Biomarker-Based Prediction of Survival and Recovery of Kidney Function in Acute Kidney Injury

Abstract

Background Acute kidney injury (AKI) affects increasing numbers of hospitalized patients, the prog-nosis remains poor. The diagnosis is still based on the 2012 published KDIGO criteria. Numerous new AKI biomarkers have been identified in recent years, they either reflect impaired excretory function or structural damage. The majority of markers are useful for AKI recognition under certain circumstances. Fewer data are available on the role of biomarkers in the prediction of in-hospital survival and renal recovery post-AKI. The current article is intended to provide information about these two aspects. Summary The following databases were screened: PubMed, Web of Science, Cochrane Library, Scopus. The period lasted from 2000 until 2022. The following terms were applied: ´AKI´ AND ´biomarker´ AND ´survival´ OR ´mortality´ OR ´recovery of kidney function´ OR ´renal recovery´ OR ´kidney recovery´. The following terms were used for additional literature search: ´TIMP-2´ AND ´IGFBP7´ and ´RNA biomarker´ AND ´hematology´. Regarding mortality, exclusively those studies were selected, that addressed the in-hospital mortality. Nine (9) studies were identified that evaluated biomarker-based pre-diction of in-hospital mortality and/or of recovery of kidney function (ROKF). A homoge-nous definition of ROKF is however missing yet. Currently, some biomarkers, meas-ured early during the course of the disease are associated with increased mortality risk and/or with a higher chance of renal recovery. Key messages • The literature provides only a few biomarker-related studies that address the is-sues of mortality and recovery. • The definition of ROKF needs to be homogenized.

Development and validation of a machine-learning model for predicting the risk of death in sepsis patients with acute kidney injury

“…Although it is generally believed that AKI is caused by sepsis in half of patients, it has been shown previously [ 25 ] that sepsis was responsible for only 23.6 % of AKI in affected patients. Therefore, AKI cannot be equated with S-AKI.…”

“…In the future, it may be possible to reduce mortality by taking these variables into consideration in clinical practice. Previous studies have suggested that biomarkers such as the fibrinogen-to-albumin ratio, urinary protein, urinary albumin, glycated hemoglobin, neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, liver-type fatty acid-binding protein [ 25 ], and other indicators can be used to predict AKI mortality accurately. Additionally, Yoo et al [ 26 ] found that the recurrent neural network model is better than classical methods for predicting the mortality of AKI patients with continuous renal replacement therapy and improves treatment outcomes by improving important predictive factors.…”

Serum Nostrin—A risk factor of death, kidney replacement therapy and acute kidney disease in acute kidney injury

“…In general, the data on biomarker-based mortality prediction in AKI are limited. We recently reviewed the literature [21] and identified six references that addressed the prediction of in-hospital death in acute kidney injury. Three studies included well known markers such as NGAL, KIM-1, L-FABP, and urinary (TIMP-2) x (IGFBP7) [22][23][24].…”

From Rare Disorders of Kidney Tubules to Acute Renal Injury: Progress and Prospective

“…The mortality rate ranges from 10% to 20% for hospitalized patients and 44.7–53% for ICU patients [ 1 ], caused by various factors such as sepsis, trauma, cardiac surgery, nephrotoxic drugs, and underlying chronic kidney disease. However, traditional biomarkers such as serum creatinine, blood urea nitrogen, neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 (KIM-1) are limited in terms of sensitivity and specificity due to factors like age, gender, muscle mass, and hydration status, which presents a challenge for the development of effective treatments for AKI [ 2 ]. Experiences from bedside and animal studies indicated the intensive correction between AKI and tubular dysfunction, injury, or programmed death.…”