Newborn Renal Tubular Acidosis Associated with Prenatal Maternal Toluene Sniffing

Erramouspe, John; Galvez, Renata; Fischel, David R.

doi:10.1080/02791072.1996.10524392

Cited by 22 publications

(5 citation statements)

References 15 publications

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“…15 In a case report by Erramouspe et al, it was established that the infant of a mother who has smelled dye thinner containing toluene during her pregnancy was born with renal tubular acidosis. 16 The reason for renal toxicity due to smelling of adhesives seems to be toluene. Because of abuse, distal renal tubular acidosis, metabolic acidosis with high anion gap, Fanconi syndrome, urolithiasis, glomerulonephritis, and Goodpasture syndrome can develop.…”

Section: Discussionmentioning

confidence: 99%

Histopathological Changes of Rat Kidney with Exposure to Chronic Thinner Inhalation

Toros¹,

Toros

Aker

et al. 2011

Renal Failure

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Introduction: Organic solvents are liquid substances commonly used in everyday life at home and in industrial workplaces. These solvents are found primarily in paint as thinner. Because other narcotics are hard to find, thinner is used as a narcotic especially among youngsters of low socioeconomic level. The aim of this study is to determine the histopathological changes of rat kidney with exposure to chronic thinner inhalation. Methods: Randomized trial -the study was conducted at the animal care facility of Haydarpasa Numune Education and Research Hospital. Forty albino Wistar male rats were used throughout the experiment. Three groups of rats inhaled thinner in a glass cage for 1, 3, and 5 weeks, respectively. Ten rats inhaled only the air in the room as the control group. Results: We observed the development of inflammation in the kidneys that became more remarkable as exposure time extended. Development of inflammation because of thinner apparently differed between the groups of week 1 and week 5. There was no difference in granuloma development. If the experiment lasted longer, there might have been granuloma development. Conclusions: Based on histopathological evaluations, it was shown that exposure to chronic thinner inhalation causes detectable damage on the kidney, which becomes more prominent as exposure period extends. As we established disorders in movement and consciousness in the rats during thinner inhalation, we can conclude that thinner also has a damaging effect upon the central nervous system.

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Section: Discussionmentioning

confidence: 99%

Histopathological Changes of Rat Kidney with Exposure to Chronic Thinner Inhalation

Toros¹,

Toros

Aker

et al. 2011

Renal Failure

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“…Exposure to large amounts of toluene can cause injury, even sudden death [15][16][17]. Therefore, analysis of metabolites in organic solvents abusers will be crucial in the forensic field because organic solvents are rapidly metabolized.…”

Section: Discussionmentioning

confidence: 99%

1H NMR spectroscopic identification of a glue sniffing biomarker

Kwon¹,

Kim²,

Kim³

et al. 2011

Forensic Science International

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“…12 The drugs associated with RTA and hyperkalemia include potassium-sparing diuretics, such as amiloride, ␤ adrenergic blockers, angiotensin converting enzyme inhibitors, cyclosporin A, and nonsteroidal anti-inflammatory drugs. 13,23 Several reports have been made of RTA in humans associated with the use of trimethoprim/sulfamethoxazole. [24][25][26][27] Trimethoprim/sulfamethoxazole is widely used in horses for the treatment of acute and some long-term infections, such as equine protozoal myelitis.…”

Section: Discussionmentioning

confidence: 99%

“…12 RTA has also been reported as a complication of inhalation of volatile organic solvents containing toluene such as acrylic paints, glues, adhesives, paint thinners, varnishes, and shoe polishes. [12][13] Three types of RTA have been described in humans: types I, II, and IV. 12 Type I or distal occurs when distal tubules are unable to excrete hydrogen ions with a resultant inability to acidify the urine.…”

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confidence: 99%

Renal Tubular Acidosis in Horses (1980–1999)

Aleman

Kuesis

Schott

et al. 2001

Veterinary Internal Medicne

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Renal tubular acidosis (RTA) is characterized by altered renal tubular function resulting in hyperchloremic metabolic acidosis. The purpose of the study was to describe RTA in 16 horses. No breed or sex predilection was found. The mean age at onset of the disease was 7 years of age. The type of diet had no apparent effect on development of RTA. The most common clinical signs were depression, poor performance, weight loss, and anorexia. Initial blood work revealed a marked hyperchloremic metabolic acidosis in all horses and a compensatory respiratory response in most horses. Sixty-three percent (10/16) of the horses had some evidence of renal damage or disease. Initial treatment consisted of large amounts of sodium bicarbonate given intravenously and orally for the prompt correction of the acidosis. Response to treatment was largely dependent on the rate of sodium bicarbonate administration. Long-term oral supplementation with NaHCO 3 was required for the maintenance of normal acid-base status in individual horses. Recurrence of RTA was noted in 56% (9/16) of the horses. Horses with evidence of renal disease had multiple relapses. RTA should be considered as a differential diagnosis in horses with vague signs of depression, weight loss, and anorexia. The pathogenesis of RTA in horses remains uncertain, but prompt recognition and early aggressive intravenous sodium bicarbonate therapy followed by long-term oral supplementation seem to be important to successful management.Key words: Hyperchloremic metabolic acidosis; Renal disease; Sodium bicarbonate. Metabolic acidosis is characterized by a decrease in pH as the result of increased endogenous production or accumulation of acid, or by the loss of bicarbonate via the gastrointestinal or urinary tract. The most common causes of metabolic acidosis with an increased anion gap (AG) include lactic acidosis, ketoacidosis, and hypovolemic shock.1 Other causes of metabolic acidosis include ingestion of compounds such as salicylate, methanol, ethylene glycol, or paraldehyde, which result in the accumulation of exogenous anions. 2Hyperchloremic metabolic acidosis with a normal AG is associated with bicarbonate loss from diarrhea or renal causes, such as renal tubular acidosis (RTA).1 Hyperchloremia develops consequent to enhanced renal conservation of chloride in the face of bicarbonate loss.1 RTA, characterized by abnormal tubular function, has been described in humans, dogs, cats, and horses. [3][4][5][6][7][8][9][10][11] In humans, RTA may be a primary condition inherited as an autosomal dominant trait.12 Further, RTA may develop secondary to a variety of conditions such as kidney disease, obstructive uropathies, nephrocalcinosis, cirrhosis, drug-or toxin-induced nephropathies, and autoimmune diseases.12 RTA has also been reported as a complication of inhalation of volatile organic solvents containing toluene such as acrylic paints, glues, adhesives, paint thinners, varnishes, and shoe polishes. 12-13Three types of RTA have been described in humans: types I, II, and IV.12...

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Newborn Renal Tubular Acidosis Associated with Prenatal Maternal Toluene Sniffing

Cited by 22 publications

References 15 publications

Histopathological Changes of Rat Kidney with Exposure to Chronic Thinner Inhalation

Histopathological Changes of Rat Kidney with Exposure to Chronic Thinner Inhalation

1H NMR spectroscopic identification of a glue sniffing biomarker

Renal Tubular Acidosis in Horses (1980–1999)

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