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Year : 2013  |  Volume : 23  |  Issue : 1  |  Page : 80-81

Benzene hexachloride poisoning with rhabdomyolysis and acute kidney injury

1 Department of Nephrology and Clinical Transplantation, Institute of Kidney Diseases and Research Center, Dr. HL Trivedi Institute of Transplantation Sciences [IKDRC-ITS], Ahmedabad, Gujarat, India
2 Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, IKDRC-ITS, Ahmedabad, Gujarat, India

Date of Web Publication16-Feb-2013

Correspondence Address:
P R Shah
Department of Nephrology and Clinical Transplantation, Institute of Kidney Diseases and Research Centre [IKDRC]- Dr. H L Trivedi Institute of Transplantation Sciences [ITS], Civil Hospital Campus, Asarwa, Ahmedabad - 380 016, Gujarat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-4065.107222

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How to cite this article:
Shah P R, Kute V B, Gumber M R, Patel H V, Patel M P, Yadav D K, Vanikar A V, Trivedi H L. Benzene hexachloride poisoning with rhabdomyolysis and acute kidney injury. Indian J Nephrol 2013;23:80-1

How to cite this URL:
Shah P R, Kute V B, Gumber M R, Patel H V, Patel M P, Yadav D K, Vanikar A V, Trivedi H L. Benzene hexachloride poisoning with rhabdomyolysis and acute kidney injury. Indian J Nephrol [serial online] 2013 [cited 2021 Sep 24];23:80-1. Available from:


A 21-year-old male was referred to our hospital for evaluation and management of renal failure. He presented with oliguria, dark color of urine, pedal edema, and muscular pain since 2 days. He had a history of ingestion of insecticidal liquid containing gamma benzene hexachloride (BHC) with a suicidal intention 3 days back. He had received gastric lavage and supportive treatment in the form of fluids at a primary care center. At the time of admission his blood pressure was 120/80 mmHg, pulse rate 90/min, respiratory rate was 24/min, and urine showed dipstick-positive proteinuria (3+) with myoglobinuria. He had tenderness of muscles (more in lower limbs) with normal tendon reflexes and altered mentation. Hematological parameters (total leukocytes 10,500/mm 3 , platelets 1.9 lac/mm 3 , hemoglobin 11.7 g/dL) and liver function tests were normal except for a mild elevation in aspartate aminotransferase (AST 94 U/L) without any evidence of hemolysis. The presence of metabolic acidosis (pH 7.18, HCO3 - 9) and rise in creatinine from 0.9 to 3.1 mg/dL prompted us to initiate him on hemodialysis. Additional evaluation revealed total serum creatine phosphokinase (CPK) of 2890 U/L (range: 20-230 U/L), lactate dehydrogenase of 360 U/L, and a rise in potassium to 6.3 mEq/L. Immunological tests like complement levels (C3), anti-nuclear antibodies, and anti-neutrophilic antibodies were unremarkable. A clinical diagnosis of BHC-induced rhabdomyolysis leading to acute kidney injury (AKI) was made. Though myoglobinuria ceased over the next 3 days and total CPK decreased to 146 U/L by the end of 1 week, he required hemodialysis on alternate days for 1 week. After 2 weeks of hospitalization and supportive care, there was a gradual improvement in urine output, and a declining trend was noticed in creatinine. Similarly, his muscular tenderness gradually improved with the disappearance of uremic symptoms and creatinine decreased to 1.2 mg/dL on the 21 st day.

Poisoning caused by industrial chemicals is an important cause of community-acquired AKI in Asia. [1],[2] Our case demonstrates AKI associated with ingestion of BHC which is very unusual. BHC is an organochlorine insecticide and acute poisoning usually leads to features of neurotoxicity like altered mentation and seizures. Other features like liver dysfunction, metabolic acidosis, and hematological and gastrointestinal toxicities have occasionally been described. [3] BHC is known to be nephrotoxic as per reports of experimental animal models, [4],[5] but reports of renal involvement in humans with myoglobinuria have not been convincingly reported in the literature. Development of muscle necrosis and AKI have been reported only in one case in 1977. [6] Rhabdomyolysis is a life-threatening condition resulting from the breakdown of skeletal muscles and commonly occurs with trauma, burns, viral infections, polymyositis, convulsions, exertion, ischemia, alcohol abuse, and various toxins. [7],[8] Other causes of myoglobinuria were safely excluded in our patient as per clinical history and temporal ingestion of BHC leading to acute presentation suggesting its etiological role. The role of dehydration and sepsis leading to AKI was ruled out in our case. Though the exact mechanism cannot be determined, generation of free radical-related oxidative damage in skeletal muscles and renal tubular cells may lead to renal toxicity.

  References Top

1.Jha V, Chugh KS. Community-acquired acute kidney injury in Asia. Semin Nephrol 2008;28:330-47.  Back to cited text no. 1
2.Jha V, Chugh KS. Nephropathy associated with animal, plant, and chemical toxins in the tropics. Semin Nephrol 2003;23:49-65.  Back to cited text no. 2
3.Nolan K, Kamrath J, Levitt J. Lindane toxicity: A comprehensive review of the medical literature. Pediatr Dermatol 2012;29:141-6.  Back to cited text no. 3
4.Andrews JE, Gray LE. The effects of lindane and linuron on calcium metabolism, bone morphometry and the kidney in rats. Toxicology 1990;60:99-107.  Back to cited text no. 4
5.Dietrich DR, Swenberg JA. Lindane induces nephropathy and renal accumulation of alpha 2u-globulin in male but not in female fischer 344 rats or male NBR rats. Toxicol Lett 1990;53:179-81.  Back to cited text no. 5
6.Munk ZM, Nantel A. Acute lindane poisoning with development of muscle necrosis. Can Med Assoc J 1977;117:1050-4.  Back to cited text no. 6
7.Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361:62-72.  Back to cited text no. 7
8.Muthukumar T, Jha V, Sud A, Wanchoo A, Bambery P, Sakhuja V. Acute renal failure due to nontraumatic rhabdomyolysis following binge drinking. Ren Fail 1999;21:545-9.  Back to cited text no. 8

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