Saudi Journal of Kidney Diseases and Transplantation

: 2009  |  Volume : 20  |  Issue : 1  |  Page : 106--111

Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis

P Kamble1, N Mohsin1, A Jha1, A Date2, A Upadhaya3, E Mohammad1, M Khalil1, A Pakkyara1, M Budruddin1,  
1 Department of Nephrology, Royal Hospital, Muscat, Oman
2 Department of Pathology, Sultan Qaboos University Hospital, Muscat, Oman
3 Department of Gastro-Enterology, Royal Hospital, Muscat, Oman

Correspondence Address:
N Mohsin
Sr. Consultant and Head of Nephrology, Royal Hospital, P.O. Box 1331, PC 111, Muscat


Selenium (Se) is an essential trace element in human and animal nutrition. It is also widely utilized in industrial processes. Reports of acute selenium toxicity in humans are rare. We report a case of a 23-year-old female who consumed about 100 mL of liquid selenite broth and presented with severe nausea, vomiting, abdominal pain, hematemesis and acute renal failure (ARF). The serum selenium level was significantly increased. Gastro-duodenoscopy revealed severe corrosive gastritis. Renal biopsy showed features of acute tubular necrosis (ATN), affecting primarily the proximal tubules. The patient was managed with gastric lavage, blood transfusions, infusion of fresh frozen plasma (FFP) and platelet concentrates and hemo­dialysis. The patient was discharged five weeks after admission and her renal functions reco­vered completely by eight weeks after admission. She continues to be on regular follow-up for any possible sequelae of mucosal corrosive damage. This case highlights a case of selenium intoxication from selenite broth resulting in ARF and corrosive gastritis. The recovery was complete.

How to cite this article:
Kamble P, Mohsin N, Jha A, Date A, Upadhaya A, Mohammad E, Khalil M, Pakkyara A, Budruddin M. Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis.Saudi J Kidney Dis Transpl 2009;20:106-111

How to cite this URL:
Kamble P, Mohsin N, Jha A, Date A, Upadhaya A, Mohammad E, Khalil M, Pakkyara A, Budruddin M. Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2023 Feb 4 ];20:106-111
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Full Text


Selenium (Se) is an ubiquitous element which is essential to the human organism and is also widely utilized in industrial processes. As an essential trace element, it plays an important role in many biochemical and physiological pathways, particularly in the activation of glutathione peroxidase (an enzyme involved in preventing oxidative damage of the cells). [1] It has been used in cancer patients to improve nutritional and immunological status. Also, it has been shown to have a protective role in preventing liver cancer and nuclear cataract. [2],[3],[4],[5]

Despite its beneficial effects, excessive doses of this element result in intoxication. Cases of acute Se intoxication occur due to excessive industrial exposure, overdose in demented patients or suicidal patients and in toddlers. Depending on the quantity and the form, symptoms and signs may vary and include excessive salivation, garlicky breath odor, nausea, vomiting, abdominal pain, ta­chycardia, hematemesis, necrosis of the liver and the kidneys, cerebral and pulmonary edema, coma and death. Currently, there are no known antidotes and the treatment remains mainly symptomatic and supportive. [6]

The selenite broth, also known as selenite enrichment culture media, is used for the isolation of Salmonella bacilli in urine and blood samples. These media contain four grams of sodium selenite (a highly toxic form of Se) dissolved in one liter base of a mixture of polypeptones.

We report a case, probably the first, of a young and previously healthy female, who consumed about 100 mL of selenite broth. She presented with manifestations of corro­sive gastritis and acute renal failure (ARF). She received a multidisciplinary management following which, made complete recovery.

