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In the current era of cardio-oncology the awareness of the cardiotoxicity of anti-cancer therapies is entering into common clinical practice, and new methods for monitoring risk and early markers are urgently needed [1–3]. One of the clear examples of cancer therapy cardiotoxicity is in patients with breast cancer over-expressing the HER2 receptor, which are currently treated with anthracyclines or taxanes and with trastuzumab. Anthracyclines and trastuzumab are both associated with cardiotoxicity [1]. Trastuzumab is associated with cardiotoxicity through a variety of HER2-related and unrelated mechanisms [4]. Concurrent use of anthracyclines and trastuzumab, while highly effective, are found to synergize in inducing cardiac damage [2]. In this issue of Internal and Emergency Medicine, Russo et al. [5] point out a new risk condition in cancer chemotherapy-associated cardiotoxicity: impaired renal function. In particular, there is renal dysfunction (RD) in a group of women with breast cancer (the ICARO cohort) with no previous signs or symptoms of heart failure and preserved LVEF who are undergoing trastuzumab treatment after chemotherapy. The authors examine this dysfunction and its relation to cardiac toxicity following trastuzumab. The heart–kidney axis is well known in cardiology, where RD often aggravates congestive heart failure. RD has now been identified as a risk factor for mortality [6], in particular increased risk for cardiovascular (CV) events. Diverse mechanisms are associated with these effects, including perturbation of the renin–angiotensin system, atrial natriuretic peptide signalling and the sympathetic baroreflex system, most of which are related to hypertension. The importance of sympathetic baroreflex signaling by the kidneys in inducing cardiac stress is increasingly recognized, to the point that trials on ablation of renal sympathetic signaling in hypertensive patients are underway [7]. However, the role of RD as a risk factor for CV events in cancer therapy has to date not been entered into the cardio-oncologic equation. Anthracyclines, taxanes or trastuzumab alone, at present are not considered to be nephrotoxic, and current guidelines do not require dose reduction in patients with RD. Russo et al. [5] report that RD, determined by estimation of GFR using creatine clearance (eGFR) with the simplified MDRD equation, assessed at baseline (prior to trastuzumab therapy, after other chemotherapies) is associated with an increased risk of cardiovascular toxicity and complications following trastuzumab. Cardiotoxicity was monitored by A. Albini (&) Research Infrastructure, IRCCS Arcispedale Santa Maria Nuova, Reggio Emilia, Italy e-mail: albini.adriana@gmail.com

Renal dysfunction and increased risk of cardiotoxicity with trastuzumab therapy: a new challenge in cardio-oncology