Acute renal failure following oxalic acid poisoning: a case report

Dassanayake, Uditha; Gnanathasan, Christeine Ariaranee

doi:10.1186/1745-6673-7-17

Cited by 29 publications

(19 citation statements)

References 9 publications

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“…Oxalic acid reacts with calcium inside renal tubules and produces calcium oxalate monohydrate crystals which are deposited in the tubular epithelium and renal tubular lumen leading to tubular obstruction and cell dysfunction [35] from oxidative stress and mitochondrial toxicity [36,37].…”

Section: Discussionmentioning

confidence: 99%

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Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid

Wijerathna

Gawarammana

Dissanayaka

et al. 2017

Clinical Toxicology

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Acute Kidney Injury (AKI) is common following deliberate self-poisoning with a combination washing powder containing oxalic acid (H2C2O4) and Potassium permanganate (KMnO4). Early and rapid increases in serum creatinine (sCr) follow severe poisoning.We investigated the relationship of these increases with direct nephrotoxicity in an ongoing multicenter prospective cohort study in Sri Lanka exploring AKI following poisoning. Multiple measures of change in kidney function were evaluated in 48 consenting patients who had serial sCr and serum cystatinC (sCysC) data available.Thirty eight (38/48, 79%) patients developed AKI (AKIN criteria). Twenty eight (58%) had AKIN stage 2 or 3. Initial increases in urine creatinine (uCr) excretion were followed by a substantial loss of renal function. The AKIN stage 2 and 3 (AKIN2/3) group had very rapid rises in sCr (a median of 118% at 24 hours and by 400% at 72 hours post ingestion). We excluded the possibility that the rapid rise resulted from the assay used or muscle damage. In contrast, the average sCysC increase was 65% by 72 hours.In most AKI, sCysC increases to the same extent but more rapidly than sCr, as sCysC has a shorter half-life. This suggests either a reduction in Cystatin C production or, conversely, that the rapid early rise of sCr results from increased production of creatine and creatinine to meet energy demands following severe oxidative stress mediated by oxalic acid and KMnO4. Increased early creatinine excretion supports the latter explanation, since creatinine excretion usually decreases transiently in AKIN2/3 from other causes.

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Section: Discussionmentioning

confidence: 99%

“…Metabolic acidosis has been recorded in oxalic acid poisoning [35,38]. Increased conversion of creatine to creatinine with acidosis may also make a minor contribution to the sCr rise [3,52].…”

Section: Discussionmentioning

confidence: 99%

Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid

Wijerathna

Gawarammana

Dissanayaka

et al. 2017

Clinical Toxicology

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“…Nasilone objawy mogą prowadzić do zgonu. Śmiertelna jednorazowa dawka doustna kwasu szczawiowego wynosi od 15 do 30 g [8,9].…”

Section: Szczawiany Egzogenneunclassified

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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“…Although intake of oxalic acid occurs as a result of its presence in the normal human diet, there exists a concern that high dietary intake of oxalic acid will increase urinary oxalate excretion. This could increase the risk of calcium oxalate (kidney stone) formation in the kidneys (Holmes et al, 2001), and of renal failure (Dassanayake U and Gnanathasan CA, 2012). The Panel noted that oxalic acid toxicity has only been reported after high intake and therefore, was unlikely in the context of a single use and low use level of Fe mTA as a food additive.…”

Section: Toxicological Data For Oxalic Acidmentioning

confidence: 99%

Scientific Opinion on the safety of the complexation product of sodium tartrate and iron(III) chloride as a food additive

2015

EFSA Journal

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European Food Safety Authority (EFSA), Parma, Italy ABSTRACTThe complexation product of sodium tartrates and iron(III) chloride (Fe mTA) is proposed for use as an anticaking agent, only in salt or its substitutes, with a maximum use level of 106 mg Fe mTA/kg salt. Fe mTA can be expected to dissociate into its constituent iron(III) and tartrate components upon ingestion. Studies in rats demonstrated that up to 90 % of ingested DL-tartrate or tartaric acid were absorbed, studies in humans suggested that only 20 % of an ingested dose of tartaric acid were absorbed. There are no ADME (absorption, distribution, metabolism and excretion) data for meso-tartrate. From a 90-day rat study, the lowest calculated BMDLs (Benchmark Dose Level) for Fe mTA were: 75 mg/kg body weight (bw) per day for males (BMDL 05 for serum bile acids) and 267 mg/kg bw per day for females (BMDL 10 for goblet cells hyperplasia). Several in vitro studies showed that there is no safety concern for genotoxicity. No reprotoxicity and developmental toxicity was reported, however no study was specifically designed for teratogenicity. SUMMARYFollowing a request from the European Commission, the Panel on Food Additives and Nutrient Sources added to Food (ANS) was asked to deliver an opinion based on a dossier presented by the applicant.According to the applicant, the complexation product of sodium tartrates and iron(III) (Fe mTA) is proposed for use, only in salt or its substitutes, as an alternative to the currently permitted anti-caking agents, with a maximum use level of 106 mg Fe mTA/kg salt.Fe mTA is a mixture of sodium tartrates [DL-and meso-tartrates] with iron(III) chloride. The proportion of each constituent comprising the mixture corresponds to 1.5 moles of tartrates (total), meso-tartrate represents approximately 65 % of the total tartrate content.The Panel noted that although there were no ADME (absorption, distribution, metabolism and excretion) data for Fe mTA, the complexation product can be expected to dissociate into its constituents iron(III) and tartrate, upon ingestion. This was supported by the weak Fe/tartrate interactions identified by electrospray mass spectrometry, where only the individual species were identified. Therefore, in addition to the data available for the Fe mTA as a compound, the Panel considered appropriate to take also into consideration the available biological and toxicological data on its individual constituents for its safety assessment, as reported in the dossier.Studies in rats demonstrated that a large proportion (55 to 90 %) of ingested DL-tartrate or tartaric acid was absorbed. The Panel noted that the retention of tartrates in the kidneys was attributed to precipitation of the poorly soluble calcium DL-tartrate in the renal tubules. The Panel noted that retention of tartrates was observed until the end of the study period (8 days after dosing), but that the actual duration of this retention was not determined. However, the Panel also noted that the metabolic fate of tartrates in humans and rats may dif...

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Acute renal failure following oxalic acid poisoning: a case report

Cited by 29 publications

References 9 publications

Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid

Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid

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

Scientific Opinion on the safety of the complexation product of sodium tartrate and iron(III) chloride as a food additive

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