Variability in urinary oxalate measurements between six international laboratories.

BACKGROUND: Hyperoxaluria is a major risk factor for kidney stone formation. Although urinary oxalate measurement is part of all basic stone risk assessment, there is no standardized method for this measurement. METHODS: Urine samples from 24-h urine collection covering a broad range of oxalate concentrations were aliquoted and sent, in duplicates, to six blinded international laboratories for oxalate, sodium and creatinine measurement. In a second set of experiments, ten pairs of native urine and urine spiked with 10 mg/L of oxalate were sent for oxalate measurement. Three laboratories used a commercially available oxalate oxidase kit, two laboratories used a high-performance liquid chromatography (HPLC)-based method and one laboratory used both methods. RESULTS: Intra-laboratory reliability for oxalate measurement expressed as intraclass correlation coefficient (ICC) varied between 0.808 [95% confidence interval (CI): 0.427-0.948] and 0.998 (95% CI: 0.994-1.000), with lower values for HPLC-based methods. Acidification of urine samples prior to analysis led to significantly higher oxalate concentrations. ICC for inter-laboratory reliability varied between 0.745 (95% CI: 0.468-0.890) and 0.986 (95% CI: 0.967-0.995). Recovery of the 10 mg/L oxalate-spiked samples varied between 8.7 ± 2.3 and 10.7 ± 0.5 mg/L. Overall, HPLC-based methods showed more variability compared to the oxalate oxidase kit-based methods. CONCLUSIONS: Significant variability was noted in the quantification of urinary oxalate concentration by different laboratories, which may partially explain the differences of hyperoxaluria prevalence reported in the literature. Our data stress the need for a standardization of the method of oxalate measurement.

Fiscal Update, June 24, 2004

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Fiscal Update, January 24, 2005

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Fiscal Update, August 24, 2005

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Fiscal Update, January 24,2006

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Fiscal Update, January 24, 2007

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Fiscal Update, August 24, 2007

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Fiscal Update, November 24, 2008

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Secure and Prepared Newsletter, April 24, 2008, Vol. 4, no. 8

A bi-weekly newsletter for those involved in the fields of homeland security and/or emergency management

Secure and Prepared Newsletter, September 24, 2009, Vol. 5, no. 19

A bi-weekly newsletter for those involved in the fields of homeland security and/or emergency management

A novel dominant mutation of the Nav1.4 alpha-subunit domain I leading to sodium channel myotonia.

BACKGROUND: Mutations in SCN4A may lead to myotonia. METHODS: Presentation of a large family with myotonia, including molecular studies and patch clamp experiments using human embryonic kidney 293 cells expressing wild-type and mutated channels. RESULTS: In a large family with historic data on seven generations and a clear phenotype, including myotonia at movement onset, with worsening by cold temperature, pregnancy, mental stress, and especially after rest after intense physical activity, but without weakness, the phenotype was linked with the muscle sodium channel gene (SCN4A) locus, in which a novel p.I141V mutation was found. This modification is located within the first transmembrane segment of domain I of the Na(v)1.4 alpha subunit, a region where no mutation has been reported so far. Patch clamp experiments revealed a mutation-induced hyperpolarizing shift (-12.9 mV) of the voltage dependence of activation, leading to a significant increase (approximately twofold) of the window current amplitude. In addition, the mutation shifted the voltage dependence of slow inactivation by -8.7 mV and accelerated the entry to this state. CONCLUSIONS: We propose that the gain-of-function alteration in activation leads to the observed myotonic phenotype, whereas the enhanced slow inactivation may prevent depolarization-induced paralysis.

You Can Fly, March 24, 2005

People in all walks of life have dreams. Is your dream to fly? Some of the most frequently asked questions about learning to fly are listed below. While they will not answer all your questions, they will send you in the right direction - up.