LETTER TO THE EDITOR
Year : 2010 | Volume
: 21 | Issue : 1 | Page : 150--152
Jet fuel intoxication and acute renal failure
King Saud University, Department of Medicine,P.O. Box 231388, Riyadh 11321, Saudi Arabia
King Saud University, Department of Medicine,P.O. Box 231388, Riyadh 11321
|How to cite this article:|
Alsuwaida A. Jet fuel intoxication and acute renal failure.Saudi J Kidney Dis Transpl 2010;21:150-152
|How to cite this URL:|
Alsuwaida A. Jet fuel intoxication and acute renal failure. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2020 Feb 23 ];21:150-152
Available from: http://www.sjkdt.org/text.asp?2010/21/1/150/58792
To the Editor,
Jet Fuel is a complex blend of paraffinic, olefinic, naphthenic and aromatic hydrocarbons. Hydrocarbons are organic substances that contain carbon and hydrogen and they are liquid at room temperature. With the exception of aromatic and halogenated compounds, most hydrocarbons are poorly absorbed through the gastrointestinal tract and cause clinical toxicity only when aspirated or inhaled.  Experimental studies have clearly shown that hydrocarbons may cause acute renal failure in animals, which is usually accompanied by acute tubular necrosis; however, in humans this phenomenon is not well recognized. ,, Similarly, the renal effects of chronic exposure are less well defined. In more recent reports, there have been several reports of glomerulonephritis in subjects with prolonged exposure to hydrocarbons. 
A 23-year-old man was presented with nausea, fatigability and bilateral flanks pain for two days. His history was relevant for work exposure to jet fuel both by inhalation and direct skin contact for one week prior to his illness. He had no fever or diarrhea. There was no history suggestive of connective tissue disease. He denied history of illicit drug use and never smoked.
On admission to a local hospital, he looked sick with elevated arterial blood pressure at 150/90 mmHg. However, the rest of his physical examination was unremarkable apart from mild bilateral renal angles tenderness. The laboratory investigations done on admission revealed hemoglobin 13 g/dL, white blood cell counts 7.07 Χ 10 9 /L with normal differential and platelet count 155 Χ 10 9 /L with a C-reactive protein 41.4 mg/L. He had normal liver function tests and coagulation profile. In addition, serum albumin was 3.7 g/dL, total cholesterol 176 mg/dL, triglycerides 153 mg/dL, serum urea 59 mg/dL, serum creatinine 4.0 mg/ dL, creatinine clearance 26 mL/min and electrolytes within normal limits. Complement C3 was 114 g/L (90-180 g/L), C4 23 g/L (10-40 g/L), IgA 193 g/L (90-395 g/L). Hepatitis B, C and HIV serology were negative. Examination of his urine revealed 2 + proteinuria with the presence of 6 to 8 leukocytes and 2 red blood cells per high-power field and no casts. The total proteinuria was 0.92 g/day. Antinuclear antibodies, anti-neutrophilic cytoplasm antibodies were also negative. Ultrasound abdomen showed normal size kidneys with minimal increase in the cortical echogenicity and 99 mTcdiethylenetriaminepentaacetic acid (DTPA) scan revealed bilaterally moderately decreased perfusion with glomerular filtration rate (GFR) of 20 mL/min.
Calcium channels blocker was administered for elevated blood pressure and he was referred to our hospital for further management. He was seen after one week in our hospital, and clinically he was feeling well with normal blood pressure and his laboratory investigations showed decreased serum creatinine to 120 ΅mol/L with bland urine sediment. Because of significant improvement in serum creatinine, kidney biopsy was deferred and antihypertensive medication was stopped due to low normal blood pressure. He came back after three weeks feeling well with normal blood pressure and a serum creatinine of 93 umol/L. He was advised to take precautions to avoid direct contact with jet fuel.
Petroleum-derived fuels and fuel oils are complex mixtures of hydrocarbons. Inhalation and percutaneous absorption are the primary routes of uptake into the peripheral blood.  Following absorption, organic solvents undergo biotransformation (which occurs primarily in the liver), or they accumulate in lipid-rich tissues such as those of the nervous system.  Metabolism in the liver results in the detoxification of the organic solvent through formation of watersoluble compounds that are excreted through urine or bile.  Therefore, the kidney is a target organ for many organic solvents including petroleum-derived or shale-oil-derived fuel vapors.
