| Abstract|| |
Glue sniffing refers to the deliberate inhalation of volatile solvents, commonly found in adhesives, for the purpose of intoxication. The globally increasing prevalence of glue sniffing suggests that physicians will encounter many such patients some time during their practice. We present a 19-year-old male who presented with acute abdomen and renal failure. He was treated conservatively and had complete recovery of renal functions in a week. The etiology of renal failure remained elusive on admission. While recovering from his illness, the patient revealed history of glue sniffing. The aim of presenting this case is to spread awareness among clinicians that glue sniffing should be considered in the differential diagnosis of unexplained acute reversible renal failure, particularly in young patients.
Keywords: Glue sniffing, Renal failure, Acute abdomen
|How to cite this article:|
Saxena SK, Ul-Haq A. Acute Reversible Renal Failure due to Glue Sniffing. Saudi J Kidney Dis Transpl 2005;16:326-9
| Introduction|| |
Unexplained acute renal failure is not an uncommon entity in clinical practice. We present a case of glue sniffing resulting in acute reversible renal failure. The etiology of renal failure remained obscure until the patient disclosed a history of glue sniffing. Glue sniffing remains one of the least discussed groups of abused substances causing renal failure. Clinicians should consider this as one of the causes of acute renal failure, particularly in adolescent and young adult patients.
| Case Report|| |
A 19-year-old male patient presented to the Al-Iman hospital, Riyadh, Saudi Arabia with complaints of generalized abdominal pain and vomiting of 10-hours duration. There was no history of diarrhea, hematemesis or malena. There was no past history of peptic ulcer disease, biliary disorder or sickle cell disease. He denied any history of non-steroidal anti-inflammatory drug ingestion and drug abuse. He was drowsy, afebrile and mildly dehydrated. His pulse and blood pressure were 100/min and 130/70 mm Hg respectively. The abdomen was diffusely tender and this was more pronounced in the right iliac fossa. There were no palpable intra-abdominal masses or hepatosplenomegaly. No free fluid was evident and normal bowel sounds were audible. Examination of other systems was unremarkable.
Investigations revealed Hemoglobin of 12.6 g/dL, White Blood Count, 16.6 x 10 9 /L with predominant polymorphs and platelet count of 214 x 10 9 /L. The serum creatinine was 424 umol/L, blood urea nitrogen was 7.1 mmol/L, potassium was 3.3 mmol/L, sodium 137 mmol/L and chloride was 123 mmol/L. Arterial blood gas analysis showed pH of 7.139, PCO2 of 9.5 mm Hg, HCO 3 of 3.1 mmol/L and PO2 of 121.5 mm Hg. Urine analysis showed pH of 7.5, Albumin 1+ with no pus cells or red blood cells. The urinary sodium was 106 mmol/L, blood urea nitrogen was 22 mmol/L, creatinine was 1854 µmol/L and the osmolality of the urine and serum were 234 and 295 respectively. Ultrasound abdomen showed that both kidneys were normal in size and parenchymal echogenicity. There were no features of obstructive uropathy. Chest X-ray and ECG were normal.
The patient was admitted by the surgical team as a case of acute abdomen, query acute appendicitis with renal failure. Urgent laparotomy was performed but no intra-abdominal surgical pathology was detected. He was then referred to the nephrology team for evaluation and management of renal failure. At this point in time, the patient was well hydrated and was normotensive. His urine output was 1450 ml in 24 hours and was treated as a case of nonoliguric acute renal failure of uncertain etiology. He was managed conservatively by appropriate care of fluid, electrolytes and nutrition with uneventful course and progressive recovery of renal functions. By day six, the blood urea nitrogen and serum creatinine levels were within normal limits with normal urine output. However, the etiology of acute reversible renal failure remained elusive. While recovering from illness in the hospital, the patient confessed that he had been sniffing glue for kicks. He used to squeeze a 50 ml tube of glue named Citex in an empty Pepsi can and sniffed the vapours for hours to feel high. He said that he used to develop abdominal pain and vomiting after each episode of sniffing. In the past, the pain used to subside spontaneously in a few hours. In the present episode however, it was severe and compelled him to visit the hospital. The patient is presently under the care of a psychiatrist for psychotherapy
| Discussion|| |
The deliberate inhalation of volatile solvents including glue sniffing, now more commonly termed as volatile substance abuse (VSA), started in early 1960, with inhalation of model aeroplane glues. The practices have diversified to include the use of adhesive cements, aerosol paints, lacquer thinners, typewriter correction fluid and fuels.  These products contain a number of volatile substances including toluene, benzene, xylene, n-hexane, methylketones, and chlorohydrocarbons. Toluene is the main toxic agent involved in glue sniffing. 
Easy availability and quick feeling of 'kicks or high' with hallucinations, euphoria and dysinhibition similar to alcohol intoxication, are major factors for increasing the prevalence of VSA including glue sniffing.  Nephrotoxic injury is mainly due to toluene and its metabolite hippuric acid. 
A review of literature revealed that wide spectrum of renal diseases may develop in association with volatile substance abuse. They include: rhabdomyolysis, myoglobinemia,  acute tubular necrosis , distal renal tubular acidosis , anti-glomerular basement membrane antibody mediated glomerulonephritis  and interstitial nephritis.  Toluene leads to distal renal tubular acidosis by inducing permeability changes in the nephron leading to back ward leakage of secreted acids. Acid retention causes calcium mobilization, hypercalciuria and renal calculi. 
In our patient, the high urinary spot sodium during the non-oliguric phase and subsequent total renal functional recovery favored a diagnosis of acute tubular necrosis as the cause of acute renal failure. Tubular injury was due to direct toxic effect of toluene or its metabolites. In most of the cases, the diagnosis is obvious by positive history of glue sniffing. Lab analysis of blood and urine samples, collected up to 24 hours post-exposure, may be helpful if the diagnosis is in doubt. Treatment is usually supportive. Recovery of renal function normally occurs quickly once exposure has ceased. Temporary renal support may be needed in certain cases taking longer time for recovery.
Apart from nephrotoxicity, VSA can cause life-threatening injuries to various other systems of the body. These include solvent encephalopathy,  solvent psychosis,  cerebral infarction,  cerebellar dysfunction,  aplastic anemia,  fulminant hepatic failure,  pulmonary hemorrhage,  as well as sudden death caused by cardiac arrhythmias.  Adolescents from unhappy and alcoholic families are found to be most prone to glue sniffing and other volatile substances abuse. 
Glue sniffing as a cause of acute renal failure is not well recognized in the Middle East. Literature search including Saudi Med Base 1979-1999, as well as manual search of relevant Saudi and other Middle East Journals did not reveal any such case being reported.
The aim of reporting this case is to highlight that glue sniffing should be included in the differential diagnosis of any young patient presenting with unexplained acute renal failure. As glue sniffing causes systemic generalized poisoning apart from renal toxicity, the patient may present with multi-system involvement. As a rule, these patients need multi-modality treatment including de-addiction therapy as well as individual and group psychotherapy.
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Shiv K Saxena
Consultant Physician and Chairman, Department of Internal Medicine and Nephrology, Al Iman General Hospital, P.O.Box. 346225, Riyadh 11381