Living donor nephrectomy is managed with:
|C||Heparinised solution at 4°C|
a. Warm ischemic injury is due to failure of oxidative phosphorylation and cell death due to adenosine triphosphate (ATP) depletion .
b. ATP is required for the cellular sodium-potassium pump to maintain a high intracellular concentration of potassium and a low internal concentration of sodium.
c. When the sodium-potassium pump is impaired, sodium chloride and water passively diffuse into the cells, resulting in cellular swelling and the “no-reflow” phenomenon after renal revascularization.
d. Cellular potassium and magnesium are lost, calcium is gained, anaerobic glycolysis and acidosis occur, and lysosomal enzymes are activated. This results in cell death.
e. During reperfusion, hypoxanthine, a product of ATP degradation, is oxidized to xanthine with the formation of free radical scavengers that cause further cell damage.
a. Cellular energy requirements are significantly reduced by hypothermia.
b. This is done by surface cooling, hypothermic pulsatile perfusion, or flushing with an ice-cold solution followed by cold storage.
c. Making the flush solution slightly hyperosmolar with impermeant solutes such as mannitol, lactobionate, raffinose, or hydroxyethyl starch helps prevent endothelial cell swelling and the “no-reflow” phenomenon.
d. When the sodium-potassium pump is impaired, there is passive transfer of ions across the cell membrane; and if the electrolyte composition of the flush solution is nearly the same as that inside the cell, electrolyte balance will be maintained.