Nifedipine and Cardiopulmonary Bypass: Effect on Renal Function

Editor, The work by Witczak et al.[1] deserves some attention. I would like to make some comments, hoping not to complicate the subject even more. Renal failure is a relevant problem associated with surgery with cardiopulmonary bypass (CPB) in adults [2]. The complication increases if we study patients with preoperative renal dysfunction [3]. The statement by the authors in the introduction and discussion that ‘CPB surgery is generally accepted to induce injury to the kidney’ could be misleading. In fact, cardiac surgery with CPB has been associated with renal dysfunction; however, this is not the CPB itself but the entire procedure, including the preoperative and postoperative course of the surgery. Preoperative renal function is the main risk factor for developing renal dysfunction postoperatively, but there are many other factors involved in this dysfunction that have not been well studied so far: fluid, inotropes, antibiotics, haemodynamic alterations and vasoconstriction to name a few. Moreover, a recent study has shown that, in patients with preoperative renal dysfunction, the incidence of postoperative renal failure is similar between on and off pump surgery [3]. No changes in glomerular filtration rate and enzymes released in this study demonstrate that the impact on renal function due to CPB in high-risk renal patients is at least discrete. Many drugs and therapies have been studied to preserve renal function under different surgical conditions: fenoldopam, nifedipine, diltiazem, verapamil, dopamine, mannitol, high blood pressure, higher haematocrit, among others. None of them have shown effective and positive results. It has been speculated that vasodilatation could reduce the incidence of renal damage, assuming that effective renal blood flow is reduced during CPB. New and old studies have shown that renal flow increases during CPB [2,4]. Filtration fraction decreases during CPB and increases in the postoperative period, so there is vasoconstriction but in the postoperative period [2]. During that period is where our therapy should be focused. To my knowledge, there is no study with strict postoperative randomization of patients with abnormal preoperative dysfunction to different ‘renal protective interventions’. Randomization under these circumstances is very complex, if not impossible, probably due to the many factors involved during this clinical period. Acknowledgement The present study is supported by a grant from FONDECYT 1030645-2003, USA.