Chronic kidney disease (uremia) has reached pandemic proportion, where more than 10% of world’s population is affected by it. Cardiovascular diseases constitute the major cause of morbidity and mortality in CKD patients, which is primarily driven by uremic solutes, unique CKD-specific risk factors. Emerging evidence points to the importance of uremic solutes in inducing hyperthrombotic phenotype across the entire spectrum of CKD. A specific group of uremic solutes generated in gut retained with renal impairment and inflicting thrombosis (gut-kidney-vascular axis) is recently termed as ‘thrombolome’. They activate specific xenobiotic pathway to upregulate highly procoagulant protein termed tissue factor (TF). Validation of this uremia-specific pathway in two large patient cohorts provides human relevance and demonstrates it as a quantifiable risk factor. Importantly, that it can be potentially modulated by food makes it a modifiable cardiovascular risk factor. Deciphering the influence of food (foodome) on the thrombolome will have deep and broad implications in patients with CKD.