Chronic Kidney Disease (CKD) is defined as kidney damage or GFR <60 mL/min/1.73m2 for >=3 months. Progressive nephron loss leads to a cascade of pathophysiological consequences: (1) Decreased GFR causes accumulation of uremic toxins (urea, creatinine, phosphate, organic acids) and inability to regulate fluid/electrolyte/acid-base balance. (2) Erythropoietin (EPO) deficiency develops because the damaged kidneys cannot produce adequate EPO, leading to normocytic normochromic anemia. (3) Phosphate-calcium imbalance: failing kidneys cannot excrete phosphate (hyperphosphatemia), which binds calcium causing hypocalcemia. Hypocalcemia stimulates parathyroid hormone (PTH) secretion (secondary hyperparathyroidism), leading to renal osteodystrophy (bone resorption to release calcium). Additionally, the kidneys cannot convert 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D (calcitriol), further reducing calcium absorption. (4) Metabolic acidosis from inability to excrete hydrogen ions and regenerate bicarbonate. (5) Uremia causes dysfunction in virtually every organ system. CKD stages by GFR: G1 (>=90, with kidney damage), G2 (60-89), G3a (45-59), G3b (30-44), G4 (15-29), G5 (<15 - kidney failure, dialysis indicated). On the exam, writers often pair stable-sounding options with unstable data—notice the mismatch before you commit. If the stem names a license or role, reread...