Oxalate in renal stone disease: the terminal metabolite that just won't go away

Marengo, Susan R; Romani, Andrea MP

doi:10.1038/ncpneph0845

Cited by 108Kidney Stones and Urolithiasis TreatmentsNephrotoxicity and Medicinal PlantsParathyroid Disorders and Treatments

Oxalate in renal stone disease: the terminal metabolite that just won't go away

Marengo, Susan R, Romani, Andrea MP·2008·Nature Clinical Practice Nephrology

DOI 10.1038/ncpneph0845

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Abstract

The incidence of calcium oxalate nephrolithiasis in the US has been increasing throughout the past three decades. Biopsy studies show that both calcium oxalate nephrolithiasis and nephrocalcinosis probably occur by different mechanisms in different subsets of patients. Before more-effective medical therapies can be developed for these conditions, we must understand the mechanisms governing the transport and excretion of oxalate and the interactions of the ion in general and renal physiology. Blood oxalate derives from diet, degradation of ascorbate, and production by the liver and erythrocytes. In mammals, oxalate is a terminal metabolite that must be excreted or sequestered. The kidneys are the primary route of excretion and the site of oxalate's only known function. Oxalate stimulates the uptake of chloride, water, and sodium by the proximal tubule through the exchange of oxalate for sulfate or chloride via the solute carrier SLC26A6. Fecal excretion of oxalate is stimulated by hyperoxalemia in rodents, but no similar phenomenon has been observed in humans. Studies in which rats were treated with (14)C-oxalate have shown that less than 2% of a chronic oxalate load accumulates in the internal organs, plasma, and skeleton. These studies have also demonstrated that there is interindividual variability in the accumulation of oxalate, especially by the kidney. This Review summarizes the transport and function of oxalate in mammalian physiology and the ion's potential roles in nephrolithiasis and nephrocalcinosis.

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The primary sources of blood oxalate are diet-derived plant sources, vitamin C degradation, and endogenous synthesis in erythrocytes and liver.
“The primary sources of blood oxalate are diet-derived plant sources, vitamin C (ascorbate) degradation, and endogenous synthesis pathways in erythrocytes and liver (27).”
From Oxalic acid and diacylglycerol 36:3 are cross-species markers of sleep debt (2015) · cites this paper as [27]

