Oxalate: From the Environment to Kidney Stones

Brzica, Hrvoje; Breljak, Davorka; Burckhardt, Birgitta C.; Burckhardt, Gerhardt; Sabolić, Ivan

doi:10.2478/10004-1254-64-2013-2428

Cited by 38 publications

(59 citation statements)

References 184 publications

(227 reference statements)

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“…Accumulating lines of evidence suggest that renal tubular cell injury and fixed crystal particles could be implicated in the pathogenesis of urolithiasis [2]–[4]. Others have postulated that excessive excretion of urinary oxalate could cause substantial damage to the renal epithelium [5].…”

Section: Introductionmentioning

confidence: 99%

C-Phycocyanin Confers Protection against Oxalate-Mediated Oxidative Stress and Mitochondrial Dysfunctions in MDCK Cells

et al. 2014

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Oxalate toxicity is mediated through generation of reactive oxygen species (ROS) via a process that is partly dependent on mitochondrial dysfunction. Here, we investigated whether C-phycocyanin (CP) could protect against oxidative stress-mediated intracellular damage triggered by oxalate in MDCK cells. DCFDA, a fluorescence-based probe and hexanoyl-lysine adduct (HEL), an oxidative stress marker were used to investigate the effect of CP on oxalate-induced ROS production and membrane lipid peroxidation (LPO). The role of CP against oxalate-induced oxidative stress was studied by the evaluation of mitochondrial membrane potential by JC1 fluorescein staining, quantification of ATP synthesis and stress-induced MAP kinases (JNK/SAPK and ERK1/2). Our results revealed that oxalate-induced cells show markedly increased ROS levels and HEL protein expression that were significantly decreased following pre-treatment with CP. Further, JC1 staining showed that CP pre-treatment conferred significant protection from mitochondrial membrane permeability and increased ATP production in CP-treated cells than oxalate-alone-treated cells. In addition, CP treated cells significantly decreased the expression of phosphorylated JNK/SAPK and ERK1/2 as compared to oxalate-alone-treated cells. We concluded that CP could be used as a potential free radical-scavenging therapeutic strategy against oxidative stress-associated diseases including urolithiasis.

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Section: Introductionmentioning

confidence: 99%

C-Phycocyanin Confers Protection against Oxalate-Mediated Oxidative Stress and Mitochondrial Dysfunctions in MDCK Cells

et al. 2014

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“…Endogenous oxalate production is thought to be fairly constant, attributing for up to 60–80% of total plasma oxalate and urinary oxalate excretion [6, 7]. Oxalate biosynthesis evolves from glyoxylate [8, 9, 10, 11] as central precursor molecule.…”

Section: Oxalate – Endogenous Productionmentioning

confidence: 99%

“…Total daily oxalate excretion by the kidney is estimated at 10–40 mg per 24 h (0.1–0.45 mmol per 24 h) in healthy children and adults, with the average excretion being slightly higher in males than in females [34, 37, 56, 57, 58]. Only a minor part is eliminated through the gastrointestinal tract [6]. Marengo et al reported fecal oxalate excretion to account for only 5–7% of the oxalate administered in rats treated with subcutaneously implanted minipumps [37].…”

Section: Hyperoxaluria – Disturbed Oxalate Homeostasismentioning

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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“…Uważa się, że jednym z podstawowych czynników sprzyjających powstawaniu szczawianów i odkładaniu się złogów są stany zapalne [3,5]. Istotne znaczenie ma także nadmierne zagęszczenie wydalanych związków na skutek ograniczenia objętości moczu [6].…”

Section: Kamica Szczawianowaunclassified

Does high-oxalate food cause oxalate stones? – Review of dietary factors affecting the risk of oxalate urolithiasis.

Kalemba-Drożdż¹

2020

Med Og Nauk Zdr.

