Acute renal failure (ARF) severely worsens prognosis of hospitalized patients. The most frequent cause of intrarenal ARF is transient or prolonged renal hypoperfusion (ischemia). Ischemia primarily affects the function and structure of tubular epithelial cells, which, in severe cases, is characterized by epithelial cell necrosis. Nevertheless, ischemia does not exclusively lead to alterations of epithelial cells but also causes interstitial inflammation and interstitial microvasculopathy. Both inflammation and microvasculopathy are particularly important in terms of postischemic kidney repair. Postischemic microvasculopathy is characterized by endothelial cell swelling with subsequent microvascular occlusion. Thus, reperfusion is inhibited (no-reflow phenomenon). Such endothelial cell dysfunction offers new therapeutic perspectives in ischemic ARF. Newer observations point towards the role of the so-called endothelial progenitor cells (EPCs) in the treatment of ARF. Systemic administration of EPCs to mice with bilateral renal ischemia mitigates postischemic endothelial cell dysfunction and protects animals from acute renal failure. 1. Introduction Acute renal failure (ARF) severely worsens prognosis of hospitalized patients. Approximately 1–5% of all patients treated in the hospital develop ARF [1]. The clinical significance of ARF results from its high mortality, which still today ranges from 30 to 70% [2]. ARF is categorized depending on its primary cause. Prerenal failure results from transient renal hypoperfusion. It is a functional response of a structurally intact kidney to hypoperfusion [3]. While postrenal ARF is caused by urinary tract obstruction with or without subsequent damage of renal tissue, intrinsic or intrarenal ARF is caused by diseases that either affect the glomeruli, the vasculature, the interstitium, or the tubules. The difference between prerenal and intrarenal failure due to hypoperfusion lies in the presence of structural tubular damage in the latter. The most frequent cause of intrarenal ARF in hospitalized patients is transient or prolonged renal hypoperfusion (ischemia reperfusion injury—IRI) [4–6]. Renal IRI is of particular importance in the setting of kidney transplantation [7]. Ischemia primarily affects the function and structure of tubular epithelial cells, which, in severe cases, is characterized by epithelial cell necrosis [8]. Nevertheless, IRI does not exclusively lead to alterations of epithelial cell function and structure but also causes interstitial inflammation and interstitial microvasculopathy (Figure 1).
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