RE:Polymyxin B haemoperfusion treatment for respiratory failure COVID-19-associated acute kidney injury: consensus report of the 25th Acute Disease Quality Initiative (ADQI) Workgroup
Although urine volume is reported infrequently, two-thirds of patients have low urinary sodium concentrations at the time of AKI, and the majority are oliguric at RRT initiation
16,17. Urinalysis and biomarkers of AKI are frequently abnormal in patients with COVID-19 and could be used to characterize AKI in these patients
5,8,16,17. For example, one study reported that among the 32% of patients hospitalized with COVID-19 for whom urinalysis was available, 42.1% had significant proteinuria, with leukocyturia and haematuria in 36.5% and 40.9%, respectively
16. Similarly, a study of urinalysis data from 442 hospitalized Chinese patients with COVID-19, proteinuria was present in 43.9% (with 30% having ≥2+ on dipstick) with significant haematuria demonstrated in 11.3%
5. Examination of urinary sediment can be an effective tool in clinical scenarios in which more than one possible cause of AKI may exist that could affect medical management, for example, to distinguish acute tubular necrosis from pre-renal AKI, although special precautions may be needed when handling biospecimens from patients with COVID-19 (ref.
63). The role of urinary markers for injury or stress in the diagnosis of COVID-19 AKI remains unclear. Patients with COVID-19 AKI and high levels of tissue inhibitor of metalloproteinases-2 and insulin-like growth factor-binding protein-7 [TIMP-2] × [IGFBP-7] were more likely to progress to RRT than patients with AKI but with low [TIMP-2] × [IGFBP-7]
64. Elevated urinary alpha1-microglobulin in hospitalized patients was associated with the subsequent development of AKI
64.
Patients with COVID-19 AKI have also been reported to have higher levels of systemic markers of inflammation, particularly ferritin, C-reactive protein, procalcitonin and lactate dehydrogenase, than patients with COVID-19 and normal kidney function17. The relationship between markers of systemic disease
(for example, ferritin, D-dimers, non-respiratory organ failure) and the severity of pulmonary disease to the development, course and outcomes of COVID-19 AKI warrants further study. Risk factors for developing severe AKI (stage 3 AKI or requiring RRT initiation) need to be explored to identify approaches to prevent AKI.
Rationale
If used, EBP therapies should be selected on the basis of the pathophysiology they are designed to target. Numerous clinical criteria, including body temperature, haemodynamic status, need for vasopressor support, respiratory status and oxygenation, multiorgan failure score, cardiac and kidney function, as well as laboratory parameters such as lymphocyte counts, concentration of cytokines, ferritin, lactate dehydrogenase, D-dimers, monocytic expression of HLA, myoglobin, troponin, C-reactive protein, endotoxin activity, procalcitonin and culture results may be useful in evaluating the suitability of a patient for initiation of EBP. However, the precise indication for EBP in patients with COVID-19 remains to be determined. EBP for endotoxin removal has been generally applied for 48 consecutive hours and for 72 h for cytokine removal in studies of septic patients and in ongoing COVID-19 trials140,146,147,148,149. However, there are limited data regarding the timing of initiation or duration of use of these therapies, and further studies are needed.
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https://www.nature.com/articles/s41581-020-00356-5