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Acute Exposure to Aliphatic Hydrocarbons

Acute Exposure to Aliphatic Hydrocarbons Acute tubular necrosis is not an uncommon phenomenon, but it rarely results from environmental factors. We describe a patient in whom acute renal failure developed 2 times after overexposure to aliphatic hydrocarbons and discuss some potential pathophysiological mechanisms. This association has rarely been reported in the literature. Considering the wide availability of aliphatic hydrocarbons in diesel fuel and solvents, associated renal toxicity is probably underrecognized. We stress the importance of identifying environmental and professional factors as causes of acute tubular necrosis.Certain hydrocarbon subclasses, such as the halogenated ones, the glycols and the toluene derivatives, are well recognized for their nephrotoxic effects.On the other hand, acute overexposure to aliphatic hydrocarbons, the straight or branched chains of carbon and oxygen, has almost never been associated with renal toxicity. We describe a patient in whom acute tubular necrosis (ATN) developed after overexposure to petroleum naphtha (aliphatic hydrocarbon) during his professional activities.REPORT OF A CASEA 43-year-old mechanic with a 48-hour history of aggressiveness and headache was brought to the emergency department at his wife's request. He also complained of having had low abdominal pain accompanied by nausea and vomiting . The results of clinical evaluations by neurology and gastroenterology consultants were noncontributory. A complete hematological and biochemical workup revealed increased values of serum urea nitrogen (40 mmol/L [112 mg/dL]) and creatinine (247 µmol/L [2.8 mg/dL]) as the only significant abnormalities. Urinary output on presentation was 30 mL/h. Renal function was normal on routine workup 2 years earlier. Despite intravenous hydration, a rapid deterioration of renal function was observed over the next 3 days, as the creatinine values increased to 862 µmol/L (9.8 mg/dL), while the level of urea nitrogen remained stable at approximately 35 mmol/L (98 mg/dL). Progressive oliguria ensued, and a transfer to our center was organized, in view of eventual dialysis.The first evaluation by a nephrologist occurred 3 days after the initial presentation to the local emergency department. At that time, the patient showed normal central nervous system function and his aggressiveness had subsided. He appeared sick and still complained of severe nausea. Physical examination, including a complete neurological evaluation, revealed an increased blood pressure (170/100 mm Hg), with distended jugular veins and pitting edema over both ankles. Biochemical and hematological evaluation again showed elevated creatinine and urea nitrogen values (999 µmol/L [11.3 mg/dL] and 30 mmol/L [84 mg/dL], respectively). The results of complete liver function tests, as well as serum calcium and phosphorus values, were normal. The creatine kinase level was initially 744 U/L, and normalized thereafter. A complete blood cell count revealed a slight normocytic anemia (hemoglobin, 117 g/L), with normal leukocyte and platelet counts. The erythrocyte sedimentation rate was 24 mm/h. The urinary sodium level was 24 mmol/L and the urinary osmolality level was 184 mmol/kg H2O. Urinalysis revealed more than 50 nondysmorphic red blood cells per high-power field. A few granular and tubular casts were observed, while no red blood cell casts were present. A renal ultrasonogram showed no evidence of hydronephrosis, but both kidneys were described as "edematous." Findings of mercapto-acetyl-triglycine renal scintigraphy (TechneScan MAG-3, Mallinckrodt, St Louis, Mo) were characteristic of ATN (Figure 1).Figure 1.Left, Serial renal scintiscan obtained 3 days after the initial presentation. Each frame represents a 4-minute interval. The last image was obtained after voiding. There is slow cortical transit, parenchymal retention, and delayed excretion, all typical of acute tubular necrosis. Right, Renal scintigraphic curves 3 days after the initial presentation. Both curves are continuously ascending; cortical retention at the end of the study was 206% in the left kidney and 181% in the right kidney (normal <35%).With respect to possible exposure to noxious agents, the patient admitted to a long smoking history, but he did not abuse alcohol and denied any illicit drug consumption. During the episode, he had only taken acetaminophen at the appropriate dosage for headaches. He denied any recent infection or significant trauma. There was no history of hypotension or dehydration. Radio-contrast products had not been used. However, the patient did report heavy respiratory and cutaneous exposure to 99% pure aliphatic hydrocarbon (petroleum naphtha) for a total of about 8 hours over the 3 days preceding his first presentation. This exposure had occurred while he had been cleaning oil pits and motor pieces with the solvent in a small room without appropriate ventilation.In the week following the patient's transfer, his creatinine and urea nitrogen values reached a maximum of 1106 µmol/L (12.5 mg/dL) and 40 mmol/L (112 mg/dL), respectively. The oliguria responded well to furosemide, and hemodialysis could be avoided. Nausea and vomiting subsided progressively. At the time of discharge, 10 days after admission, the patient was well, his serum creatinine level was 453 µmol/L (5.1 mg/dL), and the results of urinalysis had normalized. He was advised to avoid any further contact with the solvent. Follow-up serum creatinine levels were 216 µmol/L (2.4 mg/dL) at 1 week, 131 µmol/L (1.5 mg/dL) at 1 month, and 97 µmol/L (1.1 mg/dL) at 2 months after discharge from the hospital. At 2 months, the findings of renal scintigraphy were completely normal (Figure 2).Figure 2.Left, Serial renal scintiscan obtained 2 months after discharge. Each frame represents a 4-minute interval. The last image was obtained after voiding. The cortical activity is symmetrical and maximal at 2 minutes 48 seconds after the injection. The parenchymal excretion is rapid, with the bladder visible from the first frame onward. Right, Renal scintigraphic curves 2 months after