Abstract
Mannitol is an osmotic diuretic that can induce acute kidney injury (AKI) and hypertonic hyponatremia. Rapid mannitol removal and the avoidance of osmotic demyelination syndrome (ODS) by overcorrecting hyponatremia during dialysis are paramount. We present a case of mannitol-induced AKI and hyponatremia in a man in his 50 s with chronic kidney disease and heart failure who was undergoing chemotherapy for seminoma. After mannitol administration as a part of the chemotherapy protocol for forced diuresis, sudden anuric AKI and subsequent volume expansion developed. An estimated mannitol concentration of 728 mg/dL calculated using the osmolar gap (OG) was treated with hemodialysis (HD). Because of concerns regarding ODS caused by rapid serum sodium (sNa) correction by HD, extracorporeal ultrafiltration was initially considered for volume reduction. However, HD was ultimately chosen for mannitol removal; therefore, instead of the measured sNa, tonicity or corrected sodium (cNa) was monitored to account for transcellular free-water shifts between the intracellular and extracellular compartments. In this case, HD effectively removed mannitol, as reflected by the decreased OG, thereby resolving AKI and hyponatremia. Furthermore, tonicity (or cNa) remained stable throughout treatment, and complications were avoided. Prioritizing tonicity (or cNa) over measured sNa is important when managing hypertonic hyponatremia caused by mannitol intoxication.