Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells.

By Jeremy S. Duffield, K. Park, L. Hsiao, V. Kelley, D. Scadden, T. Ichimura, Joseph V. Bonventre. Journal of Clinical Investigation, 2005

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Update on mechanisms of ischemic acute kidney injury. (2006, background): “First, the number of bone marrow–derived MSC that finally appear in the postischemic kidney is very small, and their detection has been fraught with technical false-positive results (116,117).”
Epithelial to Mesenchymal Transition induces cell cycle arrest and parenchymal damage in renal fibrosis (2015, unknown): “Chronic kidney disease is associated with inadequate cell cycle progression of the tubular epithelial cells, which arrest in the G2/M phase 25,26,43,44 .”
Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis. (2010, methodology): “To preserve native red fluorescent protein (RFP) epifluorescence which we found was quenched by prolonged fixation, some kidneys were fixed in PLP fixative (4% paraformaldehyde PFA , 75 mmol/L L-lysine, 10 mmol/L sodium periodate) for 1 hour or 2 hours at 4°C, cryopreserved in 18% sucrose, and froze”
Cellular and molecular mechanisms in kidney fibrosis. (2014, unknown): “Other markers have been proposed, including fibroblast specific protein–1 (FSP-1; also known as S100A4), heat shock protein–47, and vimentin, but studies have shown these to be highly unreliable markers of myofibroblasts (14–18).”