Changes in Cardiovascular Calcification After Parathyroidectomy in Patients With ESRD

doi:10.1053/j.ajkd.2005.04.035

American Journal of Kidney Diseases

Volume 46, Issue 3, September 2005, Pages 464-469

https://doi.org/10.1053/j.ajkd.2005.04.035 Get rights and content

Background: The effect of parathyroidectomy on vascular calcification in patients with end-stage renal disease has been a subject of interest for many years, although studies in this area have not been definitive. The purpose of this investigation is to determine changes in vascular calcification after subtotal parathyroidectomy by using fast-gated helical computed axial tomographic imaging to measure coronary and carotid artery calcification. Methods: Computed tomographic imaging was performed at baseline and in follow-up on 10 patients who had undergone subtotal parathyroidectomy and 10 reference patients who had not undergone parathyroidectomy. Results: Patients who underwent subtotal parathyroidectomy had a mean change in coronary calcification of −92.3 ± 469/y, and reference patients had a mean change of +479 ± 630/y (P = 0.03). The 2 parathyroidectomy patients with the highest baseline scores had significant declines in both coronary and carotid calcification. Conclusion: In this study, subtotal parathyroidectomy is associated with a significant decrease in vascular calcification in 2 of 10 dialysis patients with high coronary artery calcium scores and stabilization in 7 of 10 patients with low baseline scores.

Section snippets

Methods

This study was approved by the Wake Forest University School of Medicine (Winston Salem, NC) Institutional Review Board.

Results

Table 1 lists baseline demographic data for the 2 groups. Parathyroidectomy patients were more likely to have elevated iPTH levels and greater serum phosphorus values.

Table 2 lists time-averaged laboratory values, time-averaged phosphate-binder dosage (in grams of elemental calcium per day), and time-averaged calcitriol-equivalent intake (in micrograms per week). Patients who underwent subtotal parathyroidectomy had lower serum calcium and higher serum phosphorus values, whereas

Discussion

The present study shows a significant decline in cardiovascular calcification in several patients with high baseline CAC scores and stabilization in 1 patient with a high baseline score. These results were in contrast to those found in a reference group of 10 other dialysis patients, for whom CAC scores increased over time in patients with high baseline scores. Other studies noted an approximate annual 25% increase in CAC scores in patients treated with calcium-based binders,¹⁰ which was

References (17)

A.J. Bleyer et al.
Sudden and cardiac death rates in hemodialysis patients
Kidney Int
(1999)
G. Chertow et al.
Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients
Kidney Int
(2002)
J. Girotto et al.
Parathyroidectomy promotes wound healing and prolongs survival in patients with calciphylaxis from secondary hyperparathyroidism
Surgery
(2001)
B. Kestenbaum et al.
Parathyroidectomy rates among United States dialysis patients1990–1999
Kidney Int
(2004)
H. Meema et al.
Arterial calcifications in severe chronic renal disease and their relationship to dialysis treatment, renal transplant, and parathyroidectomy
Radiology
(1976)
A. Parfitt
Soft-tissue calcification in uremia
Arch Intern Med
(2004)
A. DeFrancisco et al.
Parathyroidectomy in chronic renal failure
Q J Med
(1985)
L. Wexler et al.
Coronary artery calcificationPathophysiology, epidemiology, imaging methods, and clinical implications
Circulation
(2004)

There are more references available in the full text version of this article.

Cited by (76)

