Alterations of Mitochondrial Properties in Folate Nephropathy

Abstract

Folate nephropathy was selected as a model to study renal mitochondrial response after tubular injury. 20 h after injection, ¹⁴C-leucine incorporation was suppressed to 20–30% of control, ¹⁴C-mannose incorporation was 63–78% greater than control while the activities of succinic dehydrogenase and monoamine oxidase were unaltered. By 40 h, ¹⁴C-leucine incorporation had been restored to control values. Also, at 20 h, ATPase activity sensitive to oligomycin inhibition had increased by 45–73%, whereas K⁺-stimulated ATPase activity was reduced in the experimental mitochondrial fractions. The results are discussed along with other studies of mitochondria in experimental renal disease.

Folic acid‐induced animal model of kidney disease

“…The first report of kidney injury induced by FA was published in Germany in 1969 137 . These studies led to the concepts of “renal folate toxicity” and “folate nephropathy” in 1970s 138–144 . Now, the procedures of FA‐induced kidney injury in mice and rats are well established and widely used.…”

“…137 These studies led to the concepts of "renal folate toxicity" and "folate nephropathy" in 1970s. [138][139][140][141][142][143][144] Now, the procedures of FA-induced kidney injury in mice and rats are well established and widely used. As outlined in Figure 1, in both mouse and rat models of acute kidney injury, a single injection of FA at a dosage of 250 mg/kg body weight intraperitoneally can cause AKI, [145][146][147] resulting in proteinuria and increased blood urea nitrogen (BUN) and creatinine.…”