Intensive care and immediate follow-up of children after renal transplantation

Abstract

The renal allograft provides a distinctive human experiment where a healthy kidney is denervated, subjected to preservation ischemia, and later engrafted into new milieu with abnormal electrolytes and hormones. Optimal postoperative management depends on a thorough understanding of peritransplant physiology. The kidney has extensive adrenergic innervation supplied by preganglionic sympathetic nerves originating from T6-L2 and postganglionic adrenergic vasomotor fibers. Denervation of the renal artery in normal kidneys results in ipsilateral natriuresis, diuresis, and impaired ability to increase renin production in response to low-sodium diet. Denervation is not permanent as reinnervation starts within 1 to 3 months and is complete by 6 months following engraftment. Preservation injury, when moderate in severity, can result in a spectrum of tubular transport defects. Cold ischemia injury afflicts the proximal tubule and results in isolated glucosuria, aminoaciduria, hyperphosphaturia, acidosis, or more generalized transport defect (Fanconi’s syndrome). Preservation injury can also cause several distal tubular transport defects resulting in acidosis and decreased urinary concentration. Severe ischemia could result in acute tubular necrosis (ATN) and early graft dysfunction. Tubular injury, residual osmolar load from pretransplant renal failure, intraoperative mannitol, and atrial natriuretic factor result in copious urine flow. Hypokalemia and hypomagnesemia may follow the diuresis. Residual hyperparathyroidism from renal failure prior to transplant may lead to increased serum calcium and decreased serum phosphorus usually resolving within 18 months.