease. Thus, we investigated the relationship of AKI severity and duration across creatinine and urine output domains with the risk for RRT and likelihood of renal recovery and survival using a large, academic medical center database of critically ill patients. We analyzed electronic records from 32,045 patients treated between 2000 and 2008, of which 23,866 (74.5%) developed AKI. We classified patients by levels of serum creatinine and/or urine output according to Kidney Disease Improving Global Outcomes staging criteria for AKI. In-hospital mortality and RRT rates increased from 4.3% and 0%, respectively, for no AKI to 51.1% and 55.3%, respectively, when serum creatinine level and urine output both indicated stage 3 AKI. Both short- and long-term outcomes were worse when patients had any stage of AKI defined by both criteria. Duration of AKI was also a significant predictor of long-term outcomes irrespective of severity. We conclude that short- and long-term risk of death or RRT is greatest when patients meet both the serum creatinine level and urine output criteria for AKI and when these abnormalities persist.

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AKI in hospitalized children: comparing the pRIFLE, AKIN, and KDIGO definitions.

Scott Sutherland, John J Byrnes, Manish Kothari … (2015)

Although several standardized definitions for AKI have been developed, no consensus exists regarding which to use in children. This study applied the Pediatric RIFLE (pRIFLE), AKI Network (AKIN), and Kidney Disease Improving Global Outcomes (KDIGO) criteria to an anonymized cohort of hospitalizations extracted from the electronic medical record to compare AKI incidence and outcomes in intensive care unit (ICU) and non-ICU pediatric populations.

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Vancomycin-induced nephrotoxicity: mechanism, incidence, risk factors and special populations. A literature review.

Sepideh Elyasi, Simin Dashti-Khavidaki, Hossein Khalili … (2012)

Treatment failures following vancomycin therapy in patients with methicillin-resistant Staphylococcus aureus infections have led to the utilization of higher doses of this antibiotic to achieve the trough concentrations of 10-20 μg/mL recommended by the Infectious Diseases Society of America clinical practice guideline. However, many questions remain on the safety of such high doses of vancomycin, specifically their nephrotoxic effects. In this review, we have collected available evidence on the nephrotoxicity of vancomycin, particularly in terms of its mechanism, incidence, predisposing factors and special target populations. The data were collected by searching Scopus, PubMed, Medline, and Cochrane database systematic reviews. The key words used as search terms were "vancomycin", "nephrotoxicity", "renal failure", "renal damage", "risk factors", "infants", "children", "adult", "elderly" and "pregnancy". We have included all relevant animal and human studies up to the date of publication. Vancomycin-induced renal toxicity was reported in 10-20 % and 30-40 % of patients following conventional and high doses of vancomycin therapy, respectively .The most probable mechanism for its nephrotoxicity can be at least partially attributable to an increased production of reactive oxygen species and oxidative stress. There are a number of different risk factors which could accelerate or potentiate the occurrence of vancomycin-induced nephrotoxicity, with the most documented risk factors being high trough vancomycin level (especially >20 mg/L) or doses (>4 g/day), concomitant treatment with nephrotoxic agents, prolonged therapy (even more than 7 days), and admittance to an intensive care unit (especially prolonged stay). It is necessary to carry out more studies, especially those focused on the association between nephrotoxicity and high trough levels of vancomycin.