SEQUENTIAL-CHANGES OF BIOCHEMICAL BONE PARAMETERS AFTER KIDNEY-TRANSPLANTATION

Background. Persistent hyperparathyroidism after renal transplantation (Rtx) has been reported in several studies. However these studies eva luated biochemical bone parameters either only during a short time per iod (up to 6 months) or for a longer time period, but with long interv als in between. Therefore, we prospectively evaluated biochemical bone parameters of kidney-transplant recipients at short intervals for 2 y ears after surgery. Methods, Biochemical bone parameters were prospect ively investigated in 129 patients 2, 3, 5, 8, 12, 18 and 24 months af ter Rtx. All patients received prednisone and cyclosporin A as immunos uppressive therapy, and 75 patients also received azathioprine. None o f the patients was treated with calcium, phosphorus, or vitamin D prep arations. Results. Serum creatinine levels decreased from 166.8 +/- 5. 4 mu mol/l to 140.0 +/- 4.9 two years after Rtx; (data are expressed a s mean +/- s.e.m.). Serum phosphorus levels increased slightly from 0. 9 +/- 0.022 mmol/l to 0.98 +/- 0.025 (12m), but remained within the lo wer normal range. We observed a rise in total and albumin adjusted cal cium concentrations 3 months after Rtx. 52% of all patients had serum calcium levels above 2.62 mmol/l (upper normal limit in our laboratory ) 3 months after renal transplantation with a gradual decrease thereaf ter. There was no correlation of calcium and PTH levels. We observed a significant rise in biochemical bone parameters from 2 to 5 months af ter renal transplantation (P < 0.001): alkaline phosphatase (AP) incre ased from 164.3 +/- 9.4 to 236 +/- 12.7 U/l (normal 50-180), bone spec ific alkaline phosphatase (BAP) rose from 17.7 +/- 1.36 to 23.2 +/- 1. 7 ng/ml (normal:4-20) and osteocalcin (OC) increased from 20.2 +/- 1.5 to 26.7 +/- 1.9 ng/ml (normal 4-12). AP and BAP levels values normali zed 12 months after renal transplantation, whereas OC was still above normal throughout the study period. Patients were subdivided into two groups: those with good and those with impaired graft functions. Patie nts with good graft function had stable serum creatinine levels (less than or equal to 132 mu mol/l or less than or equal to 1.5 mg/dl) well below the mean serum creatinine concentration during the study period . The significant changes in AP, BAP, and OC occurred irrespective of renal function. However, patients with impaired graft function (n = 65 ) had significantly higher PTH-levels (70 pg/ml higher) than patients with good graft function (n = 64), P < 0.01. PTH was positively correl ated with serum creatinine (r = 0.81, P < 0.001). Moreover, patients w ith low 25 (OH) vitamin D levels (n = 63) had significantly higher PTH concentrations (between 40 and 80 pg/ml, P < 0.01) throughout the stu dy period compared to patients (n = 66) with a sufficient 25(OH) D sup ply irrespective of graft function. There was a negative correlation o f 25(OH)D levels and PTH; (r = -0.49, P < 0.001). 1,25(OH)(2)D3 (evalu ated in 24 patients) levels increased from 46.5 +/- 6.6 to 76.9 +/- 7. 6 pg/ml (normal:35-90) at 12 months. Conclusion, Hypercalcaemia is a c ommon phenomenon in the early period after kidney transplantation and occurs in the presence of low normal phosphorus levels. It is most pro bably related to improved PTH action and l-hydroxylation of vitamin D. The rise in biochemical bone parameters between 3 and 5 months occurs irrespective of graft function and normalization is only achieved 1 y ear after transplantation. PTH is constantly elevated for up to 2 year s after kidney transplantation and is most probably related (a) to imp aired graft function and (b) to suboptimal 25 OH vitamin D supply.