It has been hypothesized that renal hypoperfusion is a factor in the progression of acute kidney injury (AKI) in severely ill COVID-19 patients. However, there is scant evidence to back up this claim. Using multiparametric magnetic resonance imaging, researchers plan to compare critically ill COVID-19 patients with and without AKI to identify changes in renal perfusion, oxygenation, and water diffusion. An observational case-control study of COVID-19-related respiratory failure in previously healthy intensive care unit patients. Raising International Standards for the Treatment of Kidney Disease Allocation to study groups was based on creatinine levels. The Mann-Whitney U test was used to sub; analyze the significant differences between groups. About 10 patients with Acute Kidney Injury (AKI) and 9 healthy controls were evaluated. In most cases, a diagnosis of AKI was made within 1 [0-2] days of the patient’s initial visit. Time-of-life and initial conditions Both groups had equal levels of plasma creatinine. Patients with AKI had lower total renal blood flow than those without the condition (median 645 [423-753] ml/min vs. 859 [746-920] ml/min, P=0.037). Cortical (76 [51-112] vs. 146 [123-169] ml/100 g/min, P=0.015) and medulla (28 [18-47] vs. 47 [38-73] ml/100 g/min, P=0.03) regional perfusion was decreased. Regional oxygenation (R2*) in the brain (17 [16-19] vs. 17 [16-18] 1/s, ns.) and the medulla (29 [24-39] vs. 27 [23-29] 1/s, ns.) were comparable between the 2 groups, as was the renal venous saturation (72% [64-75] vs. 72% [63-84], ns.). Total, cortical, and medullary renal blood flows were all lower in severely ill COVID-19 patients with AKI compared to those of patients without AKI, yet there were no discernible variations in renal oxygenation between the 2 groups.