Laboratory Investigation of Acute Kidney Injury

Publication Date: May 11, 2021
Last Updated: November 21, 2023

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# FINDING(S) AND/OR RECOMMENDATIONS Target Group
Laboratory Clinician
1 Monitor blood creatinine and/or urine output routinely for patients at risk of having or developing AKI. Frequency of length of monitoring should be individualized based on the clinical situation and degree of risk. X
2 Once clinical diagnosis of AKI is confirmed, we recommend further classification of the prerenal and intrinsic processes within each setting. X
3 Only employ creatinine assays with intra-laboratory analytical variability ≤ 3.4% for detection of AKI. X
4 Implement the use of +0.20 mg/dL (∼20 µmol/L) or +20% (whichever is greater), as new thresholds for diagnosing AKI. X X
5 Laboratories measuring creatinine with analytical methods with poor precision (CVA > 3.4%), including point-of-care technologies, require the use of a higher clinical cut-off for the diagnosis of AKI (refer to Table 3). X X
6 There is currently no evidence to suggest that any particular algorithm or approach to baseline creatinine definition is superior to another in terms of clinical outcomes. X X
7

The fractional excretion of sodium (FENa) is used to improve the diagnostic performance of the urine sodium test in assessing the cause of AKI by standardizing it to creatinine excretion:

Values < 1% are suggestive of prerenal, and values < 0.2% are suggestive of hepatorenal syndrome (HRS) in the appropriate clinical setting

X
8 Urine microscopy can help differentiate prerenal azotemia from acute tubular necrosis. It can also help with the diagnosis of less common causes of AKI, such as glomerulonephritis and acute interstitial nephritis. X
9 The use of a urine sediment scoring system based on the number of granular casts and renal tubular epithelial cells (RTEC) per high-power field in order to differentially diagnose AKI is recommended (see Table 4). X
10 Cystatin C may be helpful in predicting renal recovery earlier than creatinine among hospitalized patients with AKI. However, the assay cannot be universally recommended due to poor standardization, the lack of availability from most vendors and high cost (in comparison with creatinine) worldwide. X X
11 Urinary [TIMP2].[IGFBP7] is not yet recommended for routine risk assessment of AKI due to the lack of evidence of benefit shown in outcome studies, high false positive rate, and limited performance studies outside of the intensive care unit or perioperative setting. X X
12 The test for urine eosinophils is not useful to confirm or exclude acute interstitial nephritis and should no longer be considered in the evaluation of AKI X X
13 The value of automated alerts and communicating results regarding the presence of AKI is unclear. Whilst there is evidence of improved clinical practice, as yet this has not been linked to improved outcomes. X X

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Laboratory Investigation of Acute Kidney Injury

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