Electrolyte abnormalities are common and potentially life-threatening across nephrology, critical care, and oncology. Recent years have added targeted, better-tolerated options for the core disturbances of sodium, potassium, and calcium.
Hyponatremia
Tolvaptan, a selective vasopressin V2-receptor antagonist, raises serum sodium in euvolemic or hypervolemic hyponatremia (SIADH, heart failure, cirrhosis). The key caveat is the risk of overly rapid correction and osmotic demyelination, so serum sodium must be monitored closely.
Hyperkalemia
Two oral potassium binders now allow chronic hyperkalemia to be managed while continuing prognostically important RAAS inhibitors and mineralocorticoid antagonists: patiromer and sodium zirconium cyclosilicate. Both effectively lower serum potassium; the main effects are gastrointestinal, with patiromer occasionally lowering magnesium. These agents have become particularly useful in enabling optimal CKD and heart-failure therapy.
Calcium and phosphate
For hypercalcemia of malignancy — especially when refractory to bisphosphonates — the RANKL inhibitor denosumab achieves normocalcemia in most patients, with hypocalcemia the main risk. Symptomatic hypophosphatemia (in critical illness or refeeding) is corrected with oral or intravenous phosphate, watching for overcorrection and hypocalcemia.
| Disorder | Therapy | Key caution |
|---|---|---|
| Hyponatremia | Tolvaptan | Osmotic demyelination if corrected too fast |
| Hyperkalemia | Patiromer, sodium zirconium cyclosilicate | GI effects; enable RAAS/MRA therapy |
| Hypercalcemia | Denosumab | Hypocalcemia |
| Hypophosphatemia | Phosphate repletion | Avoid overcorrection |
Further reading: tolvaptan in hyponatremia (SALT trials); patiromer and sodium zirconium cyclosilicate in hyperkalemia; denosumab for hypercalcemia of malignancy.