 Case Report

A 23-year-old, unmarried, employed female, with no past history of any psychiatric or medical illness, was admitted to our hospital through the accident and emergency depart­ment. Her chief complaints were nausea, vomiting, (4 to 5 times without hematemesis or garlicky smell) and epigastric pain of one day's duration. She also gave history of pa­ssing two to three loose stools with mucus but, without blood. The patient denied any history of intake of any illicit drugs or che­micals at the time of admission. On exami­nation, she was conscious, well oriented with stable vitals. There was mild epigastric ten­derness. The remainder of the systemic exa­mination was unremarkable. The laboratory investigations on admission showed a white blood cell count of 5.9 × 10 9 /L, hemoglobin of 12.8 gm/dL and platelet count of 270 × 10 9 /L. The blood urea was 3 mmol/L and the serum creatinine was 51 µmol/L. Serum elec­trolytes and liver function tests (LFT) were normal. The patient was treated as a case of gastro-enteritis with intravenous fluids, anti­emetics and histamine-2 receptor antagonists (ranitidine). The patient's condition did not improve over the next 36-48 hours as the abdominal pain and vomiting increased. She did not have hematemesis. She remained con­scious and oriented, but she appeared slightly apprehensive and had developed tachycardia. She also developed oligo-anuria with impair­ment of renal functions. The serum creatinine rose to 692 µmol/L and the blood urea to 25.8 mmol/L. The serum sodium (Na) was 142 mmol/L, potassium (K) 5.1 mmol/L and chlo­ride (Cl) 115 mmol/L. The hemogram, LFT and coagulation profile were within normal limits. The electrocardiogram showed sinus tachycardia without ST segment and T wave changes. The patient was taken into confi­dence by a lady physician and on detailed en­quiry, it was revealed that the patient had "accidentally" consumed about 100 mL of selenite broth from a local hospital labora­tory, one day prior to her hospital admission. The patient said that she hid the information for fear of social stigma and medico-legal enquiry. Blood samples showed elevated Se levels at 1.7 µmol/L (normal: 0.75 to 1.51 µmol/L). Urine samples were not available as the patient was anuric. Hemodialysis was ini­tiated with the continuation of supportive treatment. A kidney biopsy was performed which showed 10 glomeruli under light mic­roscopy, all of which looked grossly normal. The proximal tubules showed epithelial nec­rosis with eosinphilic cell debris filling the tubular basement membrane area. The distal tubular epithelium was largely preserved ex­cept for some intraluminal debris which was probably washed down from the proximal segments. The interstitium and the vascular­ture were unremarkable [Figure 1]. Tissue for immunofluorescence contained four glomeruli; none showed positive staining.

During the course of her stay in the hospital, the patient developed hematemesis. Her vitals remained stable. The coagulation profile was mildly deranged. The patient received blood transfusions, fresh frozen plasma (FFP) and platelet infusions. A gastro-duodenoscopy (OGD) was performed and showed severe hemorrhagic gastritis. She was started on pro­ton pump inhibitors (PPI) and sucralfate. Hemodialysis was continued without heparin. She had another bout of hematemesis 48­hours later. A second OGD was performed and showed large clots on the gastric greater curvature along with diffuse mucosal and submucosal hemorrhages. The esophagus was relatively spared. The findings were sugges­tive of severe corrosive hemorrhagic gastritis [Figure 2]. Intravenous PPI, octreotide, FFPs and blood were administered. The bleeding stopped and the condition of the patient im­proved progressively. Dialysis was discon­tinued in the fourth week of hospitalization and she was discharged a week later. Renal functions recovered completely by the eighth week of her illness. Periodic follow-up up to six months from discharge did not reveal any possible late sequelae of Se toxicity such as alopecia, abnormality of the fingernails or gas­tric strictures.


Selenium (Se) is an essential dietary trace element with anti-oxidant properties due to its role in activation of glutathione peroxidase, an enzyme involved in preventing oxidative damage to cells. It also plays an important role in many biochemical and physiological processes including the biosynthesis of co­enzyme Q (a component of mitochondrial electron transport system), regulation of the ion fluxes across membranes, maintenance of integrity of keratins and stimulation of anti­body synthesis. [1] There is some evidence sug­gesting that adequate dietary supplementation of Se may provide protection against some cancers. Se is currently used in hyperalimen­tation and total parenteral nutrition. [7],[8]

There appears to be a relatively narrow range between levels of Se intake resulting in deficiency and those causing toxicity. [9] The recommended daily allowance (RDA), for adults, by the Federal Drug Administration (FDA) is 50-200 µg.

Selenium is a grey metalloid element of the sulfur group discovered in 1817 by Berzelius who named it after Selene, the Greek God­dess of the moon. It is widely used in many commercial applications, thus constituting a common source of human exposure. [6],[10] Industrial uses include solar energy, semi-conduc­tor processing and the manufacturing of elec­tronics and ceramics. [10],[11],[12],[13],[14] It is present in steel and copper alloying, metal pigmentation in photographic cells, glass and paint manufac­turing, rubber vulcanization, nutritional sup­plements and Selsun TM shampoo. Also, it is mixed with various compounds utilized for polishing and bluing the exterior metallic surfaces of handguns. [10],[11] In selenite enrich­ment media (selenite broth), selenium is used to selectively isolate Salmonella bacilli from urine and blood samples. [15]

Acute poisoning with Se or its compounds, especially the fatal ones, occurs extremely rarely in humans. Marco Polo gave the first account of Se toxicity which he observed du­ring his travel in western China in the 13 th century. He linked the sloughing off of the hooves of horses to their consumption of cer­tain plants rich in very high concentration of Se. [8] In humans, acute Se intoxication can occur due to industrial exposure, accidental overdose in demented or suicidal patients and in toddlers. Acute oral exposure can result in excessive salivation, garlicky breath odor, shallow breathing, diarrhea, continuous vomi­ting, mucosal irritation, hematemesis, abdo­minal pain, tachycardia, hemolysis, necrosis of the liver and the renal tubules (resulting in ARF), cerebral and pulmonary edema, para­lysis, convulsions, coma and death. [11],[13],[16],[17]

