[Acute kidney injury caused by acute dimethyl oxalate poisoning: a case report].

Dimethyl oxalate is one of the occupational toxic chemicals and causes strong renal toxicity. On May 16, 2023, a patient with acute dimethyl oxalate poisoning was admitted to Dingxi People's Hospital. The patient presented with nausea, vomiting, lumbar distension, weakness, poor appetite, anuria, and rapidly progressing acute kidney injury. Renal biopsy confirmed acute oxalate nephropathy. After symptomatic supportive treatments such as blood purification, anti-oxidative stress, glucocorticoid, fluid supplementation, alkalized urine, anti-infection, controlling blood pressure, calcium supplementation and anemia correction, the patient's symptoms disappeared, and the kidney function basically returned to normal. This case suggested that the etiology of patients with acute kidney injury must be clearly identified, and renal biopsy was an important examination method. For patients suffering from acute dimethyl oxalate poisoning, comprehensive treatment based on blood purification should be performed as soon as possible, aiming to improve the prognosis.

A review of oxalate poisoning in domestic animals: tolerance and performance aspects.

Published data on oxalate poisoning in domestic animals are reviewed, with a focus on tolerance and performance. Oxalic acid is one of a number of anti-nutrients found in forage. It can bind with dietary calcium (Ca) or magnesium (Mg) to form insoluble Ca or Mg oxalate, which then may lead to low serum Ca or Mg levels as well as to renal failure because of precipitation of these salts in the kidneys. Dietary oxalate plays an important role in the formation of Ca oxalate, and a high dietary intake of Ca may decrease oxalate absorption and its subsequent urinary excretion. Oxalate-rich plants can be supplemented with other plants as forage for domestic animals, which may help to reduce the overall intake of oxalate-rich plants. Non-ruminants appear to be more sensitive to oxalate than ruminants because in the latter, rumen bacteria help to degrade oxalate. If ruminants are slowly exposed to a diet high in oxalate, the population of oxalate-degrading bacteria in the rumen increases sufficiently to prevent oxalate poisoning. However, if large quantities of oxalate-rich plants are eaten, the rumen is overwhelmed and unable to metabolize the oxalate and oxalate-poisoning results. Based on published data, we consider that <2.0% soluble oxalate would be an appropriate level to avoid oxalate poisoning in ruminants, although blood Ca level may decrease. In the case of non-ruminants, <0.5% soluble oxalate may be acceptable. However, these proposed safe levels of soluble oxalate should be regarded as preliminary. Further studies, especially long-term studies, are needed to validate and improve the recommended safe levels in animals. This review will encourage further research on the relationships between dietary oxalate, other dietary factors and renal failure in domestic animals.

Plants Containing Urinary Tract, Gastrointestinal, or Miscellaneous Toxins that Affect Livestock.

Whether exposed by grazing toxic range or pasture plants or by eating contaminated feed, there are plant toxins that produce urinary tract disease, gastroenteritis, and other miscellaneous or multisystemic diseases. Diagnosis can be challenging and requires incorporation of field studies, clinical signs, gross and microscopic pathology, and chemical identification of plants, toxins, and metabolites in animal samples. The objectives of this review are to introduce poisonous plants that commonly poison livestock in North America; describe clinical and pathologic lesions they produce in livestock; and present current technology available to identify poisoning, treat affected animals, and minimize or avoid poisoning additional animals.

Acute Oxalate Nephropathy due to "Averrhoa Bilimbi": A Case Report.

Averrhoa bilimbi found in bilimbi tree is a well known fruits of warm climates, found throughout Bangladesh, India, Myanmar and South East Asian countries. This fruit contents high level of oxalate. Acute renal failure due to tubular necrosis caused by oxalate crystal has been reported. We present a patient who developed acute kidney injury following ingestion of bilimbi fruit juice and had complete recovery with conservative management and concluded that star fruit and bilimbi fruit juice should be avoided in CKD and on dialysis patients.

Renal failure in a guinea pig (Cavia porcellus) following ingestion of oxalate containing plants.

A 1-year-old guinea pig presented with anorexia, lethargy, and weight loss, 1 week after ingesting a peace lily leaf. Laboratory findings were suggestive of renal failure and included elevated blood urea nitrogen and creatinine with concurrent isosthenuria. The guinea pig was euthanized 1 month later due to worsening clinical signs.

Plasma oxalic acid and calcium levels in oxalate poisoning.

Observations are reported on five cases of suicide or attempted suicide by poisoning with oxalic acid or ethylene glycol. Elevated oxalic acid levels were observed in the plasma, stomach contents, and a number of tissues. Raised oxalic acid levels in plasma were associated with reduced total and ultrafilterable calcium levels. It is suggested that the reduction in plasma total calcium level is due mainly to the deposition of calcium oxalate in the soft tissues, but inhibition of the parathyroid glands may be a contributory factor. Microscopic examination of various tissues indicated that oxalic acid is deposited in the tissues in two forms: (1) crystalline calcium oxalate dihydrate in the kidney and (2) a non-crystalline complex of calcium oxalate and lipid in liver and other tissues.

Urolithiasis in railroad shopmen in relation to oxalic acid exposure at work.

