Is low pre-transplant parathyroid hormone a risk marker for cardiovascular disease in long-term follow-up of renal transplant recipients?

Isaksson, Elin; Almquist, Martin; Seeberger, Astrid; Sterner, Gunnar

doi:10.1007/s10157-018-1543-9

Cited by 7 publications

(7 citation statements)

References 26 publications

(29 reference statements)

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“…In contrast, Isaksson et al showed that lower PTH levels in the pre-transplant period are associated with a higher risk of cardiovascular events in the post-transplant period [119]. The association of low PTH levels with worse cardiovascular outcomes has already been demonstrated in dialysis patients and this is one of the hypotheses that explains the finding of this study [25][26][27]119]. Another possible explanation is bone disease associated with reduced PTH, usually with low remodeling.…”

Section: -Abnormalities Of Ckd-mbd Biochemical Parameters After Kidne...contrasting

confidence: 52%

“…Roodnat et al showed that high PTH levels in the pre-kidney transplant period were associated with a higher risk of graft loss [117]. In contrast, Isaksson et al showed that lower PTH levels in the pre-transplant period are associated with a higher risk of cardiovascular events in the post-transplant period [119]. The association of low PTH levels with worse cardiovascular outcomes has already been demonstrated in dialysis patients and this is one of the hypotheses that explains the finding of this study [25][26][27]119].…”

Section: -Abnormalities Of Ckd-mbd Biochemical Parameters After Kidne...mentioning

confidence: 99%

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Mineral and Bone Disease After Kidney Transplantation: Risk of Fracture, Graft Dysfunction and Mortality - a Review

Penido¹

2022

IJCN

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The mineral and bone disease of chronic kidney disease (CKD-MBD) is a combination of three components: abnormalities in calcium, phosphorus, PTH, fibroblast growth factor 23 (FGF23) and vitamin D metabolism; abnormalities of bone metabolism, mineralization, volume, growth and strength; and vascular and other soft tissue calcification. During the natural course of kidney disease, there is an increase in FGF23 levels, inhibition of calcitriol production, secondary hyperparathyroidism, hypocalcemia and hyperphosphatemia. These changes have consequences on the cardiovascular and bone systems. Regarding cardiovascular disease, left ventricular hypertrophy is highlighted, associated with an increase in FGF23 and vascular calcification, directly related to hyperphosphatemia. The main types of bone disease are cystic fibrous osteitis (high turnover) and adynamic bone disease (low turnover), both of which are associated with a high risk of fracture in this population. Successful kidney transplantation (KT) does not fully correct the mineral, bone and cardiovascular abnormalities generated by CKD-MBD. In the first months after transplantation, PTH and FGF23 levels remain elevated in most patients. There is an increase in the production of calcitriol by the graft. These are the main alterations responsible for a mineral phenotype that resembles primary hyperparathyroidism, with hypercalcemia, hypophosphatemia and elevated PTH levels. Cardiovascular disease does not revert after KT and the transplant patient has a higher cardiovascular risk than the general population. In relation to bone disease, in addition to the pre-existing bone alteration, specific factors of the post-KT period add damage to the bone, especially the use of corticosteroids. The main types of bone disease in renal transplant patients are bone fracture, renal osteodystrophy, osteoporosis and osteonecrosis. CKD-MBD is a complex disease that affects patients with CKD, increasing their morbidity and mortality. KT does not fully reverse the disease and still adds other specific risk factors that make its approach challenging. This review sought to show the association between the bone mineral disease of chronic kidney disease and the risk of fractures, vascular and other tissue calcifications, graft dysfunction and kidney transplant patient mortality.

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Section: -Abnormalities Of Ckd-mbd Biochemical Parameters After Kidne...contrasting

confidence: 52%

Section: -Abnormalities Of Ckd-mbd Biochemical Parameters After Kidne...mentioning

confidence: 99%

Mineral and Bone Disease After Kidney Transplantation: Risk of Fracture, Graft Dysfunction and Mortality - a Review

Penido¹

2022

IJCN

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“…Another contributing factor could be that the prolonged survival time among PTX patients, presented in our former study, might increase the risk of having CVE at some point after PTX. In recent years, more attention has been given to the fact that not only high levels of PTH but also very low levels of PTH are associated with increased mortality [34] and CVE [35,36]. One of the common complications of PTX is low levels of PTH after the procedure, so this could partly explain the higher risk of CVE for PTX patients.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular and Cerebrovascular Events After Parathyroidectomy in Patients on Renal Replacement Therapy

et al. 2019

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Background A majority of patients with end-stage renal disease suffer from secondary hyperparathyroidism, which is associated with osteoporosis and cardiovascular disease. Parathyroidectomy (PTX) is often necessary despite medical treatment. However, the effect of PTX on cardio-and cerebrovascular events (CVE) remains unclear. Data on the effect of PTX from population-based studies are scarce. Some studies have shown decreased incidence of CVE after PTX. The aim of this study was to evaluate the effect of PTX on risk of CVE in patients on renal replacement therapy. Methods We performed a nested case-control study within the Swedish Renal Registry (SRR) by matching PTX patients on dialysis or with functioning renal allograft with up to five non-PTX controls for age, sex and underlying renal disease. To calculate time to CVE, i.e., myocardial infarct, stroke and transient ischemic attack, control patients were assigned the calendar date (d) of the PTX of the case patient. Crude and adjusted proportional hazards regressions with random effect (frailty) were used to calculate hazard ratios for CVE. Results The study cohort included 20,056 patients in the SRR between 1991 and 2009. Among these, 579 patients had undergone PTX, 423 during dialysis and 156 during time with functioning renal allograft. These patients were matched with 1234 dialysis and 736 transplanted non-PTX patients. The adjusted hazard ratio (HR) with 95% confidence interval (CI) of CVE after PTX was 1.24 (1.03-1.49) for dialysis patients compared with non-PTX patients. Corresponding results for patients with renal allograft at d were HR (95% CI) 0.53 (0.34-0.84). Conclusions PTX patients on dialysis at d had a higher risk of CVE than patients without PTX. Patients with renal allograft at d on the other had a lower risk after PTX than patients without PTX.

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“…The rate of hypoparathyroidism following surgical intervention in SHPT varied between 16.6% and 18.1% (36). Low levels of PTH before KT were associated with an increased risk of post-KT vascular events (37). Marked hypoparathyroidism and hypocalcemia related to pre-KT parathyroidectomy might also lead to slow allograft function, and suboptimal allograft function is significantly related to the diffuse hypoperfusion of the glomeruli (38).…”

Section: 2mentioning

confidence: 99%

Timing of parathyroidectomy for kidney transplant patients with secondary hyperparathyroidism: A practical overview

Wang

et al. 2022

BST

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Is low pre-transplant parathyroid hormone a risk marker for cardiovascular disease in long-term follow-up of renal transplant recipients?

Cited by 7 publications

References 26 publications

Mineral and Bone Disease After Kidney Transplantation: Risk of Fracture, Graft Dysfunction and Mortality - a Review

Mineral and Bone Disease After Kidney Transplantation: Risk of Fracture, Graft Dysfunction and Mortality - a Review

Cardiovascular and Cerebrovascular Events After Parathyroidectomy in Patients on Renal Replacement Therapy

Timing of parathyroidectomy for kidney transplant patients with secondary hyperparathyroidism: A practical overview

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