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Czy szczaw powoduje kamicę szczawianową? Przegląd czynników dietetycznych wpływających na ryzyko wystąpienia tej choroby Does high-oxalate food cause oxalate stones? -Review of dietary factors affecting the risk of oxalate urolithiasis. Kalemba-Drożdż M. Czy szczaw powoduje kamicę szczawianową? Przegląd czynników dietetycznych wpływających na ryzyko wystąpienia tej choroby. StreszczenieWprowadzenie. Kamica szczawianowa jest najczęściej występującym typem kamicy nerkowej, stanowiąc 70-80% przypadków tego schorzenia. W określonych warunkach, takich jak: wysokie stężenie kanalikowe kwasu szczawiowego, wysokie stężenie wapnia, uszkodzone nabłonki kanalików, zakażenia układu moczowego i stres oksydacyjny, mogą się wytrącać szczawiany wapnia, co prowadzi do tworzenia kamieni nerkowych. Cel pracy. Celem pracy jest przegląd dostępnej literatury naukowej dotyczącej możliwości modyfikowania ryzyka wystąpienia kamicy szczawianowej przez czynniki dietetyczne. Stan wiedzy. Szczawiany występują w większości pokarmów roślinnych. Przykładami produktów szczególnie zasobnych w kwas szczawiowy są: szczaw, rabarbar, boćwina, soja i kakao. Jednakże zaledwie 10% krążącego w krwiobiegu kwasu szczawiowego pochodzi bezpośrednio z pożywienia, zaś 90% jest produktem metabolizmu wątrobowego, a jego głównym prekursorem jest hydroksyprolina, aminokwas typowy dla kolagenu i elastyny, czyli białek zwierzęcych. Na wzrost ryzyka kamicy szczawianowej ma również wpływ zbyt niska podaż płynów, nadmierna suplementacja witaminami, a także wysoki poziom spożycia cukrów prostych i sodu. Produkty roślinne, choć stanowią źródło kwasu szczawiowego, zawierają również przeciwutleniacze, przede wszystkim polifenole i witaminy, a także kwas cytrynowy i potas, które redukują ryzyko formowania się złogów szczawianu wapnia. Podsumowanie. Zmiana diety na bogatą w warzywa, owoce i zioła oraz redukcja spożycia białek zwierzęcych, głównego źródła hydroksyproliny, powinny stanowić podstawę profilaktyki kamicy szczawianowej. Słowa kluczoweszczawiany, kwas szczawiowy, kamica szczawianowa, dieta roślinna, kwas glioksalowy, hydroksyprolina Abstract Introduction.Oxalate urolithiasis is the most common type of kidney stones, accounting for 70-80% of cases. Under certain conditions, such as high oxalic acid concentration, high calcium levels, damaged tubular epithelium, urinary tract infections and oxidative stress, calcium oxalates may precipitate and initiate the formation of kidney stones. Objective. The aim of the study is to review the available literature on the possibility of dietary factors to modify the risk of oxalate urolithiasis. State of Knowledge. Oxalates are found in most plant foods; sorrel, rhubarb, chard, soy and cocoa are examples of high-oxalate foods. However, only 10% of oxalic acid which circulates in the bloodstream originates directly from food, and 90% is a product of hepatic metabolism. Its main precursor is hydroxyproline, the amino acid typical for animal proteins: collagen and elastin. The increase in the risk of oxalate urolithiasis is also af...

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Oxalate: From the Environment to Kidney Stones

Cited by 38 publications

References 184 publications

C-Phycocyanin Confers Protection against Oxalate-Mediated Oxidative Stress and Mitochondrial Dysfunctions in MDCK Cells

C-Phycocyanin Confers Protection against Oxalate-Mediated Oxidative Stress and Mitochondrial Dysfunctions in MDCK Cells

Oxalate, inflammasome, and progression of kidney disease

Does high-oxalate food cause oxalate stones? – Review of dietary factors affecting the risk of oxalate urolithiasis.

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