discharge. Each curve shows a normal monoexponential decrease after its initial peak.Despite our explicit warnings, the patient reexposed himself to the same product a few months later, but for a shorter period. During the ensuing 24 hours, nausea, vomiting, and dizziness reappeared, and the patient was immediately reevaluated by a nephrologist. The serum creatinine level had increased again, this time to a maximum of 163 µmol/L (1.8 mg/dL), with recurrence of the image suggestive of ATN on the renal scintiscan (Figure 3). Two days after this second exposure, all symptoms had subsided; 4 days later, the serum creatinine level was 132 umol/L (1.5 mg/dL).Figure 3.Left, Serial renal scintiscan on reexposure to aliphatic hydrocarbons. Each frame represents a 4-minute interval. The last image was obtained after voiding. The cortical transit is again delayed and incomplete. Right, Renal scintigraphic curves on reexposure to aliphatic hydrocarbons. Both curves are flat. Cortical retention at the end of the study was 90% in the left kidney and 140% in the right kidney (normal <35%).COMMENTHydrocarbons are organic compounds mainly containing hydrogen and carbon atoms. They are generally subdivided according to their chemical conformation into such classifications as aliphatic (straight or branched chains), aromatic (containing a ring structure), and halogenated.These different structures are responsible for particular toxicological profiles. While the halogenated hydrocarbons are well recognized for their hepatotoxicity and nephrotoxicity, acute poisoning with aliphatic hydrocarbons manifests predominantly as gastrointestinal, tracheobronchial, pulmonary (aspiration), or central nervous system symptoms.In 1988, Phillips et alpublished an extensive review on the renal effects of hydrocarbon exposure, with the exclusion of some well-known nephrotoxins, ie, halogenated compounds, toluene-containing solvents, and glycols. In their detailed review, a few paragraphs address the topic of acute overexposure to petroleum distillates. These products, derived from petroleum processing, are essentially made of aliphatic hydrocarbons and are used as fuel (diesel) or solvents in both domestic and professional applications. We have identified only 4 cases involving acute renal toxic reactions related to petroleum distillates.In 3 cases, the patients were men who either had respiratory or cutaneous contact with diesel oil used as a solvent. The other case involved oral ingestion of refined petrol.Gastrointestinal or central nervous system symptoms, oliguria, and ATN occurred in all 4 cases.Phillips and colleagues concluded their article by quoting the observation made earlier by Barrientos et al: ". . . the scarcity of reports of renal failure caused by petroleum products, notwithstanding the profusion of products and their uses, is notable." This statement appears to have remained accurate over the years, since we were not able to find another case report of an acute renal toxic reaction associated with aliphatic hydrocarbon exposure since 1988.We believe our case to be of particular interest, since, to our knowledge, it is the first one that has involved an aliphatic hydrocarbon other than diesel oil. The chemical compound incriminated herein is a popular paint thinner that is easily available for both professional and domestic use. The patient brought us the original container, making the exact identification of the product possible. The information obtained from the distributing company indicated that the thinner was made of 99% pure aliphatic hydrocarbons with chains containing 5 to 13 carbons. In our view, the absorption of the product occurred principally by inhalation, although cutaneous contact could also be partially responsible.As the literature on this topic is limited, it is not surprising that very few pathophysiological mechanisms have been proposed to explain this unusual nephrotoxic reaction. Some authors have suggested that direct tubular toxicity could lead to a vasomotor-mediated secondary shutdown in renal perfusion, leading to acute renal failure.We can also postulate that the toxic compound, or the inflammatory mediators it generated, can induce vasoconstriction in the vascular bed of the kidney, particulary in the deep cortical zone and in the medulla. One might also postulate a hypersensitivity to the product, since only 4 cases, including ours, have been reported despite the wide use of the product. The fact that renal insufficiency relapsed later after 1 brief reexposure also supports this hypothesis.In conclusion, we report a case of ATN associated with aliphatic hydrocarbon overexposure. The presentation and subsequent clinical course are very similar to those in the few other cases previously described. Massive exposure to petroleum distillates may on rare occasions cause reversible acute renal failure. This case again emphasizes the importance of identifying and documenting environmental factors as causes of unexplained renal injury, since this phenomenon is underrecognized and treatable.RHDreisbachHydrocarbons.In: Handbook of Poisoning: Prevention, Diagnosis and Treatment. 11th ed. Los Altos, Calif: Lange Medical Publications; 1983:206-215.SCPhillipsRLPetroneGPHemstreetA review of the nonneoplastic kidney effects of hydrocarbon exposure in humans.Occup Med.1988;3:495-509.PHAyresDWTaylorSolvents.In: Hayes AW, ed. Principles and Methods of Toxicology. New York, NY: Raven Press; 1989:111-135.MReidenbergDVPowersRWSevyAcute renal failure due to nephrotoxins.Am J Med Sci.1964;247:25-29.ABarrientosMTOrtunoJMMoralesAcute renal failure after use of diesel fuel as shampoo.Arch Intern Med.1977;137:1217.AJCrispAKBhallaBIHoffbrandAcute tubular necrosis after exposure to diesel oil.BMJ.1979;279:177.SJanssenSvan der GeestSMeijerDRAUgesImpairment of organ function after oral ingestion of refined petrol.Intensive Care Med.1988;14:238-240.Accepted for publication March 26, 1998.Reprints: Serge Langlois, MD, Nephrology Service, CHUQ, Pavillon L'Hôtel-Dieu de Québec, 11 Côte du Palais, Quebec City, Quebec, Canada G1R 2J6. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Internal Medicine American Medical Association

