O impacto da doença mineral óssea após o transplante renal no risco de fratura, disfunção do enxerto, ritmo de filtração glomerular e mortalidade

Abstract

Introduction: Chronic kidney disease - mineral and bone disorder (CKD-MBD) contributes to the high morbimortality of patients with CKD. Kidney transplantation (KTx) is the optimal form of renal replacement therapy; however, it does not completely reverse CKD-MBD. Objectives: To analyze the impact of CKD-MBD on clinical outcomes after TxR. To evaluate the evolution of biochemical parameters of mineral and bone metabolism and the prevalence of mineral disorders over the period from 12 months before through the first year after KTx. Methods: This is a retrospective cohort of dialysis patients undergoing kidney transplantation between 2008 and 2018 at Santa Casa de Belo Horizonte. The variables of mineral and bone metabolism studied were calcium, phosphorus, parathyroid hormone (PTH), vitamin D and alkaline phosphatase (AP). The outcomes were fracture, graft failure, glomerular filtration rate (GFR) in the first year after KTx and death. Results: There was a significant increase in calcemia and a reduction in phosphatemia and in PTH levels in the first year after KTx. Six months after KTx, rates of hypercalcemia and hypophosphatemia were 16% and 45%, respectively. Fifty-two percent of patients had persistent hyperparathyroidism in the first year of KTx. AP levels before KTx were significantly lower in the group that suffered fracture. No variable studied was associated with graft failure. The GFR was significantly higher in the group of patients who had calcium levels < 8.5 mg/dl in the post-KTx period (0 to 3 months) when compared to the group with calcium between 8.5 and 10.5 mg/dl. The group of patients with post-KTx PTH levels (0 to 6 months) < 150 pg/ml had significantly higher GFR compared with the group with PTH levels > 300 pg/ml. The group that died had significantly lower levels of pre-KTx PTH. In the multivariate analysis, no parameter of bone and mineral metabolism was associated with fracture, graft failure and death. Discussion: Only about 15% of the evaluated patients had data on mineral and bone metabolism after KTx. There was an increase in calcemia and a reduction in phosphatemia and in serum PTH in the first months after KTx, reflecting, among other factors, the restoration of renal function and high levels of PTH. The association between calcium and PTH after KTx with GFR probably reflects the effect of the functioning graft on these variables and not the opposite. The multivariate analysis showed that CKD-MBD markers do not explain fracture, graft failure and death. Conclusions: Despite the high morbimortality associated with CKD-MBD, routine biochemical parameters available for its diagnosis did not explain serious outcomes in kidney transplant patients, indicating that there are several other factors that contribute to these outcomes. In addition, there is a need for other markers for a better approach of CKD-MBD.