Repair and recovery of acute kidney injury

Acute kidney injury (AKI) may result from ischemic or toxic insult to renal tubular cells. The cellular damage involves several forms of injury: acute inflammatory response, sublethal damage, cell death through apoptosis and necrosis, and shedding of cells into the tubular lumen. The underlying mechanism of these different forms of injuries comprises of a complex interplay of inflammatory cytokines/chemokines, reactive oxygen species, and apoptotic factors. However, the kidney has a remarkable capacity to repair itself following AKI and thereby recover renal functions. The recovery process is associated with repopulation of damaged renal tubules by proliferation of tubular epithelial cells by several mechanisms.The mechanisms underlying cellular proliferation and regeneration are incompletely understood. The cells potentially involved in the regenerative process after AKI include endogenous renal tubular cells, ‘organ-specific’ adult renal stem cells, and bone marrow-derived (BMD) stem cells. However, the relative roles of each of these populations of cells in the recovery process after AKI remains uncertain. Surviving renal tubular epithelial cells proliferate and migrate to the denuded areas of the tubule. Renal stem cells also proliferate and contribute to repopulation of the renal tubular epithelium. Emerging evidence suggest an extremely important role of BMD mesenchymal stem cells (MSC). These cells do not proliferate and repopulate the tubular epithelium rather they contribute in the recovery and regeneration process predominantly by secreting several types of growth factors, such as insulin-like growth factor-1 (IGF-1) and others. These growth factors enhance proliferation of tubular epithelial cells. Employing allogenic MSCs may hold the potential for future prevention and early treatment of AKI in clinical setting.