Folic Acid Kidney Fibrosis Model
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Chronic kidney diseases result from recurrent or progressive injuries in glomeruli, tubules, interstitium and/or vasculature. In order to study pathogenesis, mechanisms and effects of interventions, many animal models have been developed, including spontaneous, genetic and induced models. We have established a folic acid nephropathy model. In this model, folic acid induces interstitial kidney fibrosis. High dosages of folic acid (250µg/g BW) given IP in mice induces folic acid crystals rapidly with tubular necrosis in the acute phase (1–14 days) and patchy interstitial fibrosis. Folic acid renal injury is induced both by crystal obstruction and direct toxic effect to tubular epithelial cells.
The folic acid-induced kidney fibrosis model can be run in either rats or mice. Typical protocol lengths are 14 days. In addition to the markers of kidney damage shown above, studies also typically involve histology and/or hydroxyproline as a biomarker of kidney fibrosis.