Acute renal failure.
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Acute Kidney Injury↗
Biomedical subjects
D S Glaser
Publications and source records attributed to D S Glaser.
Utility of the serum osmol gap in the diagnosis of methanol or ethylene glycol ingestion.
Ingestion of methanol or ethylene glycol is a toxicologic emergency. The osmolal gap has been widely advocated as a screen for serum methanol or ethylene glycol. Unfortunately, for several reasons the osmolal gap fails in this capacity. First, an accurate serum osmolality can often not be obtained. Second, the calculated serum osmolarity will vary greatly, depending on the formula used to estimate it. Third, ethylene glycol has such a large molecular weight that even toxic amounts may contribute minimally to a patient's overall osmolality. Finally, because of metabolism, little ethylene glycol or methanol may be present when a patient presents with toxicity. These limitations invalidate the osmolal gap as a screen for ethylene glycol or methanol ingestion.
Blood Chemical Analysis↗
Preheparin lipoprotein lipolytic activities: relationship to plasma lipoproteins and postheparin lipolytic activities.
To determine the putative metabolic relevance of preheparin versus postheparin lipoprotein lipases, the relationships of both pre- and postheparin lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) to plasma triglycerides, low density lipoprotein (LDL) cholesterol, and high density lipoprotein (HDL) cholesterol were determined in 93 men. Relationships of preheparin lipases to their respective postheparin lipases were also examined. Although relationships between the preheparin lipases and plasma triglycerides and HDL cholesterol were not apparent, both preheparin LPL (rs = 0.306, P = 0.0036) and HTGL (rs = 0.348, P = 0.0008) correlated with LDL cholesterol, a relationship not seen with either postheparin lipase. Both postheparin LPL (rs = 0.515, P = 0.0001) and postheparin HTGL (rs = -0.228, P = 0.0028), however, correlated with HDL cholesterol. In addition, postheparin LPL was inversely correlated with postheparin HTGL (rs = -0.363, P = 0.0003), whereas the relationship between preheparin LPL and preheparin HTGL was positive (rs = 0.228, P = 0.0009). Overall, these data point to differences between pre- and postheparin lipases in their relationships to lipoproteins, and one to another. The relationships of LDL cholesterol to both preheparin LPL and HTGL suggest that displacement of active forms of both lipases from their endothelial binding sites may mark triglyceride-rich lipoproteins or their remnants for metabolic pathways that lead to LDL.
Adult↗