Physiology Of Renal Hypothermia

Renal metabolic activities are predominantly aerobic and hence the kidney is susceptible to damage from warm ischemia. Almost immediately after renal arterial occlusion, adenosine triphosphates in the kidney cells break down to monophosphate nucleotides to provide energy for cellular integrity. With increasing duration of ischemia, there is influx of salt and water into the cell resulting in cellular edema and eventually cell death.

Canine studies have shown that warm ischemic intervals of up to 30 minutes can be tolerated by the kidney, with eventual full recovery of function. With greater periods of warm ischemia, there is significant immediate functional loss with either incomplete or absent delayed recovery of renal function. The proximal tubular cells are the most susceptible and show varying degrees of necrosis, while the glomeruli and blood vessels are generally spared. In humans, 30 minutes is the maximum tolerable period of warm ischemia, before permanent damage may ensue (1). Anecdotally, a solitary kidney has been shown to be more resilient to ischemic damage as compared to bilaterally normal kidneys. The exact mechanism remains uncertain.

A variety of techniques have been described to minimize warm ischemic damage due to hilar occlusion. These include preoperative and intraoperative hydration, minimize traction on the renal artery and intraoperative administration of mannitol. Hypothermia is the most commonly employed technique for protecting the kidneys from ischemic damage (2). Lowering renal temperature reduces energy-dependent metabolic activity of the cortical cells which leads to decreased consumption of oxygen and reduced breakdown of ATP. A negative effect of hypothermia is inactivation of the sodium-potassium pump at the cellular level, which ultimately allows salt and water to enter the cell. These effects are completely reversible at temperatures above 4°C. With further fall in temperature, formation of ice crystals and irreversible cell damage occurs. For practical purposes, a uniform temperature of 20°C to 25°C has been found adequate to maintain renal function even after three hours of arterial occlusion.

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