Three cases are described in which renal cell carcinomas occurred in renal allografts. In the first 2 cases, the renal cell carcinomas were found accidentally in the recipient room. The tumors were resected at the time of transplantation and the kidneys were left in place. The patients died 10 and 3 years after transplantation, respectively, with well functioning renal allografts and without any tumor manifestations. In the 3rd case, a renal cell carcinoma was found 3 yr after transplantation in a cadaveric allograft from a donor with a brain tumor. A transplantectomy was performed and the patient was regrafted after 1 yr and now has an excellent renal function and no signs of tumor manifestations.

The efficacy and toxicity of cyclosporine (CsA) treatment for graft-versus-host disease (GVHD) was studied in 53 bone marrow transplant recipients. No correlation was found between acute or chronic GVHD and CsA dosage (daily or cumulative) or CsA plasma levels. Acute nephrotoxicity developed in 63% of the patients. Patients with nephrotoxicity had significantly higher CsA plasma levels during the first month after transplantation compared with patients without nephrotoxicity (P less than 0.05) although the cumulative CsA doses did not differ. Children had significantly fewer episodes of nephrotoxicity compared with adults (P less than 0.01). In spite of this, children received a significantly higher cumulative CsA dose (P less than 0.001). However, CsA plasma levels did not differ between children and adults, suggesting a difference in availability or elimination of the drug. Hypertension developed in 28% of the patients. Hypertensive patients tended to be younger compared with normotensive patients (P = 0.07). Nephrotoxicity tended to be less common in patients with hypertension (P = 0.06). No correlation existed between hypertension and CsA dose or CsA plasma levels. In conclusion, no correlation was found between CsA dose and GVHD or CsA toxicity, and in the single patient CsA plasma levels were of no value in predicting side effects of CsA treatment.

In 92 renal transplant recipients, serum or plasma levels of neopterin were significantly elevated during pretransplant uremia, rejection, cyclosporin A induced nephrotoxicity and cytomegalovirus (CMV) infections. In patients with normal serum creatinine (less than 115 mumol/l) 71% had elevated serum neopterin levels. None of 19 cyclosporin A treated patients with stable renal function had a normal level of neopterin compared to 50% for patients treated with azathioprine (p less than 0.05). Due to the dependency on renal function the serum levels of neopterin could not distinguish between rejection and cyclosporin A induced nephrotoxicity. Marked increases in neopterin levels were seen during infections and especially during CMV infection. Determination of neopterin levels may be helpful in the diagnosis of CMV infection.

Following pretreatment with at least 5 blood transfusions to 58 nontransfused uremic patients, 23 (40%) formed lymphocytotoxic antibodies against B cells and 9 (15%) against T cells as well. Significantly more (p less than 0.01) patients with polycystic kidney disease (6/16) formed T cell antibodies compared to patients with other diseases. The presence of antibodies delayed kidney transplantation, since significantly more (p less than 0.01) patients without antibodies (28 out of 35) received kidney grafts than patients with antibodies (9 out of 23). 5 patients received kidney grafts despite the occurrence of antibodies against donor B cells, but 3 of the patients lost their grafts within 1 month. In vitro lymphocyte subpopulations were studied in 4 patients before and after each of the planned blood transfusions. No persistent changes in lymphocyte responses to phytohemagglutinin and in mixed lymphocyte culture were seen. T cell subpopulations identified by monoclonal antibodies were unchanged, but the proportion of macrophages/monocytes (OKMl-positive cells) increased from 22 +/- 6 to 46 +/- 10% (p less than 0.05).

A group of 28 untransfused uremic patients was given five or more units of stored blood as pretreatment for kidney transplantation; 9 patients formed lymphocytotoxic antibodies against B cells and 1 patient developed multispecific antibodies against both B and T cell panels (greater than 80% reactivity). During the same period 22 previously transfused patients received up to five transfusions as pretreatment for kidney transplantation. B cell antibodies were formed by 10 patients, and 4 of these patients also formed T cell antibodies, 2 with broad reactivity. Cellular immune reactivity in vitro was studied on frozen cells from 17 randomly chosen patients. After five blood transfusions no significant changes were seen in blood lymphocyte responses to phytohemagglutinin (PHA), Concanavalin A (Con A), or in mixed lymphocyte cultures (MLC) and cell-mediated lympholysis (CML). After transfusion 3 patients got Non-A, non-B hepatitis and were withdrawn for up to six months from the transplantation list because of increased S-ALAT and S-ASAT. Of the 50 patients, 27 have received kidney grafts, 6 out of 20 who were sensitized, and 21 out of 30 who were nonsensitized. Because of positive crossmatches no patient with multispecific T cell antibodies has received a graft. We conclude that our transfusion regimen for kidney recipients has rendered barely one-third of the patients sensitized (mostly against B cells) and 3 out of 50 hypersensitized. No effect on T cell reactivity could be seen following five planned transfusions. Because fewer patients with antibodies received grafts (30% with antibodies, as compared with 70% without [P less than 0.01]) the blood transfusions seem to have led to a selection effect.

ABSTRACT. A 17‐month‐old boy who contracted a severe generalized BCG infection is reported. He was treated for 2 years with streptomycin, isoniazide and rifampicin and is now, at the age of 5 years, apparently cured. The boy had an unexplained discrepancy between humoral and cellular PPD reactivity for several years, but conventional immunological studies including plasma immunoglobulin levels, blast transformation as well as MLC reactivity were all normal. This is, to the best of our knowledge, the first child reported who has survived a generalized BCG infection.

The impact of renal graft survival of a low relative response (RR) in mixed lymphocyte culture (MLC) and HLA-D/DR compatibility was analyzed. Ninety-five recipients and donors of cadaver kidneys and 58 intrafamilial, HLA-haploidentical, recipient-donor pairs in a Stockholm series constituted the case material. The gene frequencies of and the correlation coefficients between the HLA-D/DR assignments were calculated from an extended material of about 400 individuals, all recipients or donors of renal grafts in Stockholm. Close correlation between the D and DR assignments existed. The combined gene frequencies of the detected D/DR antigens were 0.67 and 0.08. The RR values in the MLC tests were widely scattered, but lower medians were found in the better D/DR-matched groups. The 1-year survival of cadaveric grafts was 69% when the RR values in the MLC between recipient and donor were below 55 and 49% when the RR values were above 55%. The difference was statistically significant (P less than 0.05). Also, significantly higher graft survival rates were obtained in transplants groups where the recipient and donors were well matched for the D and DR antigens. In the transplant groups where no D/DR incompatibility existed, the 1-year graft survival was 93 and 89%, respectively, when the RR values in the MLC tests between recipients and donors were below 55%. We concluded that a close correlation existed between cellular and serological HLA-DS typing. A beneficial effect was noted on graft survival of matching for these antigens.