Renal Transplantation between HL-A Identical Donor-Recipient Pairs: <i>FUNCTIONAL AND MORPHOLOGICAL EVALUATION</i>

H. F. Seigler; J. C. Gunnells; R. R. Robinson; F. E. Ward; D. B. Amos; D. T. Rowlands; P. M. Burkholder; W. J. Klein; D. L. Stickel

doi:10.1172/JCI107147

Renal Transplantation between HL-A Identical Donor-Recipient Pairs: FUNCTIONAL AND MORPHOLOGICAL EVALUATION

H. F. Seigler, J. C. Gunnells Jr., R. R. Robinson, F. E. Ward, D. B. Amos, D. T. Rowlands, P. M. Burkholder, W. J. Klein, and D. L. Stickel

Published December 1, 1972 - More info

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Abstract

16 patients underwent renal transplantation from a sibling donor who was prospectively determined to be ABO compatible and HL-A identical with the recipient. Unidirectional mixed leukocyte reactions were performed; in each instance, lymphocyte stimulation in either direction was not observed.

The plasma creatinine 10-68 months after transplantation in these 16 patients ranged between 0.9 and 1.9 mg/100 ml. The creatinine clearance ranged from 48 to 113 ml/min, and the blood urea nitrogen (BUN) ranged between 12 and 35 mg/100 ml. Urine protein excretion varied from 0.11 to 1.86 g/day. Six patients exhibited no detectable clinical episodes of acute rejection; they were treated with azathioprine alone and each of them demonstrated normal or near normal renal histology when biopsy specimens were obtained more than 6 months after transplantation. Nine patients experienced acute rejection episodes that required the use of steroid therapy. The severity of these rejection episodes was variable; they included a mild reduction in renal function with an immediate steroid-induced restoration of function and eventual discontinuance of steroid therapy to severe reduction in function requiring prolonged and moderate doses of steroids without return to normal renal function. Renal histological observations in this group ranged from mild to marked cellular and structural changes which fit the criteria of the rejection. One patient demonstrated a gradual loss of renal function with heavy proteinuria. Biopsy of this allograft demonstrated the recurrence of original disease, i.e., lobular glomerulonephritis.

The marked variability in the clinical course and allograft morphology in these 16 patients could be explained by antigenic differences at non-HL-A loci. The presence of minor histocompatibility loci has been well documented in other mammalian species and they are most certainly present in man. The need for their identification and definition is stressed.

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