Dorman H R, Sondheimer J H, Cadnapaphornchai P
Department of Medicine, Wayne State University, School of Medicine, Detroit, Michigan.
Medicine (Baltimore). 1990 May;69(3):153-9. doi: 10.1097/00005792-199005000-00003.
Mannitol is widely used to reduce intracranial pressure and is protective against ischemic and nephrotoxic acute renal failure. However, the capacity of this seemingly innocuous agent to produce acute renal failure is not well recognized. We report herein the clinical course of 8 cases of mannitol-induced acute renal failure. In addition, we reviewed all previously reported cases of mannitol-induced renal failure. In the present series, acute oliguric renal failure developed within 3.5 +/- 1.1 (mean +/- SD) days after receiving daily and total mannitol doses of 189 +/- 64 g and 626 +/- 270 g, respectively, over 3.5 +/- 1.5 days. The peak serum creatinine was 5.7 +/- 2.7 mg/dl and peak osmolal gap was 74 +/- 39 mOsm/kg water. Renal tubular epithelial cells containing vacuoles were seen in the urinary sediments of 6 patients. Renal function improved rapidly upon discontinuation of mannitol and/or removal of mannitol by hemodialysis. In those previously reported cases in which the baseline renal function was normal, acute renal failure developed after receiving total mannitol doses of 1171 +/- 376 g. The peak osmolal gap was 107 +/- 17. In contrast, in those with underlying renal compromise, renal function worsened after a total mannitol dose of 295 +/- 143 g. The pathogenesis of mannitol-induced renal failure is not yet established but may be associated with renal vasoconstriction produced by high concentrations of mannitol. This may be averted in clinical practice by monitoring the osmolal gap, rather than serum osmolality alone, when using mannitol infusions for the treatment of intracranial hypertension.
甘露醇被广泛用于降低颅内压，对缺血性和肾毒性急性肾衰竭具有保护作用。然而，这种看似无害的药物导致急性肾衰竭的能力尚未得到充分认识。我们在此报告8例甘露醇诱发急性肾衰竭的临床过程。此外，我们回顾了所有先前报道的甘露醇诱发肾衰竭的病例。在本系列中，急性少尿性肾衰竭在分别于3.5±1.5天内每日及总共接受189±64 g和626±270 g甘露醇剂量后3.5±1.1（均值±标准差）天内发生。血清肌酐峰值为5.7±2.7 mg/dl，渗透压差值峰值为74±39 mOsm/kg水。6例患者的尿沉渣中可见含有空泡的肾小管上皮细胞。停用甘露醇和/或通过血液透析清除甘露醇后，肾功能迅速改善。在那些先前报道的基线肾功能正常的病例中，在接受总共1171±376 g甘露醇剂量后发生急性肾衰竭。渗透压差值峰值为107±17。相比之下，在那些有潜在肾脏损害的患者中，在总共接受295±143 g甘露醇剂量后肾功能恶化。甘露醇诱发肾衰竭的发病机制尚未明确，但可能与高浓度甘露醇引起的肾血管收缩有关。在临床实践中，当使用甘露醇输注治疗颅内高压时，通过监测渗透压差值而非仅监测血清渗透压，可能避免这种情况。
