Volatile solvent abuse caused glomerulopathy and tubulopathy in street children


Olgar S., ÖKTEM F., Dindar A., KILBAŞ A., Turkoglu U. D. , ÇETİN H. , ...More

HUMAN & EXPERIMENTAL TOXICOLOGY, vol.27, no.6, pp.477-483, 2008 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 27 Issue: 6
  • Publication Date: 2008
  • Doi Number: 10.1177/0960327108092292
  • Title of Journal : HUMAN & EXPERIMENTAL TOXICOLOGY
  • Page Numbers: pp.477-483

Abstract

Substance misuse among street children is a significant problem in developing countries. Volatile substances are the most abused agents. According to case reports, chronic renal diseases are common among substance-abusing street children. In this study, we examined the renal findings of 42 volatile substance-abusing street children and compared them with results from 49 healthy children (control). The street children's weight, height, and blood pressure were lower than the controls' (P < 0.05). However, their blood alkaline phosphatase and creatinine phosphokinase levels were higher (P < 0.05), and total blood protein, creatinine, and phosphorus levels were lower than the controls' (P < 0.05). Furthermore, the street children's glomerular filtration rates were within normal limits (P < 0.05), their urinary N-acetyl-beta-glucosaminidase (NAG), beta(2)-microglobulin, microlbumin, protein, calcium, phosphorus, sodium, potassium, and chloride excretions were higher, and tubular phosphate reabsorption were lower than the controls' [P < 0.05). Volatile substances have been charged with causing distal tubular disease, but increased urinary protein, NAG, beta(2)-microglobulin, microalburnin, and electrolyte excretions also result from glomerular, proximal, and distal tubular influences. We believe that increased volatile substance products in the renal parenchyma are responsible for glomerular and tubular damage. Volatile substance-abusing street children should be examined for glomerular and proximal tubular function and distal tubular acidosis.