Soejima Ayaka, Ogata Masatomo, Takaki Ryo, Matsuda Takuya, Watanabe Shiika, Shibagaki Yugo, Yazawa Masahiko
Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1, Sugao, Miyamae-Ku, Kawasaki, Kanagawa, Japan.
Department of Nephrology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki-Shi, Nagasaki, 852-8501, Japan.
CEN Case Rep. 2025 Jun 29. doi: 10.1007/s13730-025-01017-x.
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.
甘露醇是一种渗透性利尿剂,可导致急性肾损伤(AKI)和高渗性低钠血症。在透析过程中迅速清除甘露醇并避免因过度纠正低钠血症而引发渗透性脱髓鞘综合征(ODS)至关重要。我们报告一例50多岁患有慢性肾脏病和心力衰竭且正在接受精原细胞瘤化疗的男性患者,发生了甘露醇诱发的AKI和低钠血症。在作为强制利尿化疗方案的一部分给予甘露醇后,突然出现无尿性AKI及随后的容量扩张。使用渗透压间隙(OG)计算得出的估计甘露醇浓度为728mg/dL,通过血液透析(HD)进行治疗。由于担心HD快速纠正血清钠(sNa)会导致ODS,最初考虑采用体外超滤进行容量减少。然而,最终选择HD来清除甘露醇;因此,监测的不是测得的sNa,而是张力或校正钠(cNa),以考虑细胞内和细胞外间隙之间的跨细胞自由水转移。在该病例中,HD有效清除了甘露醇,OG降低即反映了这一点,从而解决了AKI和低钠血症。此外,整个治疗过程中张力(或cNa)保持稳定,避免了并发症。在处理甘露醇中毒引起的高渗性低钠血症时,将张力(或cNa)置于测得的sNa之上是很重要的。