In Reply

We thank Drs. Mets and Hennrikus for their constructive and relevant comments regarding our recently published case scenario.¹  They rightly underline that preoperative therapy with either an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker is a recognized risk factor for postoperative acute kidney injury. More importantly, they mention this therapy as a more credible etiology of acute kidney injury than hypotension itself. We support their statement, because ACE inhibitors reduce the efferent arteriole vascular tone with decreased glomerular filtration pressure and then glomerular filtration rate, especially during episodes of hypotension.²  This mechanism of reduced glomerular filtration rate corresponds to acute kidney injury definition, which may occur even with a relatively maintained renal perfusion pressure. If these different renal targets of ACE inhibitors might have negative effect, they can also be positive especially when the renin–angiotensin system is strongly stimulated as observed in cardiac failure.³  In this context, perioperative treatment with ACE inhibitors has been shown protective for renal function.^4,5  The authors thank Drs. Mets and Hennrikus for their very relevant comment, which stimulates research on continuation or not of ACE for renal and nonrenal outcome with predictable differences according to the degree of renin–angiotensin system stimulation. The second point raised by their comment concerned the use of neosynephrine, a pure α-agonist, to maintain arterial blood pressure during prolonged hypotension. We agree that it was a mistake to use such a drug instead of norepinephrine, which combines α- and β-agonist effects (which was used as second-line therapeutics). Systemic blood flow (cardiac output) and regional blood flow are expected higher with norepinephrine than with a pure α-agonist. The intention presenting this case, a frequent scenario for anesthesiologists, was to emphasize the need for an adequate preoperative cardiovascular evaluation and an adapted intraoperative hemodynamic monitoring for patient at risk of acute kidney injury. In addition to the consequences of perioperative ACE administration, this case stimulates the discussion on the “reflex” of using a pure α-receptor agonist to correct hypotension, forgetting the risk of reduction in flow. Avoidance of blinded fluid and/or vasopressors administration during major surgery may therefore reduce the need of an intensive care unit rescue and improve outcome.