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Improving acute kidney injury diagnostic precision using biomarkers.

ABSTRACT: Acute kidney injury (AKI) is common in hospitalized patients of all ages and is associated with significant morbidity and mortality. Accurate prediction and early identification of AKI is of utmost importance because no therapy exists to mitigate AKI once it has occurred. Yet, serum creatinine lacks adequate sensitivity and specificity, and quantification of urine output is challenging in incontinent children without indwelling bladder catheters. Integration of clinically available biomarkers have the potential to delineate unique AKI phenotypes that could have important prognostic and therapeutic implications. Plasma Cystatin C, urine neutrophil gelatinase associated lipocalin (NGAL) and the urinary product of tissue inhibitor metalloproteinase (TIMP-2) and insulin growth factor binding protein-7 (IGFBP7) are clinically available. These biomarkers have been studied in heterogenous populations across the age spectrum and in a variety of clinical settings for prediction of AKI. The purpose of this review is to describe and discuss the clinically available AKI biomarkers including how they have been used to delineate AKI phenotypes.

SUBMITTER: Hasson D

PROVIDER: S-EPMC9046880 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Improving acute kidney injury diagnostic precision using biomarkers.

Hasson Denise D Menon Shina S Gist Katja M KM

Practical laboratory medicine 20220409

Acute kidney injury (AKI) is common in hospitalized patients of all ages and is associated with significant morbidity and mortality. Accurate prediction and early identification of AKI is of utmost importance because no therapy exists to mitigate AKI once it has occurred. Yet, serum creatinine lacks adequate sensitivity and specificity, and quantification of urine output is challenging in incontinent children without indwelling bladder catheters. Integration of clinically available biomarkers ha ...[more]

PMID: 35494424

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Project description:The National Institute for Health and Care Excellence (NICE) state that acute kidney injury (AKI) is seen in 13-18% of all people being admitted to hospital and that other patients will further go on to develop AKI during their time in hospital, with around 30-40% being in the operative setting. AKI has an estimated inpatient mortality of 20-30% in the UK and can lead to long-term morbidities like chronic kidney disease.[2] AKI is under-recognised and badly managed despite its prevalence and seriousness, with NCEPOD report stating that only 50% of patients with AKI received good care, that there was poor assessment of risk factors for AKI, and there was an unacceptable delay in recognising post-admission AKI in 43% of patients.[4] Baseline data collected on the urology ward in Ninewells Hospital, showed that only five of 22 (23%) patients undergoing urological surgery had post-operative creatinine measured on the ward within 48 hours (the primary method for detecting AKI). Excluding patients who were discharged the same day 5/16 (31%) received the blood test. The aim of the project was to increase the number of patients returning to ward 9 post-surgery who receive a serum creatinine measurement within two days of their urological surgery, excluding daycases. Specifically, we wanted the reliability of this measurement to be 95% or over in ward 9 by 30 July 2014. This was to be done by raising awareness around AKI on ward 9 and changing protocol so that every patient staying on ward 9 beyond their day of surgery should receive a post-operative creatinine. This would be tested for a set amount of time to see if patients with AKI were being missed. Despite not being able to implement a set protocol, the percentage of patients receiving post-operative creatinine measurements on ward 9 after a urological surgery still increased significantly. By interacting with the urology team and presenting our data, the knowledge and comprehension of the problem was altered. This lead to a change in culture and a significant increase in the number of post-operative creatinine measurements being taken. Through building relationships on the ward and sharing our data and knowledge there was an increase from 27% of patients receiving post-op creatinine in our first week of collecting data, to 87% in our last week on ward 9. However, without a set tool or change in protocol this change appears to have not been sustainable as the percentage dropped to 42% two weeks later.

Project description:Introduction: The incidence of acute kidney injury (AKI) related to vancomycin is variable, and several risk factors related to the treatment and patients may explain the nephrotoxicity. The role of urinary biomarkers in AKI related to vancomycin is unknown. Objective: The aim of this study was to evaluate the role of urinary IL-18, KIM-1, NGAL, TIMP-2, and IGFBP7 as diagnostic and prognostic predictors of AKI related to vancomycin. Methods: A prospective cohort study of patients receiving vancomycin and admitted to wards of a public university hospital from July 2019 to May 2020 was performed. We excluded patients that had AKI before starting vancomycin, hemodynamic instability, inability to collect urine, and chronic kidney disease stage 5. Results: Ninety-four patients were included, and the prevalence of AKI was 24.5%, while the general mortality was 8.7%. AKI occurred 11 ± 2 days after the first vancomycin dose. The most frequent KDIGO stage was 1 (61%). There was no difference between patients who developed and did not develop AKI due to gender, length of hospital stay, dose, and time of vancomycin use. Logistic regression identified age (OR 6.6, CI 1.16-38.22, p = 0.03), plasmatic vancomycin concentrations between 96 and 144 h (OR 1.18, CI 1.04-1.40, p = 0.04), and urinary NGAL levels between 96 and 144 h (OR 1.123, CI 1.096-1.290, p = 0.03) as predictors of AKI. The time of vancomycin use (OR 4.61, CI 1.11-22.02, p = 0.03), higher plasmatic vancomycin concentrations between 192 and 240 h (OR 1.02, CI 0.98-1.06, p = 0.26), and higher cell cycle arrest urinary biomarkers TIMP-2 multiplied by IGFBP-7 between 144 and 192 h (OR 1.33, CI 1.10-1.62, p = 0.02; OR 1.19, CI 1.09-1.39, p = 0.04, respectively) were identified as prognostic factors for non-recovery of kidney function at discharge. Conclusion: AKI related to vancomycin was frequent in patients hospitalized in wards. Age, plasmatic vancomycin concentrations, and NGAL between 96 and 144 h were identified as predictors of AKI related to vancomycin use. Plasmatic vancomycin concentrations and urinary NGAL were predictors of AKI diagnosis within the next 5 days. The urinary biomarkers of cell cycle arrest TIMP-2 and IGFBP-7 and the duration of vancomycin use were associated with non-recovery of kidney function at hospital discharge moment.

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Improving acute kidney injury diagnostic precision using biomarkers.

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Improving acute kidney injury diagnostic precision using biomarkers.

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