Organic solvents, commonly used in the automobile industry, have been reported to lead to kidney injury. These involve almost any compartment of the kidney i.e. glomerulus, tubules or vasculature. Moreover, these substances also aggravate the progression of underlying kidney diseases (1–5). Occupational health hazards are the known contributors to morbidity and mortality of workers in the industry. The factors contributing to this risk include the extent of exposure, ventilation maintenance, access to fluid intake, etc. A paint reducer, an organic solvent frequently used in the automobile manufacturing and repair industry, is one such risk factor. Reducers are volatile solvents consisting of a mixture of organic compounds like aromatic hydrocarbons, halogenated hydrocarbons and naphtha, toluene, xylene, acetone, hexane, benzene and methyl isobutyl ketone etc. (6–8).

Toluene is a common constituent in many industrial solvents and has a known toxicity profile that shows environmental, accidental and intentional poisoning. Toluene finds its use in paints, paint reducers, polishing solvents, cleaning products, glues, adhesives, etc. (9). It is also a drug that substance abusers easily lay hands-on as an inhaled substance (glue sniffing). It leads to significant acute neurological effects such as euphoria followed by depression. The toxicity of toluene has been reported in the literature and impacts any organ system (10, 11). It is metabolised via cytochrome p-450 into hippuric acid and benzocaine acid and is excreted through the urine (11–13). It can also result in rhabdomyolysis, myoglobinemia, distal renal tubular acidosis (RTA) and acute tubular necrosis (14–18). The other clinical conditions that arise are a fulminant hepatic failure, lung haemorrhage, solvent encephalopathy, solvent psychosis, cerebral infarction, cerebellar dysfunction, cardiac arrhythmias and death (19–26). In this series, we report our experience with AKI because of toluene-based paint reducers.

Organic solvents, particularly toluene-based, have become a common occupational hazard and a frequent abused substance. These cause acute neurological symptoms, severe metabolic abnormalities and associated organ injury. One of the predominantly observed side effects of toluene intoxication is metabolic acidosis. Organic solvents can also result in liver injury and rhabdomyolysis. Some risk factors that suggest poor outcomes include altered mental status, renal failure and severe acidemia. Although our patients had both organ impairment and altered mental status, they managed to do well (11).

Toluene causes glomerular and tubular damage, Fanconi syndrome and hematuria. Proteinuria is common, although it seldom is in the nephrotic-range levels. Occupational exposure of toluene in patients with established glomerulonephritis is a known risk factor for progression to end-stage renal disease. Direct induction of acute tubular necrosis and acute oliguric renal failure are also associated with toluene intoxication (5, 15, 16, 27–29). Rhabdomyolysis results either because of direct toluene muscular injury or prolonged immobility. They are usually seen with ingestion of toluene, but is reported in patients with thinner intoxication by inhalation (5, 30–32). Moreover, electrolyte abnormalities like hypokalemia and hypophosphatemia can also result in rhabdomyolysis and hence AKI.

The muscular phosphate depletion from severe hypophosphatemia impairs ATP production, which leads to muscle injury by altering the oxygen-haemoglobin dissociation curve (33, 34). Type 1 distal RTA which is characterized by an inability to lower urine pH, despite acidemia results, in hyperchloremic metabolic acidosis with hypokalemia. The degree of hypokalemia is also an important factor and can lead to rhythm abnormality and or hypokalemic paralysis. The primary suggested mechanism in toluene-induced type 1 distal RTA is an inability of the distal tubule to excrete hydrogen ions and an increased production of hippuric acid by toluene metabolism (16, 35). Management of acute toluene-based solvent toxicity is largely conservative, and the measures taken are influenced by the severity of organ involvement. Broadly it involves correction of the electrolytes, acid-base and fluid abnormalities. The management focuses on aggressive potassium replacement, maintaining hydration and close monitoring of the cardiac rhythm. Large doses of bicarbonate and potassium replacement are often needed. Patients should be closely observed for the development of organ dysfunction. Rhabdomyolysis should be ruled out in patients particularly, with impaired renal parameters. A timely introduction of renal replacement therapy is needed. Mild transaminitis, which is reversible, has been previously reported in the literature (10, 32).

Organic solvent exposure may result in acute tubular necrosis, rhabdomyolysis, RTA and AKI irrespective of the route intake. Clinical suspicion of organ dysfunction and failure and timely induction of supportive care leads to good outcomes.