Peri-operative fluid strategy and post-operative acute kidney injury in cardiac surgery patients: any role for pre-operative statin therapy?

Acute kidney injury (AKI) is a common complication associated with increased morbidity and mortality in cardiac surgery patients. In this context, the recent paper by Kim et al., showing that a peri-operative liberal ‘saline- and starch-based’ fluid management significantly enhanced the incidence of severe post-operative AKI in off-pump cardiac surgery patients, is to be acclaimed [1]. With regard to the potential culprit(s) triggering this AKI, the authors pointed at ‘usual suspects’ such as excess chloride and intrinsic starch-induced renal tubular lesions. However, it is noteworthy that patients in the at-risk group were less likely (p = 0.001!) to be receiving statins before surgery [1]. Statins may prevent kidney injury through inhibition of post-operative inflammatory processes. Compared with statin-naive subjects, cardiac surgery patients taking statins indeed had reduced levels of circulating C-reactive protein, tumour necrosis factor alpha, myeloperoxidase, and pro-inflammatory interleukin (IL)-1, IL-6, and IL-8 and higher concentrations of the anti-inflammatory IL-10 [2]. The largest meta-analysis to date, including nearly 60,000 cardiac surgery patients, revealed a 13 % reduction of post-operative AKI in patients pre-operatively treated with statins [3]. Whether statins embrace the kidney as friend or foe is debatable but probably depends upon the type of study cohort (e.g. septic vs. non-septic), the intervention (e.g. surgery), and pre-existing chronic kidney disease. For example, agent-dependent ‘high potency’ statin doses increase the risk of AKI in a general patient population [4] whereas the use of corresponding high doses in cardiac surgery patients appears to exhibit a reno-protective effect [5].