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Kidney Stone Disease: An Update on Current Concepts
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Oxalic acid and diacylglycerol 36:3 are cross-species markers of sleep debt
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Cellular adaptive response of distal renal tubular cells to high-oxalate environment highlights surface alpha-enolase as the enhancer of calcium oxalate monohydrate crystal adhesion
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A Conserved Active Site Tyrosine Residue of Proline Dehydrogenase Helps Enforce the Preference for Proline over Hydroxyproline as the Substrate
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Glyoxylate is a substrate of the sulfate-oxalate exchanger, sat-1, and increases its expression in HepG2 cells
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GC−MS Metabolomic Analysis Reveals Significant Alterations in Cerebellar Metabolic Physiology in a Mouse Model of Adult Onset Hypothyroidism
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Idiopathic Osteoporosis and Nephrolithiasis: Two Sides of the Same Coin?
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Oxalate content of selected breads and crackers
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Zn2+ regulates human oxalate metabolism by manipulating oxalate decarboxylase to treat calcium oxalate stones
Wu, F., Cheng, Y., Zhou, J., Liu, X., Lin, R., Xiang, S., Liu, Z., & Wang, C. (2023) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2023.123320 · Cited by 23 · see citing works
Structure and mechanism of oxalate transporter OxlT in an oxalate-degrading bacterium in the gut microbiota
Jaunet‐Lahary, T., Shimamura, T., Hayashi, M., Nomura, N., Hirasawa, K., Shimizu, T. M., Yamashita, M., Tsutsumi, N., Suehiro, Y., Kojima, K., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-36883-5 · Cited by 23 · see citing works
Lanthanum Carbonate Inhibits Intestinal Oxalate Absorption and Prevents Nephrocalcinosis After Oxalate Loading in Rats
Robijn, S., Vervaet, B. A., Höppe, B., D’Haese, P. C., & Verhulst, A. (2012) · The Journal of Urology · doi:10.1016/j.juro.2012.12.004 · Cited by 23 · see citing works
Enteric hyperoxaluria in chronic pancreatitis
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Artificial light at night causes an unexpected increase in oxalate in developing male songbirds
Raap, T., Pinxten, R., & Eens, M. (2018) · Conservation Physiology · doi:10.1093/conphys/coy005 · Cited by 23 · see citing works
Probiotics and dietary manipulations in calcium oxalate nephrolithiasis: two sides of the same coin?
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High expression of SLC26A6 in the kidney may contribute to renal calcification via an SLC26A6-dependent mechanism
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Biochemical properties and oxalate‐degrading activity of oxalate decarboxylase from bacillus subtilis at neutral pH
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Human SLC26A1 Gene Variants: A Pilot Study
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Colorimetric detection of oxalate in aqueous solution by a pyrogallol red‐based Cu2+ complex
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Current updates on metabolites and its interlinked pathways as biomarkers for diabetic kidney disease: A systematic review
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Global Trends in Kidney Stone Awareness: A Time Series Analysis from 2004–2023
Aiumtrakul, N., Thongprayoon, C., Suppadungsuk, S., Krisanapan, P., Pinthusopon, P., Mao, M. A., Arayangkool, C., Vo, K. B., Wannaphut, C., Miao, J., et al. (2024) · Clinics and Practice · doi:10.3390/clinpract14030072 · Cited by 20 · see citing works
Oxalate nephropathy in systemic sclerosis: Case series and review of the literature
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Cell death‑related molecules and targets in the progression of urolithiasis (Review)
Wu, L., Xue, X., He, C., Lai, Y., & Tong, L. (2024) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2024.5376 · Cited by 19 · see citing works
A Case of Oxalate Nephropathy: When a Single Cause Is Not Crystal Clear
Marques, S., Santos, S., Fremin, K., & Fogo, A. B. (2017) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2017.05.022 · Cited by 19 · see citing works
Osteoporosis is a Predictive Factor for Nephrolithiasis in an Adult Free-Living Caucasian Population From Southern Italy: A Longitudinal Retrospective Study Based on a General Practice Database
Rendina, D., D’Elia, L., Evangelista, M., FILIPPO, G. D., Giaquinto, A., Barone, B., Piccinocchi, G., Prezioso, D., & Strazzullo, P. (2020) · Calcified Tissue International · doi:10.1007/s00223-020-00737-9 · Cited by 19 · see citing works
Development of a New Colorimetric Chemosensor for Selective Determination of Urinary and Vegetable Oxalate Concentration Through an Indicator-Displacement Assay (IDA) in Aqueous Media
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Recent Advances of Oxalate Decarboxylase: Biochemical Characteristics, Catalysis Mechanisms, and Gene Expression and Regulation
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Second Prize: Hydroxyproline-Induced Hyperoxaluria Using Acidified and Traditional Diets in the Porcine Model
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Dietary Induction of Long-Term Hyperoxaluria in the Porcine Model
Patel, S. R., Penniston, K. L., Iwicki, L., Saeed, I. A. M., Crenshaw, T. D., & Nakada, S. Y. (2011) · Journal of Endourology · doi:10.1089/end.2011.0182 · Cited by 18 · see citing works
Selective recognition of oxalate in water: effect of pH on binding strength and sensing mechanisms
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In female rats, ethylene glycol treatment elevates protein expression of hepatic and renal oxalate transporter sat-1 (Slc26a1) without inducing hyperoxaluria
Breljak, D., Brzica, H., Vrhovac, I., Micek, V., Karaica, D., Ljubojević, M., Sekovanić, A., Jurasović, J., Rašić, D., Peraica, M., et al. (2015) · Croatian Medical Journal · doi:10.3325/cmj.2015.56.447 · Cited by 15 · see citing works
Effect of different brewing times on soluble oxalate content of loose-packed black teas and tea bags
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(2018) · PeerJ · doi:10.7287/peerj.5192v0.1/reviews/3
Peer Review #3 of "High expression of SLC26A6 in the kidney may contribute to renal calcification via an SLC26A6-dependent mechanism (v0.2)"
(2018) · PeerJ · doi:10.7287/peerj.5192v0.2/reviews/3
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Kidney
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Peer Review #1 of "High expression of SLC26A6 in the kidney may contribute to renal calcification via an SLC26A6-dependent mechanism (v0.2)"
(2018) · PeerJ · doi:10.7287/peerj.5192v0.2/reviews/1
Peer Review #2 of "High expression of SLC26A6 in the kidney may contribute to renal calcification via an SLC26A6-dependent mechanism (v0.1)"
(2018) · PeerJ · doi:10.7287/peerj.5192v0.1/reviews/2
Peer Review #2 of "High expression of SLC26A6 in the kidney may contribute to renal calcification via an SLC26A6-dependent mechanism (v0.2)"
(2018) · PeerJ · doi:10.7287/peerj.5192v0.2/reviews/2
Peer Review #1 of "High expression of SLC26A6 in the kidney may contribute to renal calcification via an SLC26A6-dependent mechanism (v0.1)"
(2018) · PeerJ · doi:10.7287/peerj.5192v0.1/reviews/1

Authors: Marengo, S. R., & Romani, A. M.
Affiliations: Case Western Reserve University (US)
Corresponding author: Marengo, Susan R
ORCID: Romani, Andrea MP
Venue: Nature Clinical Practice Nephrology
Publisher: Springer Science and Business Media LLC
Published: 2008-06-03
Volume: 4
Issue: 7
Pages: 368-377
ISSN: 1745-8323 (ISSN-L)
1745-8331
DOI: 10.1038/ncpneph0845
OpenAlex: W1985972696
Cited by: 106
References: 120
Citations by year: 2026: 2 · 2025: 4 · 2024: 6 · 2023: 7 · 2022: 6 · 2021: 4 · 2020: 4 · 2019: 3 · 2018: 14 · 2017: 8 · 2016: 6 · 2015: 7 · 2014: 3 · 2013: 8 · 2012: 5
FWCI: 1.00
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Reviews Nephrology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01dk073730-03)
National Heart, Lung, and Blood Institute (HL-18708, P01HL018708)
National Institute of Diabetes and Digestive and Kidney Diseases (DK073730)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Kidney Stones and Urolithiasis Treatments
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Nephrotoxicity and Medicinal Plants
Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
Keywords: oxalate, kidney stones, calcium oxalate nephrolithiasis, nephrocalcinosis, SLC26A6, proximal tubule, oxalate excretion, oxalate accumulation, renal physiology, dietary oxalate
MeSH terms: Animals, Humans, Kidney, Kidney Calculi, Oxalates, Risk Factors, Ion Transport

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Oxalate in renal stone disease: the terminal metabolite that just won't go away

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