Acute Exposure to Aliphatic Hydrocarbons

JAMA Internal Medicine , Volume 158 (16) – Sep 14, 1998

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American Medical Association
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Copyright 1998 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
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2168-6106
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2168-6114
DOI
10.1001/archinte.158.16.1821
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Abstract

Acute tubular necrosis is not an uncommon phenomenon, but it rarely results from environmental factors. We describe a patient in whom acute renal failure developed 2 times after overexposure to aliphatic hydrocarbons and discuss some potential pathophysiological mechanisms. This association has rarely been reported in the literature. Considering the wide availability of aliphatic hydrocarbons in diesel fuel and solvents, associated renal toxicity is probably underrecognized. We stress the importance of identifying environmental and professional factors as causes of acute tubular necrosis.Certain hydrocarbon subclasses, such as the halogenated ones, the glycols and the toluene derivatives, are well recognized for their nephrotoxic effects.On the other hand, acute overexposure to aliphatic hydrocarbons, the straight or branched chains of carbon and oxygen, has almost never been associated with renal toxicity. We describe a patient in whom acute tubular necrosis (ATN) developed after overexposure to petroleum naphtha (aliphatic hydrocarbon) during his professional activities.REPORT OF A CASEA 43-year-old mechanic with a 48-hour history of aggressiveness and headache was brought to the emergency department at his wife's request. He also complained of having had low abdominal pain accompanied by nausea and vomiting . The results of clinical evaluations by neurology and gastroenterology consultants were noncontributory. A complete hematological and biochemical workup revealed increased values of serum urea nitrogen (40 mmol/L [112 mg/dL]) and creatinine (247 µmol/L [2.8 mg/dL]) as the only significant abnormalities. Urinary output on presentation was 30 mL/h. Renal function was normal on routine workup 2 years earlier. Despite intravenous hydration, a rapid deterioration of renal function was observed over the next 3 days, as the creatinine values increased to 862 µmol/L (9.8 mg/dL), while the level of urea nitrogen remained stable at approximately 35 mmol/L (98 mg/dL). Progressive oliguria ensued, and a transfer to our center was organized, in view of eventual dialysis.The first evaluation by a nephrologist occurred 3 days after the initial presentation to the local emergency department. At that time, the patient showed normal central nervous system function and his aggressiveness had subsided. He appeared sick and still complained of severe nausea. Physical examination, including a complete neurological evaluation, revealed an increased blood pressure (170/100 mm Hg), with distended jugular veins and pitting edema over both ankles. Biochemical and hematological evaluation again showed elevated creatinine and urea nitrogen values (999 µmol/L [11.3 mg/dL] and 30 mmol/L [84 mg/dL], respectively). The results of complete liver function tests, as well as serum calcium and phosphorus values, were normal. The creatine kinase level was initially 744 U/L, and normalized thereafter. A complete blood cell count revealed a slight normocytic anemia (hemoglobin, 117 g/L), with normal leukocyte and platelet counts. The erythrocyte sedimentation rate was 24 mm/h. The urinary sodium level was 24 mmol/L and the urinary osmolality level was 184 mmol/kg H2O. Urinalysis revealed more than 50 nondysmorphic red blood cells per high-power field. A few granular and tubular casts were observed, while no red blood cell casts were present. A renal ultrasonogram showed no evidence of hydronephrosis, but both kidneys were described as "edematous." Findings of mercapto-acetyl-triglycine renal scintigraphy (TechneScan MAG-3, Mallinckrodt, St Louis, Mo) were characteristic of ATN (Figure 1).Figure 1.Left, Serial renal scintiscan obtained 3 days after the initial presentation. Each frame represents a 4-minute interval. The