Dichloroacetate treatment accelerates development of pathology in rodent autosomal recessive polycystic kidney disease.

American Journal of Physiology, Renal Physiology

PubMedID: 25234313

Gattone VH, Bacallao RL. Dichloroacetate treatment accelerates development of pathology in rodent autosomal recessive polycystic kidney disease. Am J Physiol Renal Physiol. 2014;307(10):F1144-8.
Dichloroacetate (DCA) is a toxicant by-product from the chlorination disinfection process for municipal water. The levels would not affect people with normal renal and liver function. However, people with impaired renal or liver function may have an increased susceptibility to DCA toxicity as those are the organs affected by DCA. People (and rodents) with polycystic kidney disease (PKD) are polyuria, drink more fluids and have both renal and liver pathology. In PKD, renal tubules and biliary epithelial cells proliferate to form cysts that can eventually cause renal and/or liver dysfunction. Therefore, PKD may be a predisposing condition with an increased sensitivity to DCA toxicity. PCK rats are an orthologous model of human autosomal recessive PKD and were treated with 75mg/l of DCA in their drinking water. Male and female PCK and male Sprague Dawley rats were treated from 4 to 8 weeks of age, after which the severity of the renal and liver pathology induced by DCA were assessed. Only male PCK rats were adversely affected by DCA treatment, with an increase in the severity of renal cystic disease evinced by an increase in cystic enlargement and proteinuria. In conclusion, the chlorination byproduct DCA may adversely affect those with a preexisting renal disease, especially those who are polydipsic like those with PKD.