Are PTH serum levels predictive of coronary calcifications in haemodialysis patients?

Coen, G; Manni, Micaela; Mantella, Daniela; Pierantozzi, Andrea; Balducci, Alessandro; Condò, Stefano; DiGiulio, Salvatore; Yancovic, Lijljana; Lippi, B; Manca, S; Morosetti, Massimo; Pellegrino, L.; Simonetti, Giovanni; Gallucci, M.; Splendiani, G

doi:10.1093/ndt/gfm370

Cited by 57 publications

(43 citation statements)

References 29 publications

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“…In fact, during the 2-yr interval, our transplant patients showed an improvement in the biochemical parameters of secondary hyperparathyroidism, possibly explained by the extension of the follow-up (7,27), which is expected to favorably affect calcification (28). They also showed an increase in serum fetuin to normal levels, indicative of lower inflammation but also of increased calcification inhibition capacity of plasma (5).…”

Section: ͻ000001mentioning

confidence: 67%

Progression of Coronary Artery Calcification in Renal Transplantation and the Role of Secondary Hyperparathyroidism and Inflammation

Mazzaferro

Pasquali

Taggi

et al. 2009

Clinical Journal of the American Society of Nephrology

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Background and objectives: Transplantation should favorably affect coronary calcification (CAC) progression in dialysis; however, changes in CAC score in the individual patient are not reliably evaluated.Design, setting, participants & measurements: The authors used special tables of reproducibility limits for each score level to study, by multislice computed tomography and biochemistries, the 2-year changes in CAC in 41 transplant patients (age 48 ؎ 13 yr, 25 men, dialysis vintage 4.8 ؎ 4.3 yr, underwent transplant 6.2 ؎ 5.5 yr prior). Thirty balanced dialysis patients served as controls.Results: In the study group, Agatston score was stable, and C-reactive protein decreased, whereas fetuin and osteoprotegerin increased. In the control group, Agatston score increased, parathyroid hormone and phosphate decreased, and inflammation markers were persistently twice as high as in the study group. With regard to individual changes, 12.2% transplant patients worsened, compared with 56.6% of patients in dialysis (P < 0.0001). Patients without calcification at entry showed slower progression in transplantation (8.3%) than in dialysis (44.4%; P < 0.034), and the difference was similar to that observed in cases with CAC (17.6% versus 61.9%; P < 0.007). Discriminant analysis indicated parathyroid hormone, the modality of therapy (dialysis or transplantation), and erythrocyte sedimentation rate as the variables most associated with worsening.Conclusions: Renal transplantation lowers but does not halt CAC progression. Inflammation and hyperparathyroidism are associated with progression in the populations studied.

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Section: ͻ000001mentioning

confidence: 67%

Progression of Coronary Artery Calcification in Renal Transplantation and the Role of Secondary Hyperparathyroidism and Inflammation

Mazzaferro

Pasquali

Taggi

et al. 2009

Clinical Journal of the American Society of Nephrology

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“…Although the consensus on Ca metabolism in ESRD suggests optimal ranges of Ca/phosphate/ PTH 36) , this issue has not been endorsed by compelling evidence. Previous studies showed the deleterious effects of excess PTH on cardiovascular events in ESRD 37) . In the present study, serum i-PTH levels are lower in moderate to severe stenosis and occlusion than in normal to mild stenosis (Table 3).…”

Section: Discussionmentioning

confidence: 91%

“…Moreover, low i-PTH levels are a risk factor for severity of stenosis independent of DM and age ( Table 4). It has been shown that low i-PTH is linked to coronary calcification in dialysis patients 37) , which is based on the notion that low bone turnover due to low PTH reflects reduced bone Ca-phosphate buffering capacity 38) . Indeed, serum Ca was higher in patients with i-PTH 150 pg/mL than in those with i-PTH ≥ 150 pg/mL (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Brachial-Ankle Pulse Wave Velocity Predicts Silent Cerebrovascular Diseases in Patients with End-Stage Renal Diseases

Washida

Wakino

Hayashi

et al. 2010

JAT

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Aim: Cerebrovascular disease (CVD) is a major determinant of the prognosis in end-stage renal diseases (ESRD). The purpose of this study was to examine whether factors associated with arterial stiffness contributed to the development of CVD in patients with ESRD. Methods: CVD (lacunes and carotid/intracranial artery stenosis) was evaluated with brain magnetic resonance imaging (MRI), and carotid/intracranial artery magnetic resonance angiography (MRA) in 44 pre-dialytic patients. The severity of CVD was evaluated by the number of lacunes and the degree of stenosis, respectively. The association between CVD and atherosclerotic parameters was evaluated. Results: Patients with severe lacunes (n 18) manifested older age, lower diastolic blood pressure, serum creatinine and albumin, and higher CRP and serum calcium than those with absent-moderate lacunes (n 26). When assessed by multivariate analysis, only baPWV was adopted as an independent risk factor for severe lacunes. Furthermore, baPWV and i-PTH were associated with the severity of carotid/intracranial artery stenosis, both of which were independent of other risk factors, including age and diabetes. Conclusions: Arterial stiffness may constitute a novel determinant predicting the severity of CVD in pre-dialytic patients besides classical risk factors. J Atheroscler Thromb, 2010; 17:165-172.

