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Eight renal allograft recipients were examined on 31 occasions following administration of 99mTc sulfur colloid and 67Ga citrate. Transplant accumulation of each agent was compared and collated with the clinical diagnosis. The procedures matched in 25 instances (81%). Gallium accumulated in the graft producing a false positive result in 2 instances of acute tubular necrosis with anuria, and failed to accumulate within the graft in one case of chronic rejection and in 2 instances of acute rejection. Both radioagents failed to accumulate in 3 patients with acute rejection following heparin therapy. These data indicate that 99mTc sulfur colloid is superior to 67Ga citrate in establishing the diagnosis of transplant rejection and also provides more timely information.

Enzymatic analysis of the venous effluent of ischemically injured kidney failed to predict accurately the ability of an isochemically injured kidney to support life. Postoperative serum assay of lactic dehydrogenase (LDH) is of value in the assessment of the functional status of the kidney and correlates with response of the rejection episode to immunosuppression. However, by itself it cannot be a sole guide to withholding of therapy. Successful treatment is associated with a decline in LDH level, and failure to return to base line serves as a guide to irreversibility of the rejection reaction.

A series of 125 renal transplants were analyzed in order to ascertain the characteristics of accelerated allograft rejection. An intense accelerated rejection could be identified within the first five days in 12 of 67 transplants (18%) with good immediate renal function. Accelerated rejection differed from the usual acute rejection reaction by higher fever, increased duration and intensity of the rejection, and increased difficulty in reversing the reaction. Accelerated rejection was reversible and associated with satisfactory renal function one year posttransplant in 58% of patients. Lymphocytotoxic and heterophil antibodies in preoperative serum and eluates of removed kidneys were not present. Contrary to recent reports, accelerated renal allograft rejection is a potentially reversible process and not necessarily due to humoral antibody presensitization.

The diagnostic accuracy, ease, and technical feasibility of imaging with 131I-or 125 I-fibrinogen, 99mTc-sulfur colloid, and 67 Ga-citrate in renal transplant rejection are compared. Radiofibrinogen data resulted from literature review, radiocolloid data from 125 studies in 52 transplant patients, and gallium citrate data from 24 examinations in seven renal transplant patients performed simultaneously with the radiocolloid studied. Specificity of graft labeling during rejection appears to be similar with radiofibrinogen, 99mTc-sulfur colloid, and 67Ga-citrate. For routine clinical use 99mTc-sulfur colloid surpasses radiofibrinogen and radiogallium because of its better imaging qualities with a permissible radiation dose, leading to better separation of positive and negative results. The 99mTc-sulfur colloid accumulates in areas of intravascular fibrin thrombosis in acute and chronic rejecting renal transplants. Hence, the mechanisms for accumulation of 99mTc-sulfur colloid and labeled fibrinogen in rejecting transplants would seem to be similar. Such physiologic properties as rapid blood clearance and such physical properties as short physical half-life combine to produce reliable graft visualization with adequate definition, thus favoring 99mTc-sulfur colloid as the single agent of choice for clinical evaluation of renal transplant rejection at this time.

Renal transplant accumulation of 99m-Tc sulfur colloid was evaluated in 41 patients. Ninety-five examinations were performed comparing transplant with bone marrow activity and clinical or pathological diagnosis. 99m-Tc sulfur colloid accumulated in acute or chronic rejection as long as the vascular supply of the grafted kidney was not severely impaired. Accumulation was marked in chronic rejection, slight in acute rejection and absent in normally functioning transplants or in those with acute tubular necrosis. In the 10 dog models, no accumulation was seen in autografted transplants and early accumulation was demonstrated within the hyperacutely rejecting kidneys of allografted dogs.

The relationship between serum lactic dehydrogenase (SLDH) values and renal allograft rejection was examined in the dog and in man. Nine dogs with renal allografts and four with autografts had similar maximal elevations of SLDH during the first five postoperative days (mean, 420 +/- 213 and 433 +/- 80 I.U. per liter, respectively). During rejection of the allografts between days 7 and 14 the maximum SLDH was 810 +/- 285 I.U. per liter, and in autografts the peak SLDH was 233 +/- 22 I.U. per liter (p less than 0.01). The isoenzyme pattern of maximum SLDH during rejection was prominent in LDH5 and corresponded with renal tissue LDH isoenzyme composition. In 93 episodes of initial acute human renal allograft rejection reactions, the SLDH peaked above 500 I.U. per liter in 23 cases and remained below 500 I.U. per liter in 70 cases. SLDH levels above 500 I.U. per liter were associated with complete rejection of the kidney in 91 percent of patients and SLDH levels persistently below 500 I.U. per liter corresponded with reversal of rejection reaction in 99 percent of patients (p less than 0.01). Marked SLDH elevation is associated with severe, usually complete renal allograft rejection and may be useful in identifying patients with irreversible rejection reactions.