Chronic kidney disease involves progressive glomerulosclerosis, tubulointerstitial fibrosis, and vascular injury driven by the final common pathways of hyperfiltration, proteinuria, and inflammation. The RAAS plays a central role: angiotensin II increases glomerular efferent arteriolar tone, raising intraglomerular pressure and accelerating nephron damage. ACE inhibitors/ARBs reduce intraglomerular pressure and proteinuria, slowing progression. SGLT2 inhibitors provide additional nephroprotection through tubuloglomerular feedback restoration, reducing hyperfiltration. As GFR declines, secondary complications develop: anemia from reduced erythropoietin, mineral bone disease (CKD-MBD) from phosphate retention and vitamin D deficiency driving secondary hyperparathyroidism, metabolic acidosis from impaired acid excretion, and cardiovascular disease (the leading cause of death in CKD). The clinician must initiate nephroprotective therapy, manage CKD-MBD, prescribe ESAs with iron optimization, plan renal replacement therapy, and coordinate transplant referral.