Abstract

Abstract Background and Aims Kidney transplant recipients can be considered as high-risk collective for pathological fractures, since diverse risk factors leading to mineral bone disorder (MBD) and osteoporosis accumulate in this setting. (Subtotal) parathyroidectomy (PTX) is indicated for ESRD patients with secondary hyperparathyroidism (sHPT) who do not respond to drug therapy adequately. This study aims to identify influencable factors that are associated with pathological fractures and bone disease in KTX recipients. Method We conducted a retrospective study involving 722 adult patients with a total of 4686 patient-years who were transplanted at our center between January 2007 and June 2015. The clinical patient data was extracted from the patients’ electronic files. Different laboratory and clinical parameters for mineral bone disorder and osteoporosis including medication were evaluated. As primary endpoint we chose fracture events that were not related to malignancies or adequate trauma. Results 47 (6,5%) of the patients suffered from pathologic fracture events during the follow-up period. 124 of the patients (17.2%) underwent PTX. In 112 of these patients (90.3%), PTX was performed prior to kidney transplantation (KTx), in 12 patients PTX took place after KTx. Median time for PTX in relation to KTx was 3.7 years prior to KTx (IQR 5.43). Only 1 (2,2%) of the patients with fracture events has received PTX beforehand compared to 124 (19,2%) of the patients without fractures. Adjusted for the well-known fracture risk factors for mineral bone disease and osteoporosis which include female sex, age and dialysis vintage, PTX remains a significant protective factor against fractures after KTx in multivariable Cox regression analysis (HR 0.124, p=0.041) and in Kaplan-Meier analysis (Figure 1). Serum calcium levels were significantly lower in patients after PTX (p<0.001). Active Vitamin D was applicated in patients after PTX more frequently (40.0% vs. 22.7%, p<0.001) Conclusion Our study reveals PTX as a protective factor regarding pathological fractures after KTx. As these patients show lower serum calcium levels, one explanation for this finding could be a more generous supplementation of these patients with active vitamin D, which is known to increase bone mineral density and to reduce fracture risk. Therefore, considering that hypoprathyroidism following PTX after KTx and low plasma-PTH levels correlate with significant decrease of renal function, patients on conservative sHPT therapy should be treated with active vitamin D preparations more generously and special attention should be paid on bone metabolism.

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