Measurement of oxalate in human plasma ultrafiltrate by ion chromatography

Manoharan, M.; Schwille, P. O.

doi:10.1016/s0378-4347(97)00310-1

Cited by 9 publications

(8 citation statements)

References 11 publications

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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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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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show abstract

“…For work up of unacidified plasma the use of a 10 000 dalton cut-off filter has also been suggested as it reflects the sieve micro architecture of renal glomeruli. Using this procedure, observations suggesting binding of oxalic acid to plasma proteins with a molecular weight higher than the cut off limit was suggested 210 , but this was later reported to be apparent and not real by the same researchers 211 .…”

Section: Liquid Chromatographymentioning

confidence: 98%

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

Elgstøen

2008

Journal of Chromatography B

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“…Urinary lithiasis is an expensive and widespread disease, and the lack of information on the possible role of oxalate in MgD is partly responsible in that there are thus far no effective drugs to prevent the formation of stones, although studies have shown that some of these patients have signs of an exogenous MgD [6]. The aim of the present study was to clarify in vivo, in isolated small intestinal loops perfused with radioactive 14 C-oxalate, whether intestinal hyperabsorption or reduced secretion is important in MgD.…”

Section: Introductionmentioning

confidence: 93%

Intestinal and renal handling of oxalate in magnesium‐deficient rats. Evaluation of intestinal in vivo¹⁴C‐oxalate perfusion

et al. 2002

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Objectives To clarify in vivo, using isolated small intestinal loops perfused with radioactive 14C‐oxalate, whether intestinal hyperabsorption or reduced secretion is important in magnesium deficiency (MgD), as this is a potential cause of calcium oxalate urolithiasis. Materials and methods Twenty‐four Sprague‐Dawley rats were either fed a standard diet (control, 12 rats) or a magnesium‐deficient diet (MgD, 12 rats) for 19 weeks. One hour before the animals were killed, a defined length of a small intestinal loop was isolated and filled with 5 mL of 0.9% NaCl and a defined amount of intravenous 14C‐oxalate applied. Using this method it was possible to determine the secretion of unlabelled oxalate into the intestinal lumen, from the specific activity in plasma. Results Plasma oxalate levels doubled under MgD; urinary calcium and phosphorus also increased significantly, while urine oxalate tended to decrease. The secretion of oxalate into the intestinal lumen of MgD animals increased significantly, by five times that of the control. The relative supersaturation for calcium oxalate remained constant. Elementary analysis of renal tissue showed an increase in calcium and phosphorus under MgD, in the sense of nephrocalcinosis, but no concretions were detected (no nephrolithiasis). Conclusion In contrast to earlier studies, there is no evidence that hyperoxaluria is responsible for the possible development of urolithiasis in MgD. This was confirmed by calcium phosphate deposits in renal tissue, even though there was no evidence of oxalate urolithiasis. The increase in plasma oxalate seems to be completely compensated by strongly increased oxalate secretion into the intestinal lumen.

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Measurement of oxalate in human plasma ultrafiltrate by ion chromatography

Cited by 9 publications

References 11 publications

Oxalate, inflammasome, and progression of kidney disease

Oxalate, inflammasome, and progression of kidney disease

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

Intestinal and renal handling of oxalate in magnesium‐deficient rats. Evaluation of intestinal in vivo¹⁴C‐oxalate perfusion

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Measurement of oxalate in human plasma ultrafiltrate by ion chromatography

Cited by 9 publications

References 11 publications

Oxalate, inflammasome, and progression of kidney disease

Oxalate, inflammasome, and progression of kidney disease

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

Intestinal and renal handling of oxalate in magnesium‐deficient rats. Evaluation of intestinal in vivo14C‐oxalate perfusion

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Intestinal and renal handling of oxalate in magnesium‐deficient rats. Evaluation of intestinal in vivo¹⁴C‐oxalate perfusion