Iron chelators do not reduce cold-induced cell injury in the isolated perfused rat kidney model.

Background: In vitro, cold-induced injury is an important contributor to renal tubular cell damage. It is mediated by iron-dependent formation of reactive oxygen species and can be prevented by iron chelation. We studied whether iron chelators can prevent cold-induced damage in the isolated perfused rat kidney (IPK) model both after cold perfusion (CP) and after cold storage (CS).

Preserved vascular reactivity of rat renal arteries after cold storage.

In cultured renal tubular cells hypothermia results in cell damage caused by iron-dependent formation of reactive oxygen species. It is unknown whether cold preservation affects function of renal vessels. Rat renal arcuate arteries were stored in a physiological salt solution at 4 degrees C for 24h and compared to control arteries (not stored).

Hypothermia causes a marked injury to rat proximal tubular cells that is aggravated by all currently used preservation solutions.

Cold preservation results in cell death via iron-dependent formation of reactive oxygen species, leading to apoptosis during rewarming. We aimed to study cold-induced damage (i.e.