Most of the evidence for the nephrotoxicity of jet fuel is based on experimental studies in animals, especially mice and rats. Pathological changes observed in male rats 14 days after exposure included the appearance of cytoplasmic droplets in the kidneys.  It was noted that these droplets were larger and more numerous in the kidneys of rats sacrificed 2 or 3 days after exposure than in those sacrificed later and correlated with the observed rise in serum creatinine. ,,
There is scarcity of reported data about hydrocarbons intoxications in humans. Kidney failure has been noted only at high, acute levels of exposures and appears reversible. Two histopathological changes have been reported in human, which include acute tubular injury and rapidly progressive glomerulonephritis (RPGN).  The acute tubular necrosis is most likely related to the direct effects of the mother compound or its toxic metabolites. However, the mechanism of glomerulonephritis is poorly understood. The most common glomerular disease reported with hydrocarbon exposure is Goodpasture's syndrome.  It is possible that the injury to the lung epithelium and exposure of the basement membrane of alveoli initiated the immunogenic responses, which cause formation of basement membrane antibodies. Bell et al. studied 50 patients who had biopsy proven proliferative glomerulonephritis and had been exposed to organic solvents, comparing them with 100 control subjects matched for age, sex, and social class.  This study demonstrates a significant statistical association, as well as a dose-response relationship between solvent exposure and glomerulonephritis, ranging from mild to chronic severe glomerulonephritis.
Physicians should search for history of hydro carbon exposure in patients with acute kidney failure. On the basis of the identified adverse health effects of solvent exposure, it is recommended that employers use engineering controls, personal protective equipment and clothing, and worker education programs to reduce exposure to these organic solvents.
|1||Litvinov T. Hydrocarbon ingestions. Entechnology 1983;62(3):142-7.|
|2||Browning E. Toxicity and metabolism of Industrial solvents. Amsterdam, the Netherlands, London, U.K., New York: Elsevier, 1965.|
|3||Thomas FB, Halder CA, Holdsworth CE, Cockrell B. In: Back PH, Lock EA (eds). Renal Heterogeneity and Target Cell Toxicity. Chichester, U.K., 1985;477-80.|
|4||Halder CA, Van Gorp GS, Hatoum NS, Warne TM. Gasoline vapor exposures. Part 1. Am Ind Hyg Assoc J 1986;47:164-72.|
|5||Brautbar N. Industrial solvents and kidney disease. Int J Occup Environ Health 2004;10:79-83.|
|6||Pederen LM. Biological studies in human exposure to and poisoning with organic solvents. Pharmacol Toxicol 1987;3:1-38.|
|7||Bergman K. Application and results of wholebody autoradiography in distribution studies of organic solvents. Crit Rev Toxicol 1983;12:59-118.|
|8||Toftgard R, Gustafsson J. Biotransformation of organic solvents: A review. Scand J Work Environ Health 1980;6:1-18.|
|9||Gopinath C, Prentice DE, Lewis J. Atlas of experimental toxicological pathology. MTP Press Limited; Boston: 1987;77-90.|
|10||Stott WT, Johnson KA, Bahnemann R, Day SJ, McGuirk RJ. Evaluation of potential modes of action of inhaled ethylbenzene in rats and mice. Toxicol Sci 2003;71:53-66.|
|11||Parker GA, Bogo V, Young RW. Acute toxicity of conventional versus shale-derived JP5 jet fuel: Light microscopic, hematologic, and serum chemistry studies. Toxicol Appl Pharmacol 1981;57:302-17.|
|12||Bogo V, Young RW, Hill TA, et al. The toxicity of petroleum and shale JP5. AFRRI SR8326; AD-A142 670. Bethesda, MD: Armed Forces Radiobiology Research Institute,1983.|
|13||Bell GM, Gordon AC, Lee P, et al. Proliferative glomerulonephritis and exposure to organic solvents. Nephron 1985;40:161-5.|