Formulas for Calculated Osmolarity and Osmolal Gap: A Study of Diagnostic Accuracy.

BACKGROUND: The osmolal gap has been used for decades to screen for exposure to toxic alcohols. However, several issues may affect its reliability. We aimed to develop equations to calculate osmolarity with improved performance when used to screen for intoxication to toxic alcohols. STUDY DESIGN: Retrospective cohort study. SETTING & PARTICIPANTS: 7,525 patients undergoing simultaneous measurements of osmolality, sodium, potassium, urea, glucose, and ethanol or undergoing similar measurements performed within 30 minutes of a measurement of toxic alcohol levels at a single tertiary-care center from April 2001 to June 2016. Patients with detectable toxic alcohols were excluded. INDEX TEST: Equations to calculate osmolarity using multiple linear regression. OUTCOMES: The performance of new equations compared with published equations developed to calculate osmolarity, and to diagnose toxic alcohol intoxications more accurately. RESULTS: We obtained 7,525 measurements, including 100 with undetectable toxic alcohols. Among them, 3,875 had undetectable and 3,650 had detectable ethanol levels. In the entire cohort, the best equation to calculate osmolarity was 2.006×Na + 1.228×Urea + 1.387×Glucose + 1.207×Ethanol (values in mmol/L, R2=0.96). A simplified equation, 2.0×Na + 1.2×Urea + 1.4×Glucose + 1.2×Ethanol, had a similar R2 with 95% of osmolal gap values between -10.9 and 13.8. In patients with undetectable ethanol concentrations, the range of 95% of osmolal gap values was narrower than previous published formulas, and in patients with detectable ethanol concentrations, the range was narrower or similar. We performed a subanalysis of 138 cases for which both the toxic alcohol concentration could be measured and the osmolal gap could be calculated. Our simplified equation had superior diagnostic accuracy for toxic alcohol exposure. LIMITATIONS: Single center, no external validation, limited number of cases with detectable toxic alcohols. CONCLUSIONS: In a large cohort, coefficients from regression analyses estimating the contribution of glucose, urea, and ethanol were higher than 1.0. Our simplified formula to precisely calculate osmolarity yielded improved diagnostic accuracy for suspected toxic alcohol exposures than previously published formulas.

Acute Kidney Injury and Renal Recovery with the Use of Aminoglycosides: A Large Retrospective Study.

BACKGROUND: Recent acute kidney injury (AKI) guidelines, based on studies performed a decade ago, recommend avoiding aminoglycosides (AGs) in patients at risk of AKI. Whether present patient characteristics and management have changed this risk is uncertain. We determined the current incidence, risk factors and outcomes of AG-AKI. METHODS: We retrospectively identified adult patients who received gentamicin or tobramycin for ≥5 days in 2 large university-affiliated centers, excluding critically ill and dialysis patients. We assessed the incidence of Risk, Injury, Failure, Loss and End-stage kidney disease criteria of AKI risk and then matched each AKI to 2 controls of same age and gender to determine factors associated with AG-AKI and its recovery, defined by a creatinine within 150% of baseline by 21 days. RESULTS: Since 2001, the frequency of AG administration and dosing declined, but the incidence of AG-AKI remained constant. Of the 562 patients who received AG for ≥5 days, 65 (12%) developed AG-AKI after 11 (IQR 8-15) days, with 56, 29 and 15% having stages 1, 2 and 3 AKI, respectively. We matched these to 130 controls. In this nested case-control study, independent AKI risk factors were vancomycin coadministration, high AG trough levels and heart failure. AG-AKI compared to AG exposure without AKI was associated with greater mortality. Renal recovery occurred in 51% of the AKI patients and was less likely with heart failure and higher AKI severity. CONCLUSION: AG administration has recently decreased but the risk of AKI remained unchanged and half of the patients did not recover. Vancomycin coadministration, high AG trough levels and heart failure independently predicted AKI.

FSGS permeability factor-associated nephrotic syndrome: remission after oral galactose therapy.

Some cases of nephrotic syndrome in focal and segmental glomerulosclerosis (FSGS) are associated with a circulating factor, the FSGS permeability factor (FSPF). Galactose has a high affinity for FSPF, and experimental data suggest that it could reduce its activity. We describe the case of a 48-year-old male with a nephrotic syndrome found to be resistant to corticosteroids, immunosuppression and plasmaphaeresis. The patient was given oral galactose as a last resort treatment, which was followed by a remission of his nephrotic syndrome that correlated with a reduction of FSPF activity. This case is the first report of a long-standing remission of an FSPF-associated nephrotic syndrome on oral galactose therapy.