Early Development of Secondary Hyperparathyroidism following Renal Transplantation

Isaksson, Elin; Sterner, Gunnar

doi:10.1159/000342811

Cited by 11 publications

(9 citation statements)

References 39 publications

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“…Levels of parathyroid hormone (PTH) are mainly used to grade the extent of sHPT and both high and low PTH have been associated with cardiovascular disease (CVD) in patients on maintenance dialysis [ 3 – 6 ]. Renal transplantation improves many of the underlying causes of sHPT and levels of PTH decrease after transplantation, even though sHPT persists in the majority of renal transplant recipients over the short as well as long term [ 7 , 8 ]. Recent studies have shown no association between post-transplant PTH and risk of vascular events [ 9 ], but have shown an association with graft failure and mortality [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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BackgroundSecondary hyperparathyroidism and altered levels of parathyroid hormone (PTH) are associated with vascular events in chronic kidney disease. After renal transplantation, this association is not clear. Pre-transplant parathyroidectomy (PTX) is common, but post-transplant data are scarce. We aimed to study the effect of PTH at the time of transplantation on risk of post-transplant vascular events in renal transplant recipients with and without pre-transplant PTX.Methods258 patients from two Swedish transplant units were followed for 6 years. Separate analyses were made for patients with or without pre-transplant PTX. Patients with no pre-transplant PTX were stratified by quartiles of PTH at time of transplantation and patients with pre-transplant PTX were stratified by above and below median levels of PTH at time of transplantation. Hazard ratios for vascular events, mortality, and graft failure were calculated in adjusted Cox regression models.ResultsIn patients with no pre-transplant PTX, the lowest quartile of PTH at transplantation had a higher risk of cardiovascular events compared to quartile 3 with an adjusted hazard ratio (95% CI) of 2.63 (1.04–6.67). In patients with pre-transplant PTX, the group below median of PTH had a higher risk of cardiovascular events with an adjusted hazard ratio (95% CI) of 18.15 (1.62–203.82) compared to patients above median of PTH.ConclusionLow levels of parathyroid hormone before transplantation were associated with increased risk of post-transplant vascular events both in patients with and without pre-transplant parathyroidectomy. Any conclusions on causal or direct effect of PTH on outcome cannot be drawn from this observational study.

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Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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“…Kidney transplantation rapidly restores GFR and the renal capacity to respond to PTH (that is, phosphaturia and tubular calcium reabsorption). 8,9 Usually, some degree of autoregulation is preserved with progressive PTH reduction and regression of parathyroid hyperplasia a few months after transplantation. However, in 20%-30% of patients, parathyroid gland resistance to inhibitory feedback persisted several years after transplantation, 9 and inappropriately high PTH levels are associated with hypercalcemia, hypophosphatemia, renal allograft calcifications and dysfunction, loss of bone mineral density (BMD) and increased risk of fracture, vascular calcification, and increased risk of cardiovascular events.…”

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confidence: 99%

A Randomized Study Comparing Parathyroidectomy with Cinacalcet for Treating Hypercalcemia in Kidney Allograft Recipients with Hyperparathyroidism

Cruzado

Moreno²,

Torregrosa

et al. 2015

JASN

139

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Tertiary hyperparathyroidism is a common cause of hypercalcemia after kidney transplant. We designed this 12-month, prospective, multicenter, open-label, randomized study to evaluate whether subtotal parathyroidectomy is more effective than cinacalcet for controlling hypercalcemia caused by persistent hyperparathyroidism after kidney transplant. Kidney allograft recipients with hypercalcemia and elevated intact parathyroid hormone (iPTH) concentration were eligible if they had received a transplant $6 months before the study and had an eGFR.30 ml/min per 1.73 m 2 . The primary end point was the proportion of patients with normocalcemia at 12 months. Secondary end points were serum iPTH concentration, serum phosphate concentration, bone mineral density, vascular calcification, renal function, patient and graft survival, and economic cost. In total, 30 patients were randomized to receive cinacalcet (n=15) or subtotal parathyroidectomy (n=15). At 12 months, ten of 15 patients in the cinacalcet group and 15 of 15 patients in the parathyroidectomy group (P=0.04) achieved normocalcemia. Normalization of serum phosphate concentration occurred in almost all patients. Subtotal parathyroidectomy induced greater reduction of iPTH and associated with a significant increase in femoral neck bone mineral density; vascular calcification remained unchanged in both groups. The most frequent adverse events were digestive intolerance in the cinacalcet group and hypocalcemia in the parathyroidectomy group. Surgery would be more cost effective than cinacalcet if cinacalcet duration reached 14 months. All patients were alive with a functioning graft at the end of follow-up. In conclusion, subtotal parathyroidectomy was superior to cinacalcet in controlling hypercalcemia in these patients with kidney transplants and persistent hyperparathyroidism.

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“…Levels of PTH accumulate during ESRD thus a rapid decrease in PTH is seen immediately after transplantation. Thereafter, levels of PTH keep decreasing slowly and stabilize after the first 6 months (Isaksson & Sterner 2012). The majority of patients have PTH levels above the reference range 1 year after transplantation (Sprague et al 2008).…”

Section: Renal Transplantationmentioning

confidence: 98%

The treatment of renal hyperparathyroidism

Almquist

Isaksson

Clyne

2020

Endocrine-Related Cancer

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Renal hyperparathyroidism (rHPT) is a complex and challenging disorder. It develops early in the course of renal failure and is associated with increased risks of fractures, cardiovascular disease and death. It is treated medically, but when medical therapy cannot control the hyperparathyroidism, surgical parathyroidectomy is an option. In this review, we summarize the pathophysiology, diagnosis, and medical treatment; we describe the effects of renal transplantation; and discuss the indications and strategies in parathyroidectomy for rHPT. Renal hyperparathyroidism develops early in renal failure, mainly as a consequence of lower levels of vitamin D, hypocalcemia, diminished excretion of phosphate and inability to activate vitamin D. Treatment consists of supplying vitamin D and reducing phosphate intake. In later stages calcimimetics might be added. RHPT refractory to medical treatment can be managed surgically with parathyroidectomy. Risks of surgery are small but not negligible. Parathyroidectomy should likely not be too radical, especially if the patient is a candidate for future renal transplantation. Subtotal or total parathyroidectomy with autotransplantation are recognized surgical options. Renal transplantation improves rHPT but does not cure it.

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Early Development of Secondary Hyperparathyroidism following Renal Transplantation

Cited by 11 publications

References 39 publications

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

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

A Randomized Study Comparing Parathyroidectomy with Cinacalcet for Treating Hypercalcemia in Kidney Allograft Recipients with Hyperparathyroidism

The treatment of renal hyperparathyroidism

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