First, the use of a vasopressor therapy as well as hypoxia-induced pulmonary vasocontraction can lead to the increasing levels of NT-proBNP.12 Second, the NT-proBNP release can also be triggered by direct involvement of the myocardium tissue by the activation of the inflammatory process, demand-supply mismatch, and oxidative stress.13 Finally, the development of acute renal failure which, by impairing its clearance, may also elevate the levels of NT-proBNP.12,13. Here, NPPB is linked to acute kidney injury.