OBJECT: Mannitol is commonly used for acute insults to the central nervous system; acute renal insufficiency is one of its side effects. The cause of mannitol-induced acute renal insufficiency (MI-ARI) is unknown, although elevated osmolality has been implicated as a risk factor. The goal of this study was to determine risk factors and outcomes of MI-ARI and to determine whether osmolality is associated with MI-ARI. METHODS: The authors retrospectively reviewed the cases of 95 patients treated with mannitol to determine if MI-ARI (an increase in the creatinine level of > 0.5 mg/dl if the baseline value is < 2 mg/dl or an increase > 1 mg/dl if the baseline value is > 2 mg/dl) is linked to elevated osmolality. The 11 patients (11.6%) in whom MI-ARI developed did not exhibit significant differences in patient age, sex, or race; history of cerebrovascular disease or smoking; baseline renal function; or Glasgow Coma Scale score from those in whom MI-ARI did not occur. Cumulative fluid balance, exposure to nephrotoxic drugs, and the peak osmolality and osmotic gap before onset of renal insufficiency were also similar in the two groups. Factors predictive of the onset of MI-ARI included a higher Acute Physiology and Chronic Health Evaluation (APACHE) II score on admission and a history of diabetes, coronary artery disease, congestive heart failure, and hypertension. The presence of congestive heart failure and a high APACHE II score were the only factors independently associated with a higher likelihood of MI-ARI according to a multivariate analysis. Renal function spontaneously returned to baseline in all patients. With maintenance of normovolemia and monitoring of the osmotic gap, MI-ARI appears to be associated with chronic insults to the kidneys such as a history of diabetes or hypertension, not mannitol dose, or osmolality. CONCLUSIONS: Use of osmolality to limit mannitol use and thus prevent MI-ARI may be unwarranted. Prospective studies are needed.
OBJECT: Mannitol is commonly used for acute insults to the central nervous system; acute renal insufficiency is one of its side effects. The cause of mannitol-induced acute renal insufficiency (MI-ARI) is unknown, although elevated osmolality has been implicated as a risk factor. The goal of this study was to determine risk factors and outcomes of MI-ARI and to determine whether osmolality is associated with MI-ARI. METHODS: The authors retrospectively reviewed the cases of 95 patients treated with mannitol to determine if MI-ARI (an increase in the creatinine level of > 0.5 mg/dl if the baseline value is < 2 mg/dl or an increase > 1 mg/dl if the baseline value is > 2 mg/dl) is linked to elevated osmolality. The 11 patients (11.6%) in whom MI-ARI developed did not exhibit significant differences in patient age, sex, or race; history of cerebrovascular disease or smoking; baseline renal function; or Glasgow Coma Scale score from those in whom MI-ARI did not occur. Cumulative fluid balance, exposure to nephrotoxic drugs, and the peak osmolality and osmotic gap before onset of renal insufficiency were also similar in the two groups. Factors predictive of the onset of MI-ARI included a higher Acute Physiology and Chronic Health Evaluation (APACHE) II score on admission and a history of diabetes, coronary artery disease, congestive heart failure, and hypertension. The presence of congestive heart failure and a high APACHE II score were the only factors independently associated with a higher likelihood of MI-ARI according to a multivariate analysis. Renal function spontaneously returned to baseline in all patients. With maintenance of normovolemia and monitoring of the osmotic gap, MI-ARI appears to be associated with chronic insults to the kidneys such as a history of diabetes or hypertension, not mannitol dose, or osmolality. CONCLUSIONS: Use of osmolality to limit mannitol use and thus prevent MI-ARI may be unwarranted. Prospective studies are needed.