Contrib Nephrol. 2007;156:340-53.
Cardiopulmonary bypass-associated acute kidney injury: a pigment
nephropathy?
Haase M, Haase-Fielitz A, Bagshaw SM, Ronco C, Bellomo R.
Department of Intensive Care, Austin Health, Melbourne, Vic.,
Australia.
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
CPBassociated 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 CPBassociated 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.
PMID: 17464145 [PubMed - in process]
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