In a recent edition of Anesthesiology, Wijk et al.¹ examine the differential effect on the kidney of cardiopulmonary bypass (CPB) with flow rates of 2.4 L/min/m² and 2.9 L/min/m². This is the latest in a suite of roughly 20 articles in the past 15 years by this Swedish group investigating the effects of CPB, medications, and various pathologic states on renal physiology.

They should be congratulated on these achievements. A review of the literature in mainstream anesthesiology journals indicates that few groups pursue this type of research, in which physiological variables are invasively measured in patients undergoing clinical care. In fact, this article has already generated 2 stand-alone editorials.^2,3 It took 4 years to recruit the 36 patients analyzed in this study, and the patients were subjected to infusions of para-aminohippuric (PAH) acid and iohexol and renal vein cannulation, in addition to their standard treatment. This invasive, and one would imagine painstaking, research provides valuable insights into potential pathophysiology and offers avenues for research for preventing renal damage associated with CPB.

In this study, the findings were relatively modest and are hypothesis generating rather than scientific conclusions with a high degree of certainty. Overall, the authors saw no difference in renal blood flow or the renal oxygen supply-demand relationship between the standard-flow and the high-flow groups. There was an increase in the glomerular filtration rate (GFR) and a 60% reduction in the release of N-acetyl-β-d-glucosaminidase, a marker of renal tubular damage, 60 minutes after the cessation of bypass, in the high-flow group. The PAH extraction in the high-flow group was reduced, which suggested a redistribution of flow away from the cortex and into the medullary regions where PAH extraction is lower. The high-flow group required less norepinephrine to maintain mean arterial pressure targets, which may have influenced some of the findings, and needed more crystalloid to maintain reservoir volume. The impact of this is unclear. Potentially confounding the findings was that the starting GFR was lower in the high-flow group (73 v 86 mL/min) despite adequate randomization strategies.