Saudi Journal of Kidney Diseases and Transplantation

LETTER TO THE EDITOR
Year
: 2010  |  Volume : 21  |  Issue : 1  |  Page : 150--152

Jet fuel intoxication and acute renal failure


Abdulkareem Alsuwaida 
 King Saud University, Department of Medicine,P.O. Box 231388, Riyadh 11321, Saudi Arabia

Correspondence Address:
Abdulkareem Alsuwaida
King Saud University, Department of Medicine,P.O. Box 231388, Riyadh 11321
Saudi Arabia




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


Full Text

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. [1] 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. [2],[3],[4] 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. [5]

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. [6] 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. [7] Metabolism in the liver results in the detoxification of the organic solvent through formation of water­soluble compounds that are excreted through urine or bile. [8] 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. [9] 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. [10],[11],[12]

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). [5] 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. [5] 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. [13] 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.

References

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