Nephrotoxins and nephrotoxic acute kidney injury
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REVIEW
Nephrotoxins and nephrotoxic acute kidney injury Amanda M. Uber 1
&
Scott M. Sutherland 1
Received: 12 August 2019 / Revised: 30 September 2019 / Accepted: 8 October 2019 # IPNA 2019
Abstract Although the concept of nephrotoxicity has been recognized for more than 80 years, interest in nephrotoxins has intensified dramatically over the past two decades. Much of this attention has rightfully been focused on pharmaceutical agents and iatrogenic harm; however, it is important for providers to recognize that nephrotoxins can be found in naturally occurring substances as well. Although nephrotoxins exist in a myriad of forms, the means by which they induce injury can be organized into a few categories. For most of these agents, regardless of the mechanism, the final common pathway is acute kidney injury (AKI). Unfortunately, therapeutic options are limited and no treatments currently exist to reverse nephrotoxic AKI once it occurs. As a result, current strategies focus on increased awareness, nephrotoxin avoidance, early injury detection, and mitigation of disease severity. The goal of this review is to summarize our current understanding of nephrotoxic mechanisms and the epidemiology of nephrotoxic AKI. Additionally, avoidance and preventative strategies are discussed, screening approaches are suggested, and chronic monitoring recommendations are made. Keywords Acute kidney injury . AKI . Nephrotoxin
Introduction The concept of “toxin nephropathy” was first introduced by Dr. George Schreiner in 1965. He coined this term to describe “any adverse functional or structural changes in the kidney due to the effect of a chemical or biological product that is inhaled, ingested, injected or otherwise absorbed, or that yields toxic metabolites with an identifiable adverse effect to the kidneys” [1]. Since that time, nephrotoxins, defined generally as agents capable of causing such a nephropathy, have been widely studied in the nephrology literature. In 1967, Balter et al. highlighted several of the more prevalent nephrotoxic exposures, focusing on hydrocarbons, heavy metals, drugs of abuse, analgesics, and antimicrobials [2]. Even then, the authors emphasized the importance of prevention and early detection. In 1987, Kleinknecht et al. provided pathologic evidence of nephrotoxicity, describing the clinical course and biopsy findings in 81 patients with
* Amanda M. Uber [email protected] 1
Department of Pediatrics (Nephrology), Stanford University School of Medicine, 300 Pasteur Drive, Room G-306 Stanford CA 94304 USA
“drug-associated renal failure” [3]. The authors identified seven major medication classes implicated in injury, including non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, glafenin, contrast media, diuretics, chemotherapy, and paracetamol. Notably, NSAIDs and antibiotics were responsible for 30% and 27% of cases, respectively. The biopsies revealed the most common pathologic findings in the setting of nephrotoxin exposure were acute tubular necrosis (ATN) and acute interstitial nephri
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