Journal of Medicine in the Tropics

: 2017  |  Volume : 19  |  Issue : 2  |  Page : 133--135

An unusual case of acute kidney injury caused by oxalic acid mistaken for common salt

Koushik Bhattacharjee, Smita S Divyaveer, Avinandan Banerjee, Vaibhav Tiwari, Tanima D Bhattacharya, Arpita Raychaudhury, Rajendra Pandey 
 Department of Nephrology, IPGMER, Kolkata, West Bengal, India

Correspondence Address:
Smita S Divyaveer
Department of Nephrology, IPGMER and SSKM Hospital, Near Ronald Ross Building, Kolkata 700020, West Bengal


Accidental exposure to chemicals and toxins is an important cause of acute kidney injury in the tropics. We report a case of a 26-year-old female who presented with acute kidney injury following a history of accidental ingestion of some white powder mistaken for table salt. Urine microscopy revealed the presence of calcium oxalate crystals. Because accidental poisoning was suspected despite normal 24-h oxalate excretion, renal biopsy was performed, which showed acute tubular injury with occasional refractile oxalate crystals. The patient improved symptomatically with conservative management and did not require haemodialysis. Subsequently, renal functioning showed an improving trend. Oxalic acid poisoning is relatively rare but is an emerging sporadic as well as epidemic poison in some regions.

How to cite this article:
Bhattacharjee K, Divyaveer SS, Banerjee A, Tiwari V, Bhattacharya TD, Raychaudhury A, Pandey R. An unusual case of acute kidney injury caused by oxalic acid mistaken for common salt.J Med Trop 2017;19:133-135

How to cite this URL:
Bhattacharjee K, Divyaveer SS, Banerjee A, Tiwari V, Bhattacharya TD, Raychaudhury A, Pandey R. An unusual case of acute kidney injury caused by oxalic acid mistaken for common salt. J Med Trop [serial online] 2017 [cited 2022 Aug 18 ];19:133-135
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Acute kidney injury following accidental exposure to chemicals and toxins differs in different geographic regions depending on the availability or industrial/domestic use of these substances.[1] We report a case of non-oliguric acute kidney injury (AKI) following an accidental intake of white powder mistaken for table salt. Although poisoning caused by plant sources of oxalic acid are known,[2],[3] to the best of our knowledge, this is the first report of oxalic acid poisoning due to the ingestion of white powder used for domestic purpose in India.


A 26-year-old female, who hails from a sub-urban area of West Bengal, presented in our institute with complaints of nausea and recurrent vomiting with vague dull upper abdominal pain. On further enquiry, she gave history of consumption of a white powder-like substance after mixing it in her dinner, which she presumed to be table salt, 4 days prior to admission. The symptoms started 10–12 h after ingestion. There was no history of decrease in urine output, haematemesis, melena or haematuria. Exact amount ingested was not known. On examination, the patient was alert, conscious and oriented with stable vitals (Pulse Rate 80/min, regular and Blood Pressure 140/80). Systemic examination was unremarkable except mild epigastric tenderness. The results of investigations conducted were as shown in [Table 1]. Urine output continued to be 1.5 to 2 L/day throughout the hospital stay. Arterial blood gas analysis revealed metabolic acidosis with normal anion gap. Urine analysis revealed occasional envelop-shaped calcium oxalate crystals. On the basis of a suspicion of oxalate poisoning, a 24-h urine oxalate level was determined, which was subsequently found to be 30.92 mg/day (the normal upper level of urinary oxalate excretion is 40 mg in 24 h), and the package of the white powder that was ingested was asked to be brought to our institute. The package was examined to determine the contents of the powder, and it was found to be oxalic acid, which is commonly found in households as a cleansing agent. An ultrasonography of the abdomen revealed the following: right kidney–10.2 cm, left kidney–11.6 cm, normal cortical echotexture and maintained corticomedullary differentiation. Due to a persistently high serum creatinine (SCr) level, renal biopsy was performed on the 6th day of her hospital stay (shown in [Figure 1],[Figure 2],[Figure 3]). The patient was managed conservatively with antacids and mucoprotective agents such as sucralfate. On day 10, following a progressive decrease in SCr levels and adequate urine output, the patient was discharged. On follow-up on day 15, she was asymptomatic, had a SCr level of 0.8 mg/dl and urea of 23 mg/dl.{Table 1}{Figure 1}{Figure 2}{Figure 3}


Oxalic acid is a toxic organic compound, commonly used as a reducing agent in photography, for bleaching and dust removal, as well as being found in certain plants and natural sources. Oxalic acid as a toxin is mostly described in the context of ethylene glycol poisoning, because it is a metabolite of ethylene glycol. Other reported cases of isolated oxalic acid poisoning involve the consumption of food, medications and plants that contain the compound, for example, star fruit and ascorbic acid.[2],[3] Oxalic acid is poorly absorbed with a bioavailability of 2–5%. It is excreted unchanged in the urine. The oral lethal dose of oxalic acid for adults is 15–30 g, although the ingestion of as little as 5 g has caused death.[4] It may have a direct corrosive effect on the eyes, skin and digestive tract after contact. However, once absorbed, oxalic acid and other soluble oxalates react with calcium in the plasma to form insoluble calcium oxalate. Calcium oxalate exists in monohydrate and dihydrate forms, which can be distinguished by the shape of the respective crystals. Calcium oxalate dihydrate crystals are octahedral. A large portion of the crystals in urine sediment will have this type of morphology, because they can grow at any pH and naturally occur in normal urine. Calcium oxalate monohydrate crystals vary in shape and can be shaped as dumbbells, spindles, ovals or picket fences, the last of which is most commonly seen due to ethylene glycol poisoning. We found oxalate crystals in our case. This could be a normal finding, but the history of accidental ingestion indicated a possible case of oxalate poisoning. The 24-h excretion of oxalate was at the upper limit of normal. This could have been due to the delay of presentation of the patient as well as renal impairment per se.

The mechanisms of renal injury include the precipitation of calcium oxalate in the renal system (the proximal tubules of the kidney) causing obstruction, which may lead to local necrosis of the tubular epithelium, energy depletion, cell swelling, calcium influx, intracellular acidosis and enzyme activation.[5],[6] Systemic formation of calcium oxalate may produce hypocalcaemia directly, although this case had no biochemical evidence. The acute renal failure of oxalate poisoning is usually managed supportively, and only a minority of reported cases required dialysis. Interstitial nephritis has been described in cases of chronic hyperoxaluria.[7],[8],[9] Such cases may benefit from a short course of steroid therapy.[10]

A huge number of cases of oxalic acid poisoning are increasingly being reported even in epidemic proportions particularly from Sri Lanka, where it is available as a cleansing agent.[11] It is also necessary to ascertain the source of AKI with oxalate crystals, because if associated with ethylene glycol poisoning other measures such as dialysis, which may help in the removal of the toxin and fomepizole, may be needed.[12] These are not indicated for oxalic acid poisoning because these measures are useful only for ethylene glycol poisoning, as they help in decreasing the concentration of toxic substances in blood caused by the metabolism of ethylene glycol.


Oxalic acid poisoning is uncommon but can cause acute kidney injury and related complications. Awareness regarding oxalic acid toxicity among primary care physicians and the general population as well as regulation of the household products with warning of toxic potential is necessary to curb the incidence of oxalic acid poisoning.

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