Chronic kidney disease now become a global health burden being the seventh leading risk factor for mortality worldwide. Chronic kidney disease is a progressive disease driven by hemodynamic and non-hemodynamic responses to nephron loss, which further facilitates kidney damage. Recent success in clinical trials that put kidney outcomes as primary or secondary outcomes have broadened our weapon to retard chronic kidney disease progression. In this lecture, I go over the current best approach in CKD management based on "KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease". Traditionally, modest dietary protein intake (0.8 g/kg body weight) and optimal blood pressure control and proteinuria reduction using ACE inhibitor or ARB remain a key intervention to retard CKD progression. In particular, a recent guideline recommends a more strict target of systolic blood pressure of <120 mmHg in CKD patients. The additional risk reduction nowadays can be achieved with the aid of pharmacological intervention using sodium-glucose cotransporter-2 inhibitors (SGLT2i), nonsteroidal mineralocorticoid receptor antagonists (ns-MRA), or glucagon-like peptide-1 receptor agonists (GLP1 RA) in diabetic or nondiabetic CKD patients having eGFR > 20~25 ml/min/1.73m2 and albuminuria > 30~200 mg/gCr. Furthermore, a pooled analysis suggests that a combination of SGLT2i, GLP-1 RA, and ns-MRA could bring a synergy effect in kidney event-free and overall survival. In patients with CKD of eGFR >15 ml/min/1.73m2 having atrial fibrillation, it is also recommended to use non–vitamin K antagonist oral anticoagulants (NOACs) in preference to warfarin based on superior thromboembolic risk reduction and comparable bleeding risk of NOAC. With these hopeful new drugs, avoidance of nephrotoxin drugs, prevention of acute kidney disease if possible, weight control, and the correction of hyperkalemia and metabolic acidosis are fundamental practices that should go in hand.