last image was obtained after voiding. There is slow cortical transit, parenchymal retention, and delayed excretion, all typical of acute tubular necrosis. Right, Renal scintigraphic curves 3 days after the initial presentation. Both curves are continuously ascending; cortical retention at the end of the study was 206% in the left kidney and 181% in the right kidney (normal <35%).With respect to possible exposure to noxious agents, the patient admitted to a long smoking history, but he did not abuse alcohol and denied any illicit drug consumption. During the episode, he had only taken acetaminophen at the appropriate dosage for headaches. He denied any recent infection or significant trauma. There was no history of hypotension or dehydration. Radio-contrast products had not been used. However, the patient did report heavy respiratory and cutaneous exposure to 99% pure aliphatic hydrocarbon (petroleum naphtha) for a total of about 8 hours over the 3 days preceding his first presentation. This exposure had occurred while he had been cleaning oil pits and motor pieces with the solvent in a small room without appropriate ventilation.In the week following the patient's transfer, his creatinine and urea nitrogen values reached a maximum of 1106 µmol/L (12.5 mg/dL) and 40 mmol/L (112 mg/dL), respectively. The oliguria responded well to furosemide, and hemodialysis could be avoided. Nausea and vomiting subsided progressively. At the time of discharge, 10 days after admission, the patient was well, his serum creatinine level was 453 µmol/L (5.1 mg/dL), and the results of urinalysis had normalized. He was advised to avoid any further contact with the solvent. Follow-up serum creatinine levels were 216 µmol/L (2.4 mg/dL) at 1 week, 131 µmol/L (1.5 mg/dL) at 1 month, and 97 µmol/L (1.1 mg/dL) at 2 months after discharge from the hospital. At 2 months, the findings of renal scintigraphy were completely normal (Figure 2).Figure 2.Left, Serial renal scintiscan obtained 2 months after discharge. Each frame represents a 4-minute interval. The last image was obtained after voiding. The cortical activity is symmetrical and maximal at 2 minutes 48 seconds after the injection. The parenchymal excretion is rapid, with the bladder visible from the first frame onward. Right, Renal scintigraphic curves 2 months after discharge. Each curve shows a normal monoexponential decrease after its initial peak.Despite our explicit warnings, the patient reexposed himself to the same product a few months later, but for a shorter period. During the ensuing 24 hours, nausea, vomiting, and dizziness reappeared, and the patient was immediately reevaluated by a nephrologist. The serum creatinine level had increased again, this time to a maximum of 163 µmol/L (1.8 mg/dL), with recurrence of the image suggestive of ATN on the renal scintiscan (Figure 3). Two days after this second exposure, all symptoms had subsided; 4 days later, the serum creatinine level was 132 umol/L (1.5 mg/dL).Figure 3.Left, Serial renal scintiscan on reexposure to aliphatic hydrocarbons. Each frame represents a 4-minute interval. The last image was obtained after voiding. The cortical transit is again delayed and incomplete. Right, Renal scintigraphic curves on reexposure to aliphatic hydrocarbons. Both curves are flat. Cortical retention at the end of the study was 90% in the left kidney and 140% in the right kidney (normal <35%).COMMENTHydrocarbons are organic compounds mainly containing hydrogen and carbon atoms. They are generally subdivided according to their chemical conformation into such classifications as aliphatic (straight or branched chains), aromatic (containing a ring structure), and halogenated.These different structures are responsible for particular toxicological profiles. While the halogenated hydrocarbons are well recognized for their hepatotoxicity and nephrotoxicity, acute poisoning with aliphatic hydrocarbons manifests predominantly as gastrointestinal, tracheobronchial, pulmonary (aspiration), or central nervous system symptoms.In 1988, Phillips et alpublished an extensive review on the renal effects of hydrocarbon exposure, with the exclusion of some well-known nephrotoxins, ie, halogenated compounds, toluene-containing solvents, and glycols. In