Liquid chromatography–tandem mass spectrometry method for routine measurement of oxalic acid in human plasma

Elgstøen, Katja Benedikte Prestø

doi:10.1016/j.jchromb.2008.07.002

Cited by 23 publications

(13 citation statements)

References 122 publications

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“…Thus, sample handling, including prevention of ascorbate conversion to oxalate, is quite important. In addition, methods for measuring oxalate, including sample type, preparation, and analysis, are not interchangeable [10][11][12]. Our study benefitted from use of a single clinical laboratory over many decades with data to support that POx results could be compared over that time period.…”

Section: Discussionmentioning

confidence: 99%

Plasma Oxalate as a Predictor of Kidney Function Decline in a Primary Hyperoxaluria Cohort

Shah

Vaughan

Enders

et al. 2020

IJMS

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This retrospective analysis investigated plasma oxalate (POx) as a potential predictor of end-stage kidney disease (ESKD) among primary hyperoxaluria (PH) patients. PH patients with type 1, 2, and 3, age 2 or older, were identified in the Rare Kidney Stone Consortium (RKSC) PH Registry. Since POx increased with falling estimated glomerular filtration rate (eGFR), patients were stratified by chronic kidney disease (CKD) subgroups (stages 1, 2, 3a, and 3b). POx values were categorized into quartiles for analysis. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) for risk of ESKD were estimated using the Cox proportional hazards model with a time-dependent covariate. There were 118 patients in the CKD1 group (nine ESKD events during follow-up), 135 in the CKD 2 (29 events), 72 in CKD3a (34 events), and 45 patients in CKD 3b (31 events). During follow-up, POx Q4 was a significant predictor of ESKD compared to Q1 across CKD2 (HR 14.2, 95% CI 1.8–115), 3a (HR 13.7, 95% CI 3.0–62), and 3b stages (HR 5.2, 95% CI 1.1–25), p < 0.05 for all. Within each POx quartile, the ESKD rate was higher in Q4 compared to Q1–Q3. In conclusion, among patients with PH, higher POx concentration was a risk factor for ESKD, particularly in advanced CKD stages.

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Section: Discussionmentioning

confidence: 99%

Plasma Oxalate as a Predictor of Kidney Function Decline in a Primary Hyperoxaluria Cohort

Shah

Vaughan

Enders

et al. 2020

IJMS

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“…Plasma or serum oxalate levels in healthy children and adults are mainly reported to be in the range of 1–3 μmol/L [57, 58, 113, 114, 115, 116]; depending on the method used, however, higher normal limits of up to 11 μmol/L have been reported [117, 118]. As GFR declines, renal oxalate clearance is decreasing, which leads to increased plasma oxalate as depicted in Figure 1C [59, 119, 120, 121, 122, 123, 124, 125].…”

Section: Oxalate and Ckdmentioning

confidence: 99%

Oxalate, inflammasome, and progression of kidney disease

Ermer

Eckardt²,

Aronson³

et al. 2016

Current Opinion in Nephrology and Hypertension

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Purpose of review Oxalate is an end product of metabolism excreted via the kidney. Excess urinary oxalate, whether from primary or enteric hyperoxaluria, can lead to oxalate deposition in the kidney. Oxalate crystals are associated with renal inflammation, fibrosis and progressive renal failure. It has long been known that as glomerular filtration rate (GFR) becomes reduced in chronic kidney disease (CKD), there is striking elevation of plasma oxalate. Taken together, these findings raise the possibility that elevation of plasma oxalate in CKD may promote renal inflammation and more rapid progression of CKD independent of primary etiology. Recent findings The inflammasome has recently been identified to play a critical role in oxalate-induced renal inflammation. Oxalate crystals have been shown to activate the nucleotide-binding domain, leucine-rich repeat inflammasome 3 (also known as NALP3, NLRP3 or cryopyrin), resulting in release of Interleukin-1β and macrophage infiltration. Deletion of inflammasome proteins in mice protects from oxalate-induced renal inflammation and progressive renal failure. Summary The findings reviewed in this article expand our understanding of the relevance of elevated plasma oxalate levels leading to inflammasome activation. We propose that inhibiting oxalate-induced inflammasome activation, or lowering plasma oxalate, may prevent or mitigate progressive renal damage in CKD, and warrants clinical trials.

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“…Thus, results using these early methods, particularly published reference ranges, are often hard to interpret. Furthermore, a number of analytic methods have been described including enzymatic oxalate oxidase [9], gas chromatography (GC) [10,11] with or without mass spectrometry (MS), liquid chromatography with and without mass spectrometry [12][13][14] and ion chromatography with or without MS detection (ICMS) [8,15].…”

Section: Introductionmentioning

confidence: 99%

Plasma oxalate: comparison of methodologies

Stokes¹,

Acquaviva‐Bourdain

Höppe

et al. 2020

Urolithiasis

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Measurement of oxalate in the blood is essential for monitoring primary hyperoxaluria patients with progressive renal impairment and on dialysis prior to transplantation. As no external quality assurance scheme is available for this analyte, we conducted a sample exchange scheme between six laboratories specifically involved with the investigation of primary hyperoxaluria to compare results. The methodologies compared were gas chromatography/mass spectrometry (GCMS), ion chromatography with mass spectrometry (ICMS), and enzymatic methods using oxalate oxidase and spectrophotometry. Although individual laboratories performed well in terms of reproducibility and linearity, there was poor agreement (absolute values) between centres as illustrated by a longer-term comparison of patient results from two of the participating laboratories. This situation was only partly related to differences in calibration and mainly reflected the lower recoveries seen with the ultrafiltration of samples. These findings lead us to conclude that longitudinal monitoring of primary hyperoxaluria patients with deteriorating kidney function should be performed by a single consistent laboratory and the methodology used should always be defined. In addition, plasma oxalate concentrations reported in registry studies and those associated with the risk of systemic oxalosis in published studies need to be interpreted in light of the methodology used. A reference method and external quality assurance scheme for plasma oxalate analysis would be beneficial.

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Liquid chromatography–tandem mass spectrometry method for routine measurement of oxalic acid in human plasma

Cited by 23 publications

References 122 publications

Plasma Oxalate as a Predictor of Kidney Function Decline in a Primary Hyperoxaluria Cohort

Plasma Oxalate as a Predictor of Kidney Function Decline in a Primary Hyperoxaluria Cohort

Oxalate, inflammasome, and progression of kidney disease

Plasma oxalate: comparison of methodologies

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