The kidneys are the primary regulators of electrolyte homeostasis, and renal dysfunction causes predictable electrolyte derangements. Hyperkalemia is the most immediately life-threatening complication of CKD/AKI: normally, the kidneys excrete 90% of daily potassium load via the ROMK channels in the collecting duct under aldosterone regulation. In renal failure, potassium accumulates, and the addition of RAAS blockers (ACEi/ARBs), potassium-sparing diuretics, or high-potassium foods can precipitate dangerous levels. ECG changes progress: peaked T waves → PR prolongation → loss of P waves → widened QRS → sine wave → cardiac arrest. Hyperphosphatemia occurs because the kidneys cannot excrete dietary phosphorus; elevated phosphorus binds serum calcium, causing hypocalcemia and stimulating PTH release (secondary hyperparathyroidism), which drives osteoclastic bone resorption (renal osteodystrophy). The failing kidney also cannot convert 25-OH vitamin D to active 1,25-dihydroxyvitamin D (calcitriol), worsening hypocalcemia. Metabolic acidosis develops because the kidneys cannot regenerate bicarbonate or excrete hydrogen ions; the anion gap may be elevated (uremic acid accumulation) or non-anion gap (from reduced ammonium excretion). Hyponatremia in CKD is usually dilutional from impaired free water excretion. The NP manages these derangements with...