Deterioration in renal function after interventional cardiac procedures has been identified not only as a procedural complication, but also as an important risk for subsequent mortality (1). Because the bulk of the early observations stemmed from iodinated contrast percutaneous procedures, the term “contrast-induced” nephropathy was customary, albeit with a doubt (2): could it be that patients’ hemodynamic instability, congestive heart failure, or procedural hypotension account for more of the detriments in renal function than the contrast media? Nephrology input in the cardiology literature recently introduced the more permissive term of contrast-associated nephropathy (3).

Noncontrast nephropathy has been well described in the cardiac surgery literature. Cardiac surgery, however, portends special risks in relation to hypotension and cardiopulmonary bypass and does not really fit the bill as analogous to noncontrast percutaneous procedures. Considerable risks of acute renal failure after different types of cardiac surgery have been reported despite the absence of contrast media use (4, 5, 6); no long-term follow-up was available in those studies. Detailed renal insufficiency data in open heart mitral valve repair or replacement surgery are scarce but indicate higher acute nephropathy after open heart surgery than percutaneous methods (7,8). In general, a longer operation was associated with acute kidney injury (AKI) in several studies (4, 5, 6, 7, 8).

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