Anti-Infective-Associated AKI: A Narrative Review of the Epidemiology, Mechanisms, Risk Factors, Biomarkers, Clinical Course, Monitoring, Prevention, and Therapeutic Strategies

TL;DR

This review discusses how certain anti-infective drugs can cause acute kidney injury, covering risk factors, mechanisms, and monitoring strategies.

Contribution

The paper provides an updated narrative review on anti-infective-associated AKI, emphasizing mechanisms and biomarkers.

Findings

Anti-infective-associated AKI is typically dose-dependent and occurs within the first two weeks of treatment.

Oxidative stress and inflammation are key mechanisms in antibiotic-related AKI.

Novel biomarkers like urinary kidney-injury molecule-1 show promise in detecting kidney damage.

Abstract

Acute kidney injury (AKI) occurs commonly in hospitalized patients, especially patients in intensive care units (ICUs). Medications are among the major causative factors of AKI. This narrative review addressed and updated different aspects of anti-infective-associated AKI, including amphotericin B, cidofovir, foscarnet, polymyxins, vancomycin, and aminoglycosides. There is no standard definition or operational criteria to describe anti-infective-associated AKI. Characteristically, it usually occurs during the first two weeks of treatment and is typically dose dependent. Functional resolution occurs, but kidney injury can affect renal functional reserve and increase susceptibility to future AKI events. A variety of pathophysiological mechanisms impacting glomerular, tubular, and interstitial components of the kidney are usually responsible for the development of AKI from anti-infective medications. Oxidative stress and inflammation play a pivotal role in the pathogenesis of antibiotic-related AKI. Numerous patient-related, medication-related, and co-administered-related scenarios have been demonstrated as risk factors for anti-infective-induced AKI. Apart from traditional indexes of kidney function (serum creatinine and urine output), novel biomarkers of kidney function (e.g., serum cystatin C) and damage (e.g., urinary kidney-injury molecule-1 and neutrophil gelatinase-associated lipocalin) have been noticed in recent clinical studies with promising findings. The efficiency of preventive strategies against anti-infective-associated AKI in most cases appears to be variable, relative, and modest. Close and regular monitoring of kidney function parameters is crucial during treatment with nephrotoxic antibiotics. Currently, there is no definitive treatment modalities for the management of AKI with anti-infectives. Therefore, supportive care is the mainstay of treatment.

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