their detailed review, a few paragraphs address the topic of acute overexposure to petroleum distillates. These products, derived from petroleum processing, are essentially made of aliphatic hydrocarbons and are used as fuel (diesel) or solvents in both domestic and professional applications. We have identified only 4 cases involving acute renal toxic reactions related to petroleum distillates.In 3 cases, the patients were men who either had respiratory or cutaneous contact with diesel oil used as a solvent. The other case involved oral ingestion of refined petrol.Gastrointestinal or central nervous system symptoms, oliguria, and ATN occurred in all 4 cases.Phillips and colleagues concluded their article by quoting the observation made earlier by Barrientos et al: ". . . the scarcity of reports of renal failure caused by petroleum products, notwithstanding the profusion of products and their uses, is notable." This statement appears to have remained accurate over the years, since we were not able to find another case report of an acute renal toxic reaction associated with aliphatic hydrocarbon exposure since 1988.We believe our case to be of particular interest, since, to our knowledge, it is the first one that has involved an aliphatic hydrocarbon other than diesel oil. The chemical compound incriminated herein is a popular paint thinner that is easily available for both professional and domestic use. The patient brought us the original container, making the exact identification of the product possible. The information obtained from the distributing company indicated that the thinner was made of 99% pure aliphatic hydrocarbons with chains containing 5 to 13 carbons. In our view, the absorption of the product occurred principally by inhalation, although cutaneous contact could also be partially responsible.As the literature on this topic is limited, it is not surprising that very few pathophysiological mechanisms have been proposed to explain this unusual nephrotoxic reaction. Some authors have suggested that direct tubular toxicity could lead to a vasomotor-mediated secondary shutdown in renal perfusion, leading to acute renal failure.We can also postulate that the toxic compound, or the inflammatory mediators it generated, can induce vasoconstriction in the vascular bed of the kidney, particulary in the deep cortical zone and in the medulla. One might also postulate a hypersensitivity to the product, since only 4 cases, including ours, have been reported despite the wide use of the product. The fact that renal insufficiency relapsed later after 1 brief reexposure also supports this hypothesis.In conclusion, we report a case of ATN associated with aliphatic hydrocarbon overexposure. The presentation and subsequent clinical course are very similar to those in the few other cases previously described. Massive exposure to petroleum distillates may on rare occasions cause reversible acute renal failure. This case again emphasizes the importance of identifying and documenting environmental factors as causes of unexplained renal injury, since this phenomenon is underrecognized and treatable.RHDreisbachHydrocarbons.In: Handbook of Poisoning: Prevention, Diagnosis and Treatment. 11th ed. Los Altos, Calif: Lange Medical Publications; 1983:206-215.SCPhillipsRLPetroneGPHemstreetA review of the nonneoplastic kidney effects of hydrocarbon exposure in humans.Occup Med.1988;3:495-509.PHAyresDWTaylorSolvents.In: Hayes AW, ed. Principles and Methods of Toxicology. New York, NY: Raven Press; 1989:111-135.MReidenbergDVPowersRWSevyAcute renal failure due to nephrotoxins.Am J Med Sci.1964;247:25-29.ABarrientosMTOrtunoJMMoralesAcute renal failure after use of diesel fuel as shampoo.Arch Intern Med.1977;137:1217.AJCrispAKBhallaBIHoffbrandAcute tubular necrosis after exposure to diesel oil.BMJ.1979;279:177.SJanssenSvan der GeestSMeijerDRAUgesImpairment of organ function after oral ingestion of refined petrol.Intensive Care Med.1988;14:238-240.Accepted for publication March 26, 1998.Reprints: Serge Langlois, MD, Nephrology Service, CHUQ, Pavillon L'Hôtel-Dieu de Québec, 11 Côte du Palais, Quebec City, Quebec, Canada G1R 2J6.

Journal

JAMA Internal MedicineAmerican Medical Association

Published: Sep 14, 1998

References