Parathyroidectomy
2022, Handbook of Dialysis Therapy
The development of secondary hyperparathyroidism is commonly observed in chronic kidney disease. In these patients, increased parathyroid hormone (PTH) synthesis and secretion, together with elevation of fibroblast growth factor 23 (FGF-23) levels, stimulate phosphaturia to prevent the accumulation of phosphate. In advanced stages of chronic kidney disease, glomerular filtration rates are so low that elevated PTH is not able to prevent the increase in serum phosphate; however, the stimulus for the progressive increase of parathyroid growth is maintained, which may even progress to nodular hyperplasia. Then, parathyroid glands fail to respond to medical therapy, and refractory hyperparathyroidism occurs. Parathyroidectomy (PTX), surgical resection of the parathyroid glands, is usually performed in cases of persistent excessive elevation of serum PTH levels associated with hypercalcemia despite available medical therapy: phosphate binders, active vitamin D, and calcimimetics. PTX can be performed using different procedures: subtotal PTX or total PTX with or without parathyroid autotransplantation. PTH oversuppression is an undesirable consequence of parathyroid surgery, which may cause the development of adynamic bone disease. Hungry bone syndrome is quite common after this surgery. However, if appropriately indicated, PTX improves survival and parameters of mineral metabolism. PTX should be considered in cases of severe hyperparathyroidism that do not respond to pharmacological treatment and with clear undesirable effects of PTH on bone and mineral metabolism.
Differentiating the causes of adynamic bone in advanced chronic kidney disease informs osteoporosis treatment
2021, Kidney International
Patients with chronic kidney disease (CKD) have an increased fracture risk because of impaired bone quality and quantity. Low bone mineral density predicts fracture risk in all CKD stages, including advanced CKD (CKD G4-5D). Pharmacological therapy improves bone mineral density and reduces fracture risk in moderate CKD. Its efficacy in advanced CKD remains to be determined, although pilot studies suggest a positive effect on bone mineral density. Currently, antiresorptive agents are the most commonly prescribed drugs for the prevention and therapy of osteoporosis. Their use in advanced CKD has been limited by the lack of large clinical trials and fear of causing kidney dysfunction and adynamic bone disease. In recent decades, adynamic bone disease has evolved as the most predominant form of renal osteodystrophy, commonly associated with poor outcomes, including premature mortality and progression of vascular calcification. Evolving evidence indicates that reduction of bone turnover by parathyroidectomy or pharmacological therapies, such as calcimimetics and antiresorptive agents, are not associated with premature mortality or accelerated vascular calcification in CKD. In contrast, chronic inflammation, oxidative stress, malnutrition, and diabetes can induce low bone turnover and associate with poor prognosis. Thus, the conditions causing suppression of bone turnover rather than the low bone turnover per se may account for the perceived association with outcomes. Anabolic treatment, in contrast, has been suggested to improve turnover and bone mass in patients with advanced CKD and low bone turnover; however, uncertainty about safety even exceeds that of antiresorptive agents. Here, we critically review the pathophysiological concept of adynamic bone disease and discuss the effect of low bone turnover on the safety and efficacy of anti-osteoporosis pharmacotherapy in advanced CKD.
Surgical Management of Secondary Hyperparathyroidism
2021, Kidney International Reports
Secondary hyperparathyroidism (SHPT) affects a majority of patients with chronic kidney disease (CKD) of stage 3 or worse. Despite the development of calcimimetics and their effectiveness in treating SHPT, many patients continue to fail medical management and should be referred to a parathyroid surgeon. In this narrative review, we summarize the indications for surgical referral, preoperative planning, intraoperative strategies to guide resection, and postoperative management. In the absence of universal guidelines, it can be difficult to determine when it is appropriate to make this referral. The majority of studies evaluating parathyroidectomy (PTX) for SHPT use the criteria of parathyroid hormone level (PTH) >800 pg/ml with hypercalcemia and/or hyperphosphatemia, which may be accompanied by symptoms such as bone pain and pruritis that can improve after surgery. Although the reported utility of the various imaging modalities (i.e., 99m-technetium-sestamibi scintigraphy with computed tomography [SPECT/CT], CT, or ultrasound) is highly variable in SHPT, SPECT/CT appears to be the most sensitive. Intraoperatively, PTH monitoring is effective in predicting long-term cure of SHPT but not in predicting hypoparathyroidism. Ectopic and supernumerary parathyroid glands are common in these patients and are often implicated in persistent or recurrent disease. Postoperatively, patients are at risk of severe hypocalcemia and hungry bone syndrome requiring close monitoring and replenishment.
Mineral Bone Abnormalities and Vascular Calcifications
2019, Advances in Chronic Kidney Disease
Citation Excerpt :
