Mannitol is an independent risk factor of acute kidney injury after cerebral trauma: a case–control study

Abstract

We retrospectively studied a random cohort of patients with cerebral trauma to investigate the risk factors of acute kidney injury (AKI) following cerebral trauma. AKI was determined using the RIFLE (risk, injury, failure, loss, or end-stage kidney) staging criteria. About 171 patients were chosen in the study, with 53 patients in AKI group and 118 patients without AKI in non-AKI group. By logistic regression analysis, univariate analysis revealed that age, hypertension, emergent surgery, systemic inflammatory response syndrome (SIRS), Glasgow coma score (GCS), sequential organ failure assessment (SOFA) score, the respiration, coagulation, and cardiovascular components of the SOFA score, mechanical ventilation time, red blood cell transfusion, plasma transfusion, and the accumulative doses of furosemide, torsemide, and mannitol were significantly related to AKI after cerebral trauma. Logistic multivariate regression analysis showed that SOFA score [odds ratio (OR) = 1.516, 95% confidence interval (CI) 1.222-1.881, p < 0.001], the accumulative doses of torsemide (OR = 0.016, 95% CI 1.002-1.031, p = 0.016), and the accumulative doses of mannitol (OR = 2.687, 95% CI 1.062-6.800, p = 0.037) were independent risk factors of AKI. This model had a good discrimination for AKI with an area under the receiver operating characteristic (ROC) curve of 0.901 (p < 0.001). The accumulative doses of mannitol as a risk factor of AKI were identified by propensity score match (PSM) method. We concluded that AKI was a common complication in patients with cerebral trauma. SOFA score and the accumulative doses of torsemide and mannitol were independent risk factors of AKI following cerebral trauma.

Increased risk of acute kidney injury associated with higher infusion rate of mannitol in patients with intracranial hemorrhage

“…13,32 However, the relationship between AKI and preexisting renal impairment has not been explored among patients treated with mannitol. 9,15 Our results demonstrate that patients with preexisting renal dysfunction showed a significant chance of developing AKI. With normal renal function, the halflife of mannitol is approximately 70 minutes, increasing to as long as 36 hours in patients with uremia.…”

Osmotic nephrosis with mannitol: review article

“…5,[11][12][13] In most cases, high-dose mannitol infusion was given. [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] During mannitol infusion, hyperosmolarity was documented by most, that is, 13 reports/series while combined hyponatremia and hyperosmolarity in 8 reports/series ( (Table 2). In our patient, it was up to 0.24 kg given over 4 days (56 hours) at a rate not faster than 0.5 g/kg/h.…”

“…17 In the setting of acute CNS (central nervous system) insult, two of the studies (Fang et al and Dziedzic et al) concluded that accumulative doses of mannitol is associated with MI-ARF while the other three (Chen et al, Gondim et al and Kim et al) suggested that mannitol is safe in patients with otherwise healthy kidneys and that MI-ARF appears to be associated with chronic insults to the kidneys such as diabetes or hypertension. 8,[17][18][19][20] Furthermore, Kim et al concluded that higher mannitol infusion rate is associated with more frequent and more severe AKI (acute kidney injury; Table 3). 18 …”

The combined use of edaravone, diuretics, and nonsteroidal anti-inflammatory drugs caused acute kidney injury in an elderly patient with chronic kidney disease

“…3). Clinical reports and animal experiments have shown that the use of edaravone, mannitol, or NSAIDs alone can cause acute renal failure [6][7][8][9][10][11][12]. Examination revealed that the patient received a score of nine on the Naranjo Adverse Drug Reaction Probability Scale [13], which indicated that the application of these drugs had a ''definite'' causal relationship with the acute kidney injury.…”