Transplantation Delayed Graft Function

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Transplantation of cadaveric kidneys is beset with a significant problem with the potential of adversely affecting transplant outcome. Difficulties derive from the periods of warm and cold ischemia that precede transplantation. The incidence of delayed graft function (defined as failure of the graft to function promptly following transplantation), usually requiring dialysis, varies widely. It may be encountered in as few as 10% of patients in some programs, but in as many as 50% of patients in others. When the effects of delayed graft function are analyzed it can be shown that it usually reduces 1-year graft survival by 10% or more and reduces the half-life of the graft by nearly 3 years. A number of regimens designed to ensure prompt graft function have been employed by various organ harvesting and transplant teams, usually involving the use of vasodilators such as calcium channel blockers, blood volume expanders such as saline solutions and hyperoncotic albumin, and diuretics such as furosemide and mannitol. Despite the many papers written on the subject there have been few that report prospective and randomized studies. Two of the best studies were authored by the same group [45, 46], who first investigated the importance of hydration in a prospective trial examining the effects of restricted fluid

TABLE 1 Effects of Moderate Hydration and Mannitol on Graft Function"





(ml ± SD)




1059 ± 371




1548 ± 622




2529 ± 675


"Data from Tiggeler [45].

"Data from Tiggeler [45].

infusion (Group 1 ), restricted fluid infusion along with 250 ml of 20% mannitol (Group 2), and moderate hydration together with 250 ml of 20% mannitol [45]. The results, showing the volume of fluid infused (V) and the incidence of acute tubular necrosis (ATN) are shown in Table 1. It can be seen that hydration with 2.5 liters of fluid and administration of mannitol, 250 ml of 20% immediately before the release of the vascular clamps, greatly reduced the incidence of ATN. The authors reported that this treatment also decreased the number of dialyses, radionuclide scans, ultrasound studies, transplant biopsies, and rejection episodes in the first 3 months post-transplantation.

In a subsequent study the same authors [46] investigated whether hydration alone, without mannitol, was sufficient to prevent ATN in the setting of either cyclosporine (CS) or azathioprine (AZ). Patients were randomly allocated to treatment with moderate hydration (2.5 liters) with or without mannitol (patients not receiving mannitol received glucose instead). The results are shown in Table 2, wherein the hydration and the hydration plus mannitol groups are designated H and H+M, respectively. It is clear from these studies that hydra-

TABLE 2 Effects of Moderate Hydration, with or without Mannitol, on Graft Function"

H 32 54

H 34 44

"Data from van Valenberg [461. *P < 0.01. **P < 0.05.

tion and mannitol, but not hydration alone, produced a highly significant reduction in the incidence of ATN. When the two immunosuppression groups are combined the difference in ATN becomes even more significant (P < 0.001).

The foregoing studies demonstrating the usefulness of mannitol in renal transplantation are in sharp contrast to those discussed under Prevention above. The reason(s) for this discrepancy is (are) elusive. One important difference between the transplanted kidney and the native kidney is the fact that the former is denervated. Whether mannitol can induce a neurally mediated injury in the intact kidney but fails to do so in the denervated transplanted kidney remains to be determined.

The experience with furosemide in preventing ATN in the transplanted kidney has been disappointing. Infusion of 200-400 mg furosemide just before restoration of renal circulation in kidney transplant recipients given mannitol did not prevent acute renal failure nor did it reduce the need for dialysis [23]. Our own observations strongly suggest that the intraoperative infusion of furosemide significantly complicates the postoperative care since it may cause massive diuresis which requires massive fluid replacement and careful and frequent monitoring of the serum electrolytes, especially K+ and Mg2+. Finally, the potential for developing pulmonary edema should be considered when using OKT3 for induction of immunosuppression. This monoclonal antibody is known to precipitate noncardiogenic pulmonary edema in overly hydrated patients.

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