Acute kidney injury (AKI) is a common and serious postoperative complication following exposure to
cardiopulmonary bypass (CPB). Several mechanisms have been proposed by which the kidney can be damaged and interventional studies addressing known targets of renal injury have been undertaken in an attempt to prevent or attenuate CPB-associated AKI. However, no definitive strategy appears to protect a broad heterogeneous population of cardiac surgery patients from CPB-associated AKI. Although the association between
hemoglobinuria and the development of AKI was recognized many years ago, this idea has not been sufficiently acknowledged in past and current clinical research in the context of cardiac surgery-related AKI.
Hemoglobin-induced renal injury may be a major contributor to CPB-associated AKI. Accordingly, we now describe in detail the mechanisms by which
hemoglobinuria may induce renal injury and raise the question as to whether CPB-associated AKI may actually be, in a significant part, a form of pigment nephropathy where
hemoglobin is the pigment responsible for renal injury. If CPB-associated AKI is a pigment nephropathy, alkalinization of urine with
sodium bicarbonate might protect from: (1) tubular cast formation from met-
hemoglobin; (2) proximal tubular cell
necrosis by reduced endocytotic
hemoglobin uptake, and (3) free
iron-mediated
radical oxygen species production and related injury.
Sodium bicarbonate is safe, simple to administer and inexpensive. If part of AKI after CPB is truly secondary to
hemoglobin-induced pigment nephropathy, prophylactic
sodium bicarbonate infusion might help attenuate it. A trial of such treatment might be a reasonable future investigation in higher risk patients receiving CPB.