It is well known that the urinary excretion of oxalic acid is one of the main determinants for urinary stone formation. From 1950 to 1978 a saturated oxalic acid solution was used in a repainting and cleaning process for railroad cars in Norwegian railroad workshops. With the use of a questionnaire, the cumulative prevalence of urolithiasis-induced colic episodes was registered in the Sundland railroad depot. Forty-two (11.9%) out of 353 male workers not exposed to oxalic acid reported having had one or more such stone colic episodes. The corresponding figure for 15 individuals who had a very high exposure to oxalic acid was 8 (53.3%). Also workers in other departments, occasionally exposed to oxalic acid, had an increased stone colic prevalence rate, a finding suggesting a positive dose-response relationship. There was an increased frequency of stone colic episodes in the age group 40-69 years. Seven heavily exposed workers in the paint shop reported initial pollakiuria and slight dysuria during the exposure. The study indicates a causal relation between urinary stone formation in the investigated railroad shopmen and their exposure to oxalic acid at work.

Oxalate nephropathy in a Tibetan spaniel litter. A probable case of primary hyperoxaluria.

Severe oxalate nephropathy with end-stage kidney lesions was found in two pups of a litter of three Tibetan Spaniels. This histopathological finding strongly suggests a primary hyperoxaluria since there was no exposure to agents capable of producing secondary hyperoxaluria. Primary hyperoxaluria has not been reported as a spontaneous disease in the dog, although it is a well-known, but rare, inherited metabolic disease of man.

Oxalate (Halogeton) poisoning of sheep: certain physiopathologic changes.

Certain clinical changes associated with acute oxalate (halogeton) poisoning were determined in sheep given (by stomach tube into the rumen) a lethal dose of Halogeton glomeratus. Plasma concentrations of calcium and calcium ion activity decreased over several hours to such low levels that tetany or coma occurred and death followed. Cerebrospinal fluid concentrations of calcium did not reflect the degree of hypocalcemia. In 2 pregnant sheep administered halogeton, the plasma concentration of calcium in the fetus did not decrease despite the appearance of severe maternal hypocalcemia. Increases in plasma total inorganic phosphate and magnesium concentrations occurred as the hypocalcemia progressed. Hyperglycemia was often marked as hypocalcemia became severe; however, as hyperglycemia increased, plasma immunoreactive insulin concentrations remained inappropriately low in relation to the plasma concentration of glucose. Intravenous infusion of a calcium solution at this time was associated with marked increase in immunoreactive insulin concentration and a decrease in glucose concentration. Ruminal activity, as measured by frequency and amplitude of contractions of the rumen, was greatly reduced as hypocalcemia progressed. Seemingly, body temperature became lowered as severity of the hypocalcemia progressed. Seemingly, body temperature became lowered as severity of the hypocalcemia increased, as determined by intramuscularly or intraperitoneally implanted temperature telemetry devices. However, the occurrence of tetany and the fleece covering could either modify or reverse this decrease in body temperature.

Oxalate (Rumex venosus) poisoning in cattle.

Fifteen range cows died of oxalate poisoning caused by ingestion of Rumex venosus. Ecchymotic and petechial hemorrhages were prominent on the abdominal serosal surfaces. Approximately 2 L of thin, yellowish fluid was in the abdominal cavity, and mesenteric lymph nodes were enlarged and edematous. Other findings included catarrhal abomasitis; enteritis; pale, edematous kidneys; congested lungs; fatty infiltration of the liver; and nephrosis. In the kidneys, birefringent crystals resembling oxalate crystals were demonstrable only when frozen sections were examined.

Acute oxalate poisoning attributable to ingestion of curly dock (Rumex crispus) in sheep.

Ten of 100 mature ewes were afflicted with acute oxalate toxicosis within 40 hours after being temporarily penned in a lot that contained considerable growing Rumex crispus (curly dock). Clinical signs of toxicosis included excess salivation, tremors, ataxia, and recumbency. Affected ewes were markedly hypocalcemic and azotemic. Oxalate crystals were not observed in urine. Gross postmortem lesions were minimal and nondiagnostic in 2 ewes that died peracutely, but perirenal edema and renal tubular degeneration were clearly observable in ewes euthanatized on the third day of toxicosis. Diagnosis of oxalate toxicosis was confirmed by histopathologic findings. Samples of Rumex spp contained 6.6 to 11.1% oxalic acid on a dry-weight basis, a concentration comparable with that in other oxalate-containing plants that have caused acute oxalate toxicosis.

Oxalate poisoning in a koala (Phascolarctos cinereus).

A case of suspected acute oxalate poisoning is reported in an aged male koala. The animal had extensive renal oxalosis and a haemorrhagic bladder wall when autopsied. The source of the oxalate was not detected.

Urolithiasis in a herd of beef cattle associated with oxalate ingestion.

An unusually high incidence of urinary calculi in a group of feeder cattle is described. Necropsy findings in one affected animal suggested that oxalates in the feed, specifically in fescue (Festuca spp.) seed screenings, may have been the cause. Low dietary calcium and decreased water intake by the cattle appear to have been predisposing factors. Control measures are discussed.