This study underscores the substantial underdiagnosis of AKI due to the failure to timely measure renal function indicators. Among the 17,269 hospitalizations analysed, only 7.0% and 9.1% could be identified as suffering from AKI strictly using AKIN or KDIGO criteria (considering the time intervals described by those criteria). Notably, in over 46% of hospitalizations, the time between SCr tests exceeded 48 h, raising concerns about the accuracy of strictly applying the time intervals outlined in these criteria. However, in 11.2% of hospitalizations, SCr elevations surpassed the limits described in both criteria, indicating a potential underestimation of AKI. This lack of timely SCr assessment could have resulted in disregarding more than 700 or 370 individuals with AKI (depending on the criteria used), translating to underestimating AKI diagnoses by 60% or 23.5% for AKIN and KDIGO, respectively. This potential AKI underdiagnose was confirmed by the statistical association between the AKI potential stages of these patients with the minimum KeGFR they reached. Also, almost 90% patients suffering unnoticed AKI were using drugs that should have dose adjustment when renal function is impaired.

A key strength of this study lies in its utilization of a real-world cohort of patients, drawing on secondary data obtained for routine patient care. Consequently, the results reflect the current practices of an average Portuguese hospital. The study underscores the imperative for a more standardized protocol to measure inpatient SCr at intervals no longer than 48 h.

The study has limitations. Firstly, it is confined to a single hospital, which lacks representation of all medical specialties, impeding the generalization of results to other European or Portuguese hospitals. The reliance on secondary data extracted from hospital records introduces a potential limitation, as accuracy was not validated on-site. However, the hospital undergoes external accreditation, including a review of medical record data quality. The use of SCr at admission as the steady-state creatinine for KeGFR may introduce inaccuracies, particularly in patients with acute SCr increases just before hospitalization. When analysing exposure to drugs requiring dose adjustment, information on any interventions conducted was unavailable, as such interventions are not recorded. However, this was beyond the scope of our analysis. Lastly, it is essential to note that all four authors are pharmacists by education. While this expertise enriches the interpretation, it is crucial to acknowledge this potential influence when analysing interpretations given.

This study specifically targeted individuals with normal kidney function at the time of admission, consequently not requiring dose adjustments for renally excreted drugs. However, the failure to timely monitor kidney function might result in overlooking potential AKI occurrences, potentially necessitating drug dose adjustments. Early identification of AKI is critical, as evidence suggests a heightened risk of CKD in patients who have experienced AKI, even in cases where the acute condition completely resolved [22]. Rapid intervention in the earliest stages of AKI could yield long-term benefits for patients [23].

The existing eGFR equations may not accurately reflect glomerular filtration in AKI, as they do in CKD [24]. KDIGO defines AKI based on SCr increases over time and reduced urine output [24]. While various biomarkers have been suggested for measuring filtration rate in AKI [25], their availability and routine use in clinical practice vary. KeGFR has emerged as a valuable alternative, particularly in conditions like AKI where SCr levels change rapidly [14] KeGFR has demonstrated high predictive power for identifying AKI [26] and allows for drug dose adjustments, similar to traditional eGFR equations [27]. Notably, KeGFR could be calculated for nearly 75% of the hospitalizations under analysis.

The management of drug therapy in patients developing AKI remains a topic of debate. Some authors advocate for considering an alternative drug with no dose adjustment requirements in CKD as a first choice [28]. While this option may not always be feasible due to the limited availability of alternative non-renally excreted drugs, it is also not necessarily the most efficient solution as it unnecessarily restricts the therapeutic portfolio. It is crucial to note that the effects of AKI on drugs extend beyond renal excretion, encompassing modifications in hepatic clearance in AKI patients [29]. AKI can increase the volume distribution for hydrophilic drugs due to the shorter half-life of albumin in these patients [30]. Alternatively, some authors advocate for increasing therapeutic drug monitoring in patients with AKI [31]. However, this option may not be universally available for all drugs in all settings. Consequently, drug dose adjustment emerges as the most pragmatic option for many patients developing AKI.

While guidelines for dose adjustment of renally excreted drug in patients with CKD are well established, guidelines in AKI are not so robust. KDIGO recommends increasing research, not only to generate guidelines for “drug dosing adjustments in patients with AKI”, but also to develop electronic tools and decision-making software “to guide drug dosage individualization” [32].

The clinical pharmacist’s role in providing dose adjustment recommendations based on observed modifications in renal function, especially in CKD, is well-documented in the literature of both developed [33, 34] and developing countries [35]. Clinical pharmacists have further demonstrated their contribution to patients recovering from an AKI episode by establishing post-discharge follow-up services [36, 37]. Pharmacists play also a crucial role in AKI prevention by monitoring nephrotoxic drug levels [38], although some studies present conflicting conclusions [39]. Initial results from a large randomized controlled trial revealed that pharmacists, as part of a trained multidisciplinary team, adjusted doses, or initiated drug level monitoring in nearly 70% of patients with AKI [40].

Pharmacists can employ intricate dosing techniques to mitigate AKI risks [19] or utilize advanced computerized decision support systems (CDSS) to aid in identifying and preventing iatrogenic risks [40]. However, irrespective of the methods employed, timely access to renal function information is imperative. Pharmacists have advocated for such access and proposed solutions for a considerable duration [41, 42]. In our study, access to SCr data, when available, was provided to hospital pharmacists. Yet, in situations where the SCr test was not conducted promptly, pharmacists should advocate for an expanded scope of practice, a concept already implemented in some countries which entails legal authorization for pharmacists to prescribe specific laboratory tests [43]. Some countries have successfully tested this expanded role, particularly in primary care, involving community pharmacists and general practitioners in the early identification of CKD [44]. However, studies suggest that the location of the clinical pharmacist may influence the delivery and acceptance of interventions [45]. On-ward pharmacists, embedded within multidisciplinary teams, are more likely to have access to all necessary indicators, enhancing the meaningful impact of their interventions [46].

KeGFR emerged as a potentially valuable metric for early AKI identification. However, its calculation, requiring three SCr values (steady state and two within a time interval), may limit its applicability in settings with suboptimal SCr measuring practices. Given the strong correlation observed in our study between KeGFR and eGFR estimated with CKD-EPI, future research should delve into the potential agreement between these two estimates using specialized analytical techniques [47].