Selenium occurs in several valency states; -2 (hydrogen selenide, sodium selenide, dimethyl selenium, selenomethionine); 0 (elemental se­lenium); +4 (selenium dioxide, selenious acid and sodium selenite); and +6 (selenic acid and sodium selenate). Toxicity of Se varies according to the valency state and the water solubility of the compound. The more soluble compounds such as sodium selenate are more toxic than the less soluble elemental sele­nium. Absorption is also more efficient after a single dose than after repetitive daily doses. Gastrointestinal absorption of the various Se compounds ranges from about 44 to 95 %. It is widely distributed in the body. Relatively high concentrations are seen in the gastric mucosa, heart, liver, kidneys, lungs, pancreas, spleen and testes. Excretion is primarily via the urine (0-15 µg/L). [18],[19],[20]

Multi-organ system involvement is known to occur in acute oral Se intoxication. The severity depends upon the dose and the type of Se compound ingested. Nantel AJ et al reported a case in which a two-year-old male child presented with severe corrosive gastritis and moderate renal, hepatic and pulmonary dysfunction after consuming 15 mL of Gun­Blue solution containing selenious acid. Plas­ma Se concentration was raised to 285 µg/L. The patient died after 17 days. [21] In another instance, where the patient presented after fatal suicidal ingestion of Gun-Blue solution, post-mortem examination revealed pulmonary edema with pleural effusion and congestion of the kidney. Necrosis of proximal tubules was noted in the kidney on histological exa­mination. The selenium levels in the tissues were 9 to 90-fold higher than in normal sub­jects, with highest tissue levels found in the lungs, kidneys and stomach. [17] In animal stu­dies, a dose dependent acute tubular necrosis (ATN) of the kidney and centrilobular liver injury is well documented. [22]

Our patient developed severe ARF requiring dialysis support. Her renal biopsy revealed proximal tubular necrosis consistent with toxic ATN [Figure 1]. The biochemical me­chanism of toxicity of Se and related com­pounds is not fully understood. However, potential mechanisms of toxicity include: [13],[17]

substitution of Se for sulfur in sulfhydryl­containing enzymes necessary for oxidative reactions in cellular respiration via effects on the mitochondrial and microsomal electron transport.mediation of oxidative stress mechanism, interference with the normal redox-regu­lating activities of glutathione peroxidase,mediation of apoptotic and free radical formation.

Our patient also had severe hematemesis due to corrosive gastritis [Figure 2] which re­quired aggressive management with multiple transfusions of blood, FFPs, platelet concen­trates, PPI and octreotide. Kise Y, et al repor­ted a case of oral Se intoxication in a 48-year-old female who had hematemesis with severe corrosive mucosal injury of the oral cavity, esophagus and stomach with deep gastric ul­cers. The patient had consumed 2000 mg of selenium dioxide (from the bottle of glass­blue). She recovered with symptomatic and supportive care. [8] Highly toxic Se compounds like sodium selenite and selenium dioxide, upon contact with water, form a weak acid (selenic acid) which is a strong oxidant and is responsible for the corrosive mucosal injury. [16]

Se clearance in humans appears to follow a two-compartment model characterized by an initial distribution phase of six hours and a final elimination half- life phase of 17.5 hours. [8],[23],[24] In humans, toxic effects have been re-ported at blood levels ranging from 0.179­7.5 µg/mL. [25] It was calculated that the patient under discussion consumed about 400 mg of sodium selenite. Her serum Se level was 1.71 µmol/L, which was moderately but signifi­cantly higher than the normal level, in a sample collected 3-4 days after Se ingestion. Hemodialysis is not an established mode of treatment for Se intoxication, but was indi­cated for the treatment of the ARF. Never­theless, a decrease in serum Se concentration has been reported with dialysis. [8],[26]

The principal treatment strategy in acute Se intoxication is to remove the patient from the source of Se and to provide symptomatic and supportive care, as currently there are no anti­dotes available. Few pharmaceutical agents such as bromobenzene, arsenic compounds and glutathione have been suggested as possi­ble antidotes, but require confirmation before putting them into practical use. [6],[8]

The terminal half-life of selenite is about four months. Hence, care should be taken to avoid further exposure to Se and to observe any late sequelae of Se toxicity such as cha­nges in hair, skin and nails or any persistent gastric symptoms. [8],[20],[25] After six months of follow-up, our patient is doing fine and looks healthy. An OGD at six years is suggested, as corrosive gastritis may cause late complica­tions like strictures or stenosis. [27]

In summary, the present case highlights the possibility of acute Se intoxication following the ingestion of selenite enrichment media (selenite broth). The clinical features included acute renal failure and corrosive gastritis with hematemesis. She recovered with multidiscip­ linary symptomatic and supportive manage­ment.


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