Biomarkers in pursuit of precision medicine for acute kidney injury: hard to get rid of customs.

Traditional acute kidney injury (AKI) classifications, which are centered around semi-anatomical lines, can no longer capture the complexity of AKI. By employing strategies to identify predictive and prognostic enrichment targets, experts could gain a deeper comprehension of AKI's pathophysiology, allowing for the development of treatment-specific targets and enhancing individualized care. Subphenotyping, which is enriched with AKI biomarkers, holds insights into distinct risk profiles and tailored treatment strategies that redefine AKI and contribute to improved clinical management. The utilization of biomarkers such as N-acetyl-ß-D-glucosaminidase, tissue inhibitor of metalloprotease-2·insulin-like growth factor-binding protein 7, kidney injury molecule-1, and liver fatty acid-binding protein garnered significant attention as a means to predict subclinical AKI. Novel biomarkers offer promise in predicting persistent AKI, with urinary motif chemokine ligand 14 displaying significant sensitivity and specificity. Furthermore, they serve as predictive markers for weaning patients from acute dialysis and offer valuable insights into distinct AKI subgroups. The proposed management of AKI, which is encapsulated in a structured flowchart, bridges the gap between research and clinical practice. It streamlines the utilization of biomarkers and subphenotyping, promising a future in which AKI is swiftly identified and managed with unprecedented precision. Incorporating kidney biomarkers into strategies for early AKI detection and the initiation of AKI care bundles has proven to be more effective than using care bundles without these novel biomarkers. This comprehensive approach represents a significant stride toward precision medicine, enabling the identification of high-risk subphenotypes in patients with AKI.

Acute kidney injury in patients with COVID-19 compared to those with influenza: a systematic review and meta-analysis.

Background: COVID-19 and influenza can both lead to acute kidney injury (AKI) as a common complication. However, no meta-analysis has been conducted to directly compare the incidence of AKI between hospitalized patients with COVID-19 and influenza. The objective of our study aims to investigate the incidence and outcomes of AKI among hospitalized patients between these two groups. Materials and methods: A systematic search of PubMed, Embase, and Cochrane databases was conducted from December 2019 to August 2023 to identify studies examining AKI and clinical outcomes among hospitalized patients with COVID-19 and influenza. The primary outcome of interest was the incidence of AKI, while secondary outcomes included in-hospital mortality, recovery from AKI, hospital and ICU stay duration. The quality of evidence was evaluated using Cochrane and GRADE methods. Results: Twelve retrospective cohort studies, involving 17,618 hospitalized patients with COVID-19 and influenza, were analyzed. COVID-19 patients showed higher AKI incidence (29.37% vs. 20.98%, OR: 1.67, 95% CI 1.56-1.80, p < 0.01, I2 = 92.42%), and in-hospital mortality (30.95% vs. 5.51%, OR: 8.16, 95% CI 6.17-10.80, p < 0.01, I2 = 84.92%) compared to influenza patients with AKI. Recovery from AKI was lower in COVID-19 patients (57.02% vs., 80.23%, OR: 0.33, 95% CI 0.27-0.40, p < 0.01, I2 = 85.17%). COVID-19 patients also had a longer hospital stay (SMD: 0.69, 95% CI 0.65-0.72, p < 0.01, I2 = 98.94%) and longer ICU stay (SMD: 0.61, 95% CI 0.50-0.73, p < 0.01, I2 = 94.80%) than influenza patients. In our study, evidence quality was high (NOS score 7-9), with low certainty for AKI incidence and moderate certainty for recovery form AKI by GRADE assessment. Conclusion: COVID-19 patients had higher risk of developing AKI, experiencing in-hospital mortality, and enduring prolonged hospital/ICU stays in comparison to influenza patients. Additionally, the likelihood of AKI recovery was lower among COVID-19 patients.

Outcomes associated with acute kidney disease: A systematic review and meta-analysis.

Background: Acute kidney disease (AKD) defines the period after kidney damage and it is a critical period of both repair and fibrotic pathways. However, the outcomes of patients with AKD have not been well-defined. Methods: In this meta-analysis, PubMed, Embase, Cochrane and China National Knowledge Infrastructure were searched on July 31,2022. We excluded studies including patients undergoing kidney replacement therapy at enrollment. The data was used to conduct a random-effects model for pool outcomes between patients with AKD and non-AKD (NKD). This study is registered with PROSPERO, CRD 42021271773. Findings: The search generated 739 studies of which 21 studies were included involving 1,114,012 patients. The incidence rate of community-acquired AKD was 4.60%, 2.11% in hospital-acquired AKD without a prior AKI episode, and 26.11% in hospital-acquired AKD with a prior AKI episode. The all-cause mortality rate was higher in the AKD group (26.54%) than in the NKD group (7.78%) (odds ratio [OR]: 3.62, 95% confidence interval [CI]: 2.64 to 4.95, p < 0.001, I2 = 99.11%). The rate of progression to end-stage kidney disease (ESKD) was higher in the AKD group (1.3%) than in the NKD group (0.14%) (OR: 6.58, p < 0.001, I2 = 94.95%). The incident rate of CKD and progressive CKD was higher in the AKD group (37.2%) than in the NKD group (7.45%) (OR:4.22, p < 0.001, I2 = 96.67%). Compared to the NKD group, patients with AKD without prior AKI had a higher mortality rate (OR: 3.00, p < 0.001, I2 = 99.31%) and new-onset ESKD (OR:4.96, 95% CI, p = 0.002, I2 = 97.37%). Interpretation: AKD is common in community and hospitalized patients who suffer from AKI and also occurs in patients without prior AKI. The patients with AKD, also in those without prior AKI had a higher risk of mortality, and new-onset ESKD than the NKD group. Funding: This study was supported by Ministry of Science and Technology (MOST) of the Republic of China (Taiwan) [grant number, MOST 107-2314-B-002-026-MY3, 108-2314-B-002-058, 110-2314-B-002-241, 110-2314-B-002-239], National Science and Technology Council (NSTC) [grant number, NSTC 109-2314-B-002-174-MY3, 110-2314-B-002-124-MY3, 111-2314-B-002-046, 111-2314-B-002-058], National Health Research Institutes [PH-102-SP-09], National Taiwan University Hospital [109-S4634, PC-1246, PC-1309, VN109-09, UN109-041, UN110-030, 111-FTN0011] Grant MOHW110-TDU-B-212-124005, Mrs. Hsiu-Chin Lee Kidney Research Fund and Chi-mei medical center CMFHR11136. JAN is supported, in part, by grants from the National Institute of Health, NIDDK (R01 DK128208 and P30 DK079337) and NHLBI (R01 HL148448-01).