Since endogenous 1:25 vitamin D (1:25VD) is principally involved with involution of secondary hyperparathyroidism post-renal transplant we correlated 1:25VD levels with intact PTH in 82 random patients with a serum creatinine of < 2 mg/dl and with normal hepatic function. All patients studied were normocalcemic with normal phosphorus and received azathioprine, cyclosporin A and prednisone. Of considerable interest, of the 42 patients studied after 2 years post-transplant, there were 8 (19%) patients with intact PTH of more than twice the upper limit of normal (normal 10-65 pg/ml) and other 15 (36%) with PTH levels above normal. Secondly, in no patient did we see 1:25VD above normal (normal 15-60 pg/ml) despite levels of PTH of > 200 pg/ml. Of concern, 20% of 73 patients had 1:25VD deficiency (< 15 pg/ml). This may not have been previously appreciated because of the number of patients studied. Like previous investigators, we failed to understand why 1:25VD levels were relatively low. There was no correlation between 1:25VD and serum creatinine. Of 25 patients with a serum creatinine of 1.4 or less, there were 10 patients (40%) with 1:25VD of less than 20 pg/ml. Since persistently high PTH can contribute to bone demineralization, which is not uncommon post-transplant, we treated 8 patients with small doses of oral 1:25VD (rocaltrol). In less than 6 months PTH levels returned to normal in 7 of the 8 patients. The current studies clearly indicate that asymptomatic hyperparathyroidism is common even after 2 years post-renal transplant. Monitoring for PTH and 1:25VD will help prevent bone disease post-transplant now that rocaltrol is available.