Thus, in the setting of cardiac surgery, hemodynamic impairment may reduce the clearance of NT-proBNP.[26] Second, systematic vasodilation and antagonism of the renin-angiotensin-aldosterone system mediated by NT-proBNP might directly lead to renal hypoperfusion and cause renal injury.[17] Furthermore, NT-proBNP may be an indicator of elevated inflammation following heart surgery, which is crucial for the emergence and progression of CSA-AKI.[27] However, further investigation is required to determine the possible mechanism underlying the interaction between CSA-AKI and NT-proBNP. Here, NPPB is linked to acute kidney injury.