Treatment of patients with chronic kidney disease (CKD) requires implementation of prevention and management strategies that reduce the risk of kidney failure and CKD-associated cardiovascular risk. Metabolic syndrome is characterised by obesity, high blood pressure, dyslipidaemia and hyperglycaemia, and is common among patients with CKD. Large-scale randomised trials have led to significant advances in the management of CKD with five pharmacotherapies now proven to be nephroprotective and/or cardioprotective in certain types of patients. Renin-angiotensin system inhibitors and sodium-glucose co-transporter 2 inhibitors slow kidney disease progression and reduce heart failure complications for most patients with CKD. In addition, statin-based regimens lower low-density lipoprotein cholesterol and reduce the risk of atherosclerotic disease (with no clinically meaningful effect on kidney outcomes). For patients with type 2 diabetes and albuminuric CKD, the non-steroidal mineralocorticoid receptor antagonist finerenone and the glucagon-like peptide-1 receptor agonist semaglutide also confer cardiorenal benefits, with semaglutide additionally effective at reducing weight. Together, these randomised data strongly suggest that metabolic syndrome mediates some of the cardiorenal risk observed in CKD. Considered separately, the trials help elucidate which components of metabolic syndrome influence the pathophysiology of kidney disease progression and which separately modify risk of atherosclerotic and non-atherosclerotic cardiovascular outcomes. As we predict complementary and different mechanisms of nephroprotection and cardioprotection for these different interventions, it seems logical that they should be deployed together to maximise benefits. Even when combined, however, these therapies are not a cure so further trials remain important to reduce the residual cardiorenal risks associated with CKD.