Erratum to Rutten et al. "Platelet density per monocyte predicts adverse events in patients after percutaneous coronary intervention" (Thromb Haemost 2016; 115: 353-360).

scribe WISN in a 52-year-old man with protein C and S deficiency four years after warfarin initiation (5). Tillou et al. describe an 84-year-old male with WISN after six months of therapy for PE with DVT (6). Gaikwad et al. describe a 31-year-old male with a DVT who presented with WISN after two months of warfarin (7). Scarff et al. describe a 43-year-old female with recent aortic and mitral valve replacement secondary to rheumatic valvular disease who developed WISN 58 days after warfarin initiation (11). Interestingly, WISN has been described in conjunction with cases of congestive heart failure (CHF) exacerbations. Teepe et al. describe the case of five recurrent episodes of WISN in a patient with protein C deficiency coinciding with CHF exacerbations (12). In addition, Humphries et al. describe a 59-year-old female with a CHF exacerbation associated with WISN after three months of warfarin therapy (13). Essex et al. describe two cases of WISN with bi-ventricular dysfunction demonstrated on TTE (14). Our patient’s TTE revealed mild-moderately dilated left and right ventricles and EF 35 %. This association requires further investigation in the future. Many cases of WISN resolve after discontinuation of warfarin and wound care therapy. Canturk et al. reported a case of WISN after two weeks of initiation of therapy for acute DVT with resolution of lesions after discontinuation of warfarin and initiation of rivaroxaban (15). It is unclear if duration of warfarin therapy prior to symptom onset affects prognosis and resolution of lesions. There are currently no cases demonstrating WISN with renal involvement in the literature. It is unclear what the significance of these findings may be in our patient. Given the pro-thrombotic state of WISN, it is possible that other organs including the kidneys and heart may be affected similarly. Of note, Brodsky et al. suggested that warfarin therapy can result in warfarin-related nephropathy by causing glomerular haemorrhage and renal tubular obstruction by RBC casts (16, 17). In addition, certain infectious processes may lead to glomerular damage as in the case of post-streptococcal glomerulonephritis, although our patient did not demonstrate such findings. In conclusion, this case highlights the importance of including WISN in the differential of any patient who presents on warfarin with skin lesions. In addition, WISN may occur at any time period after initiation of warfarin, possibly affecting other organ systems. Finally, novel anti-coagulants may serve as an appropriate alternative therapy after diagnosis.