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“…In the long-term, this phenomenon is maladaptive as it leads to bone demineralization (renal osteodystrophy). In these scenarios, PTH is believed by some investigators to enhance coronary artery calcifications 15 and lead to the aforementioned microvascular calcification, intimal hypertrophy, and thrombosis, which in turn leads to ischemia and subsequent calciphylactic ulcers. 16 More recently, fibroblast growth factor 23 (FGF-23) has been established as an important player in the regulation of phosphate-vitamin D homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Calciphylaxis presenting in early chronic kidney disease with mixed hyperparathyroidism

Brucculeri¹,

Haydon²

2011

IJNRD

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Calciphylaxis is a disabling and life-threatening complication that primarily affects patients who are dialysis dependent. Reports have grown in the literature of cases occurring in those who have advanced chronic kidney disease (pre-end-stage renal disease) or in the setting of transplantation. There are also a few reports of cases occurring in those without any form of chronic kidney disease but with primary hyperparathyroidism. This disease entity is characterized by calcification, intimal hypertrophy, and thrombosis of small vessels that result in necrotizing, nonhealing ulcers -many of which are life threatening. Although several strategies aimed at treating and preventing this affliction have been reported in the literature, the outcome for most patients with calciphylaxis remains quite poor. We describe a patient with comparatively early stage-3 chronic kidney disease who developed calciphylaxis in the setting of both primary and secondary hyperparathyroidism. Predictably, after subtotal parathyroidectomy, her wounds did not completely heal and her biochemical markers of hyperparathyroidism did not completely normalize until her underlying secondary hyperparathyroidism was treated medically. It was only after initiating cinacalcet that the patient experienced complete wound healing and resolution of her calciphylaxis. It also supports other authors' findings that cinacalcet may be an important adjunct in the treatment of calciphylaxis. Keywords: calciphylaxis, chronic kidney disease, cinacalcet, parathyroidectomy Case reportA 66-year-old Caucasian woman with a medical history significant for chronic kidney disease (CKD) stage 3, hypertension, and morbid obesity was followed regularly at our nephrology and hypertension clinic. She was being treated aggressively for her hypertension, proteinuria, hyperuricemia, and secondary hyperparathyroidism (SHPT). Her baseline creatinine fluctuated between 1.5 mg/dL and 2.0 mg/dL, and eGFR (6 variable Modification of Diet in Renal Disease) between 24 and 34 mL/min/1.73 m 2 . Her home medications included paricalcitol, gemfibrozil, febuxostat, pantoprazole, furosemide, lisinopril, latanoprost ophthalmic, and ferrous sulfate. Our patient had never taken warfarin, vitamin D, or any oral phosphate binders. In 2009, her intact parathyroid hormone (PTH) levels were noted to be rising despite her receiving oral paricalcitol 1 mcg daily. The dose was eventually adjusted up to 2 mcg daily without controlling her PTH which climbed as high as 216 pg/mL. Her calcium levels climbed from 9.0 to 10.4 mg/dL but never higher. Her serum phosphorous levels ranged from 2.9 to 3.7 mg/dL before, during, and after subsequent treatment. Most importantly, the Ca 2+ × PO 4 2-solubility product was never greater than 33.7. In August 2010, she presented with painful eruptions and ulcerations along the medial aspects of her thighs Dovepress submit your manuscript | www.dovepress.com

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Are PTH serum levels predictive of coronary calcifications in haemodialysis patients?

Cited by 57 publications

References 29 publications

Progression of Coronary Artery Calcification in Renal Transplantation and the Role of Secondary Hyperparathyroidism and Inflammation

Progression of Coronary Artery Calcification in Renal Transplantation and the Role of Secondary Hyperparathyroidism and Inflammation

Brachial-Ankle Pulse Wave Velocity Predicts Silent Cerebrovascular Diseases in Patients with End-Stage Renal Diseases

Calciphylaxis presenting in early chronic kidney disease with mixed hyperparathyroidism

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