Application of Lithium Assay kit LS for quantification of lithium in whole blood and urine.

A commercially available kit for the quantitation of lithium, the Lithium Assay kit LS, was originally developed to measure lithium in serum or plasma using a conventional microplate reader. We investigated whether use of the kit could be extended to quantify lithium in whole blood and urine samples collected at autopsy. The calibration curve for whole blood showed good linearity ranging from 0.5 to 20 µg/mL with a coefficient of determination of 0.998 when samples were pretreated with methanol followed by acetonitrile. Moreover, for urine, we obtained excellent linearity with a coefficient of determination of 0.999 without any pretreatment. The accuracies and precisions were 106.3-174.7% and 1.9-18.1% for whole blood and 83.3-118.8% and 5.7-33.8% for urine. The values in the lower concentration range (0.5-1 µg/mL) were not satisfactory, whereas those in the higher range (2-20 µg/mL) were acceptable. The Lithium Assay kit LS was successfully applied to the measurement of lithium in whole blood and urine samples collected at autopsies. This method appears to be useful for forensic toxicological investigations because of its simplicity and speed.

Empagliflozin-Mediated Lithium Excretion: A Case Study and Clinical Applications.

BACKGROUND Empagliflozin selectively reduces apical sodium-glucose co-transporter 2 function in the proximal convoluted tubules, increasing sodium and glucose excretion in the urine, ultimately reducing glucose reabsorption in the kidneys for diabetic management. Lithium, the gold-standard treatment for bipolar disorder, also utilizes sodium transporters in the proximal convoluted tubules. CASE REPORT Presenting with a manic relapse of refractory schizoaffective disorder, our patient was found to have subtherapeutic levels of lithium on admission due to poor outpatient medication compliance. Restoration to therapeutic lithium levels allowed inpatient blood glucose measurements, which led to a new diagnosis of type 2 diabetes mellitus. Given his comorbid severe hepatic impairment, obesity, and prior pancreatitis, the patient was started on empagliflozin to safely manage this new diagnosis without collateral organ injury. Routine monitoring found reproducible and clinically significant decreases in serum lithium levels in the presence of empagliflozin therapy, without obvious confounding factors. Subsequent discussion with specialist teams resulted in trialling metformin, which adequately controlled the new diabetic diagnosis without inpatient complications. CONCLUSIONS We suspect that empagliflozin reduced sodium-glucose and lithium-glucose reabsorption in the proximal connecting tubules, thereby increasing the renal excretion of sodium, glucose, and lithium. Applications include awareness of the interaction between these medications, support for the role of physiological SGLT-2-mediated lithium transport, and the possibility of using empagliflozin and other SGLT-2 inhibitors to treat life-threatening lithium toxicity.