Recurrent Renal Dysfunction Secondary to Probable Piperacillin-Tazobactam–Induced Acute Interstitial Nephritis

Parsels, Katie A; Seabury, Robert W.; Darko, William; Probst, Luke A.; Steele, Jeffrey

doi:10.1177/1060028020936778

Cited by 2 publications

(2 citation statements)

References 5 publications

(8 reference statements)

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“…In the case of pseudo-AKI caused by medications such as cobicistat, SCr concentrations can increase by about 0.2-0.4 mg/dL [20]. Similarly, dolutegravir recipients may experience a modest, non-progressive SCr increase (about 0.14 mg/dl) within two weeks after initiation of therapy [22].…”

Section: Diagnostic Biomarkersmentioning

confidence: 99%

“…Table 1 List of drugs/drug classes associated with pseudo-AKI and their possible mechanism(s) † Pseudo-AKI via inhibiting organic anion transporters 1 & 3 in proximal tubule has also been reported with antibiotic combinations such as piperacillin/tazobactam or vancomycin plus piperacillin/tazobactam [17,18]. Nevertheless, interstitial nephritis due to piperacillin/tazobactam has been documented in the literature [19,20]. Thus, it seems prudent not to place piperacillin/tazobactam into the "neither dysfunction nor damage" category ‡ Sulfamethoxazole/trimethoprim should be discriminated from trimethoprim alone and viewed as an independent agent because of described interstitial nephritis or crystal nephropathy cases induced by sulfamethoxazole/trimethoprim [21].…”

Section: Dysfunction Without Damage Mechanismsmentioning

confidence: 99%

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Moving toward a contemporary classification of drug-induced kidney disease

Karimzadeh,

Barreto,

Kellum

et al. 2023

Crit Care

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Drug-induced kidney disease (DIKD) accounts for about one-fourth of all cases of acute kidney injury (AKI) in hospitalized patients, especially in critically ill setting. There is no standard definition or classification system of DIKD. To address this, a phenotype definition of DIKD using expert consensus was introduced in 2015. Recently, a novel framework for DIKD classification was proposed that incorporated functional change and tissue damage biomarkers. Medications were stratified into four categories, including “dysfunction without damage,” “damage without dysfunction,” “both dysfunction and damage,” and “neither dysfunction nor damage” using this novel framework along with predominant mechanism(s) of nephrotoxicity for drugs and drug classes. Here, we briefly describe mechanisms and provide examples of drugs/drug classes related to the categories in the proposed framework. In addition, the possible movement of a patient’s kidney disease between certain categories in specific conditions is considered. Finally, opportunities and barriers to adoption of this framework for DIKD classification in real clinical practice are discussed. This new classification system allows congruencies for DIKD with the proposed categorization of AKI, offering clarity as well as consistency for clinicians and researchers.

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Section: Diagnostic Biomarkersmentioning

confidence: 99%