The endothelial damage of pulsatile renal preservation and its relationship to perfusion pressure and colloid osmotic pressure.

To evaluate the effects of pulsatile preservation, 34 heterotopic renal autografts with immediate contralateral nephrectomy were divided into four groups with either the pulsatile preservation or cold storage technique. Group I had pulsatile preservation with plasma-albumin perfusate at a mean pressure of 60 mm. Hg and a colloid osmotic pressure (COP) of 20 to 50 cm. H2O. Group II had pusatile preservation with the same plasma-albumin perfusates as in Group I, but at a mean pressure of 30 mm. Hg. Group III had pulsatile preservation with albumin-phosphate buffer solution at a mean pressure of 30 mm. Hg. Group IV used cold storage technique. Group I demonstrated severe endothelial destruction and denuding of basement membrane. The changes were inversely related to COP. None of these kidneys functioned and, following transplantation, had persistent severe tubular damage and plugging of glomerular capillary loops with platelets, fibrinogen, and white cells. In Groups II and III, there were minimal changes, consisting of widening of the endothelial pores and focal endothelial damage. All of these kidneys functioned following reimplantation with minimal ultrastructural alterations. Group IV had no glomerular changes following preservation or following transplantation. All preservation techniques produced proximal tubular damage. There is a definite mechanical lesion associated with pulsatile preservation, which can be minimized by utilizing low perfusion pressures and solutions of high colloid osmotic pressure and which has the potential of producing a picture resembling hyperacute rejection following transplantation.