Intraoperative hypotension (IOH) invariably follows the induction of general anesthesia during surgical operations. The current prevailing and predominant consensus acknowledges that IOH has immense clinical benefits such as reduced bleeding, less need for blood transfusions, and shorter surgery times and yet without significant adverse renal, hepatic, and neurological consequences. Nonetheless, our critical analysis of the surgery-acute kidney injury (AKI) literature exposed the fact that historical research had studied younger patients, with normal kidney function, involved procedures with short surgery times while concurrently excluding patients with advanced chronic kidney disease (CKD) and/or uncontrolled hypertension. We report on two patients seen in the Renal Unit of Mayo Clinic Health System, Northwestern Wisconsin, USA, to exemplify the causative relationship between IOH and postoperative AKI. Sun et al. (2015) recently demonstrated that postoperative AKI was associated with sustained intraoperative hypotensive periods of mean arterial pressure (MAP) <55 and <60 mmHg, respectively, in a graded pattern. Our experiences provide an impetus for new randomized clinical trials to determine safe levels of IOH during operations and whether interventions that promptly treat IOH, or better still that prevent IOH, and that are tailored to suit individual patient physiology, would reduce the risk of AKI. We posit that IOH is a neglected cause of postoperative AKI. We call for a preventative nephrology paradigm shift and the targeting of MAP ≥60 mmHg and/or systolic blood pressure ≥90 mmHg during surgical procedures. Particularly, in Sub-Saharan Africa with its paucity of renal replacement therapy options to manage kidney failure, every effort to limit AKI, syndrome of rapid onset end-stage renal disease, and exacerbation of kidney dysfunction in general, must be vigorously applied.