Urinary bladder cancer accounted for around 570,000 new cancer cases and about 200,000 deaths worldwide in 2020, making it the tenth most commonly diagnosed cancer [1]. Bladder cancer manifests either as non-muscle-invasive cancer or a muscle-invasive form (MIBC); the latter form accounts for approximately 25% of cases at diagnosis. Urothelial MIBC was, prior to the introduction of neoadjuvant chemotherapy (NAC), associated with a poor prognosis, with a 5-year overall survival (OS) post-RC of 50%. The current treatment regimen in Europe for MIBC includes NAC in medically fit patients and radical cystectomy (RC) [2]. The inclusion of NAC pre-RC aims to eradicate micro-metastatic dissemination and has been shown to significantly increase survival compared with RC only [3,4]. We previously showed that chemo-responding patients who downstaged with complete response (CR) to pT0N0M0) had an absolute risk reduction of 31% for death at the five-year median observation time (OS) [5]. The NAC regimen for MIBC patients in Sweden in most centers consists of a cisplatin-based combination of methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC), while in patients who are ineligible for cisplatin, a carboplatin-gemcitabine combination is used [6]. Eligibility for NAC, according to Swedish guidelines, are age ≤ 75 years, renal function with eGFR > 50–60, no hearing impediments, and acceptable comorbidities [7]. NAC treatment is generally well tolerated; however, adverse events, including thromboembolic events (TEEs). have been shown to occur during and after NAC treatment [8,9]. Eriksson et al., using a multicenter clinical dataset, showed serious grade 4 TEEs in patients treated with NAC. In addition, acute kidney injury and chronic kidney disease were seen in 41% and 11% of patients, respectively [10]. Interestingly, 30% of patients receiving NAC had to terminate the treatment prematurely. Among these patients, 62% of terminations were due to acute kidney injury. There was a significant association between decreased kidney injury and increased downstaging, possibly reflecting the effect of completed intended NAC cycles on downstaging, as reported earlier [5]. Renal impairment is a fraught consequence of cisplatin-based combinations and one of the key determinants for NAC eligibility [7,11]. Mehrazin et al., in a recent study, showed a continued decline in eGFR rates in MIBC-NAC patients after discharge. In their study, the rate of decline was related to eGFR rates at discharge, with up to 43% of the patients showing a decline [12]. Deep vein thrombosis (DVT) and pulmonary embolism (PE) are two lethal complications during NAC and RC. Endothelial damage and the hypercoagulable state during cancer treatment continues post treatment [13]. Thromboprophylaxis pre- and post-surgery has become a standard in tertiary care centers and is highly encouraged as a quality-of-care indicator [14]. Low-molecular-weight heparin (LMWH) is frequently prescribed for the prevention and treatment of TEEs in patients [15]. LMWH provides a reduction in the incidence of venous thromboembolism and requires minimal monitoring [16,17]. However, combined with impaired renal function, the major mode of excretion for LMWH, there is an increased risk of supratherapeutic accumulation of LMWH with an associated risk of major bleeding [12]. To the best of our knowledge, no international or national guidelines exist advocating LMWH as prophylaxis against TEEs amongst MIBC-NAC patients during the NAC period. In this retrospective study, we investigate the incidence of NAC-induced renal impairment in our research database. The objective was to assess the incidence of patients with NAC-induced TEEs who may not have benefited from LMWH if prophylaxis had hypothetically been used.