The theory that cancer may arise under conditions of reduced immune capacity is supported by observations of humans with immune deficiencies such as occur following organ transplants. However, no study on humans has been done in which the reference population was the same as that in which the cancer cases arose and in which there was a sufficiently long period of follow-up. Information on 5,692 Nordic recipients of renal transplants in 1964-1982 was linked with the national cancer registries (1964-1986) and population registries. Person-years at risk were calculated from the date of first transplantation until death or the end of the study period and were multiplied by the appropriate age- and calender-specific incidence rates to obtain the expected numbers of cancers. Standardized incidence ratios (SIR) were calculated after stratification by a number of recorded variables. Altogether, 32,392 person-years were accrued, and 471 cancers occurred, yielding overall SIR of 4.6 (95% CI, 4.0 to 5.2) for males and 4.5 (95% CI, 4.0 to 5.2) for females. Significant overall 2- to 5-fold excess risks in both sexes were seen for cancers of the colon, larynx, lung and bladder, and in men also for cancers of the prostate and testis. Notably high risks, 10-fold to 30-fold above expectation, were associated with cancers of the lip, skin (non-melanoma), kidney and endocrine glands, also with non-Hodgkin's lymphoma, and in women also with cancers of the cervix and vulva-vagina. Among a number of donor and recipient variables studied, including tissue types and compatibility (ABO, HLA, DR), age below 45 years at the time of transplantation was the most important determinant for increased risk at most sites. Kidney transplantation increases the risk of cancer in the short and in the long term, consistent with the theory that an impaired immune system allows carcinogenic factors to act. The tumor risk is small in comparison with the benefits of transplants, but patients should be followed up for signs of cancer.

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Nineteen consecutive patients receiving renal transplants underwent prospective evaluation of their calcium homeostasis for 1 year after transplantation to characterize indices of hyperparathyroidism (HPT) amelioration. All but one underwent dialysis, and six had vitamin D supplementation before grafting. The rapid falls in serum creatinine concentrations and increased creatinine clearances the first weeks after grafting were accompanied by rapidly reversed hypercalcemia and hypermagnesemia, induced hypophosphatemia, maintained parathyroid hormone (PTH) excess and calcitriol deficiency, and decreased alkaline phosphatases. At 3 months when the serum calcitriol had started to rise, serum PTH levels were the lowest and parathyroid responses to induced hypocalcemia the least abnormal. This was coupled to peaks in serum calcium, 24-hour urine calcium excretions, and serum alkaline phosphatase levels. All patients had subnormal creatinine clearances at the study end, and normal serum PTH occurred in only seven of them. Arbitrary subgrouping of the material was performed according to posttransplant creatinine clearance and serum PTH levels. More satisfactory graft function related to lower serum PTH values and less abnormal parathyroid responses to induced hypocalcemia, earlier and higher rises in serum calcitriol, and higher urine calcium excretion. Patients with mild HPT at the study end generally had higher creatinine clearance, lower serum PTH, calcium, and alkaline phosphatase values, and lower urine calcium excretion. Moreover, they had fewer prevalent signs of radiologic bone involvement before grafting. These temporal diversities in conjunction with the variable graft function and intensity of immunosuppression provide a complex interaction in renal transplant recipients, which should be considered in the light of improved function of the PTH/PTHrP receptor in bone and kidney and cation receptors in the parathyroid and kidney.