On the other hand, low PTH levels are observed in kidney disease patients with adynamic bone disease, which is associated with VC; however, PTH is likely not the primary factor in the pathophysiology of adynamic bone-associated VC given the complexity of the disease.90 Among end-stage kidney disease patients with secondary hyperparathyroidism, parathyroidectomy91 and treatment with cinacalcet plus low-dose calcitriol compared to vitamin D analogs92 attenuates the progression of VC; however, it is difficult to distinguish if this observation is due to decreased PTH levels, concurrent changes in calcium and phosphorus levels, specific medication effects (eg, an effect on vascular CaSR), or other factors such as an increase in levels of the VC inhibitor, fetuin-A.93 FGF23 is a 251-amino acid protein synthesized and secreted by osteocytes and osteoblasts.
Vascular calcification (VC) is common in chronic kidney disease, increases in prevalence as patients progress to end-stage renal disease, and is significantly associated with mortality. VC is a complex and highly regulated process similar to bone formation whereby hydroxyapatite crystals deposit in the intimal or medial layer of arteries. Mineral bone abnormalities are common in chronic kidney disease; reduction in glomerular filtration rate and changes in vitamin D, parathyroid hormone, and fibroblast growth factor 23 result in the dysregulation of phosphorus and calcium metabolism. Cell culture studies, animal models, and observational and clinical studies all suggest this abnormal mineral metabolism plays a role in the initiation and progression of VC in kidney disease. This review will focus on these mineral bone abnormalities and how they may contribute to mechanisms that induce VC in kidney disease.
Impacts of parathyroidectomy on calcium and phosphorus metabolism disorder, arterial calcification and arterial stiffness in haemodialysis patients
2019, Asian Journal of Surgery
Citation Excerpt :
Some scholars22,23 believe that patients with refractory SHPT should be treated with surgical resection of the parathyroid as early as possible, as this might slow the process of atherosclerosis. Bleyer et al5 compared ten PTX uremic patients with ten patients without PTX, and used MSCT to determine the CAC scores. The average annual change in CAC scores of the PTX patients was significantly lower than in the control group, among whom the scores of two cases that originally had high scores were significantly reduced, and those of the seven cases that originally had low scores were maintained within the preoperative range.
Secondary hyperparathyroidism (SHPT) and calcium and phosphorus metabolism disorder are important complications in haemodialysis patients. Parathyroidectomy (PTX) may prevent or delay the progress of vascular calcification in haemodialysis patients.
To investigate the impacts of PTX on calcium and phosphorus metabolism, arterial calcification and arterial stiffness in haemodialysis patients with SHPT.
Twenty-one SHPT-haemodialysis patients were selected for PTX. The preoperative and postoperative 1-year scores of coronary artery calcification were measured via multislice spiral CT, along with the brachial-ankle pulse wave velocity (baPWV), and preoperative and postoperative 1-year indexes such as calcium, phosphorus, calcium-phosphorus product concentration and parathyroid hormone (PTH) level were compared.
Compared with the preoperative score, the postoperative 1-year coronary artery calcification score was significantly reduced; the mean baPWVs of the bilateral limbs were reduced; and the levels of serum calcium, phosphorus, calcium-phosphorus product concentration and PTH were all reduced; all differences were statistically significant (P < 0.05).
PTX can be used to correct calcium and phosphorus metabolism disorder, reduce arterial calcification, and improve arterial stiffness.
Facing cinacalcet-induced hypocalcemia: sit back and relax?
2018, Kidney International
A post hoc analysis of data from the EVOLVE study demonstrates that cinacalcet-induced hypocalcemia is common, mostly asymptomatic, and resolves spontaneously. These findings are reassuring and may warrant therapeutic inertia. However, previous studies in parathyroidectomized patients suggest that calcium repletion may be beneficial and safe from bone and cardiovascular perspectives, respectively, and as such call into question the appropriateness of a “sit back and relax” attitude toward cinacalcet-induced hypocalcemia.

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Originally published online as doi:10.1053/j.ajkd.2005.04.035 on July 12, 2005.

Supported in part by a grant from the National Kidney Foundation of North Carolina, Inc.

View full text

Original investigationDialysis therapyChanges in Cardiovascular Calcification After Parathyroidectomy in Patients With ESRD

Section snippets

Methods

Results

Discussion

Kidney Int

Kidney Int

Surgery

Kidney Int

Arterial calcifications in severe chronic renal disease and their relationship to dialysis treatment, renal transplant, and parathyroidectomy

Radiology

Soft-tissue calcification in uremia

Arch Intern Med

Parathyroidectomy in chronic renal failure

Q J Med

Coronary artery calcificationPathophysiology, epidemiology, imaging methods, and clinical implications

Circulation

Original investigation
Dialysis therapy
Changes in Cardiovascular Calcification After Parathyroidectomy in Patients With ESRD