Are calcium oxalate crystals involved in the mechanism of acute renal failure in ethylene glycol poisoning?

McMartin, Kenneth E.

doi:10.3109/15563650903344793

Cited by 92 publications

(53 citation statements)

References 87 publications

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“…In many studies with duration of 4 weeks or 30 days, renal injury occurs through exposure to ethylene glycol, while longer (4-8 weeks) EG-Drinking model studies are required for the occurrence of urolithiasis. In this regard EG-drinking model studies are warranted (28). In this study, it may be more appropriate to mention a renal injury effect rather than urolithiasis.…”

Section: Resultsmentioning

confidence: 99%

Nephroprotective and antioxidative effects of royal jelly on ethylene glycol induced nephropathy in rats

ASLAN

2017

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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Summary: Antioxidative and nephroprotective effects of royal jelly against ethylene glycol induced renal injury were examined in this study. Five groups of rats were used. Rats in Group 1 served as control. Rats in Group 2 received ethylene glycol (1%) in drinking water, while those in Group 3 received 100 mg/kg of royal jelly through oral gavage. Group 4 served as protective group and received ethylene glycol 1% in drinking water and 100 mg/kg of royal jelly administered. Group 5 served as treatment group and received ethylene glycol 1% in the drinking water for the initial 15 days, followed by 100 mg/kg of royal jelly administered last 15 days. Oxidative stress was induced by ethylene glycol. Royal jelly was found to reduce renal damage with measured BUN and CREA (creatinine) levels. It was considered that royal jelly has positive effects on antioxidant system and decreased effects on lipid peroxidation. Royal jelly may have positive nephroprotective effects on the injury induced by ethylene glycol exposure. Particularly, the effects observed in the treatment group were remarkable.Keywords: Antioxidant, calcium oxalate, ethylene glycol, nephropathy, royal jelly. Ratlarda etilen glikolün indüklediği nefropatide arı sütünün nefroprotektif ve antioksidatif etkileriÖzet: Bu çalışmada ratlarda etilen glikolün oluşturduğu renal hasara karşı arı sütünün antioksidatif etkileri incelendi. Ratlardan 5 çalışma grubu oluşturuldu. 1. grup kontrol grubu olarak belirlendi. 2. gruptaki ratlara etilen glikol, içme suyunda (%1 oranında) verildi. 3. gruptaki ratlara her gün oral gavajla 100 mg/kg arı sütü verildi. 4. grup koruyucu grup olarak belirlendi ve 30 gün boyunca içme suyunda etilen glikol (%1) verilirken, oral gavajla 100 mg/kg arı sütü verildi. 5. grup tedavi edici grup olarak belirlendi ve çalışmanın ilk 15 günü etilen glikol (%1) içme suyunda, son 15 gün 100 mg/kg arı sütü oral gavajla verildi. Etilen glikolün oksidatif stresi indüklediği görülmüştür. Ölçülen BUN ve CREA (kreatinin) düzeylerinden arı sütünün böbrek hasarını azalttığı bulundu. Arı sütünün antioksidatif sistemi desteklediği, lipid peroksidasyonunu azaltıcı etki gösterdiği düşünülmektedir. Etilen glikol maruziyetiyle oluşturulan hasara karşı arı sütünün olumlu etkileri olduğu söylenebilir. Arı sütü uygulamasıyla tedavi edici grupta elde edilen sonuçlar özellikle dikkat çekicidir.

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Section: Resultsmentioning

confidence: 99%

Nephroprotective and antioxidative effects of royal jelly on ethylene glycol induced nephropathy in rats

ASLAN

2017

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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“…Nephrotoxicity due to oxalic acid poisoning is probably similar to AKI after ethylene glycol poisoning, as the latter is metabolised to oxalic acid [38][39][40].…”

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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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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“…Other rare causes include chronic pancreatitis (7), ethylene glycol (8), vitamin C (9), ingestion of foods with high levels of oxalate (10)(11)(12), and complication of some medications (3,13,14).…”

Section: Introductionmentioning

confidence: 99%

Primary Hyperoxaluria: A Case Report and Review of the Literature

2017

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Oxalate nephropathy is a rare cause of renal failure. Primary Hyperoxaluria (PH) is due to glyoxylate metabolism disorders with specific hepatic enzyme deficiencies. Secondary hyperoxaluria is caused by increased intestinal absorption, excessive dietary intake or excessive intake of oxalate precursors. This study reports on a 4-month-old male with high serum creatinine level, low serum sodium and calcium, high uric acid, and low urine specific gravity. Sonography showed calcification of medullary papilla (nephrocalcinosis). In kidney biopsy, many polarizing intra-tubular and interstitial calcium oxalate crystals, mild patchy lymphocytic infiltration, and interstitial fibrosis were noted. Despite supportive therapies and correction of fluid and electrolyte abnormalities, the patient gradually became oliguric progressing to anuria, and was placed on peritoneal dialysis.

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Are calcium oxalate crystals involved in the mechanism of acute renal failure in ethylene glycol poisoning?

Cited by 92 publications

References 87 publications

Nephroprotective and antioxidative effects of royal jelly on ethylene glycol induced nephropathy in rats

Nephroprotective and antioxidative effects of royal jelly on ethylene glycol induced nephropathy in rats

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

Primary Hyperoxaluria: A Case Report and Review of the Literature

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