scholarly journals Parathyroidectomy May Cause Remission of Uraemic Tumoral Calcinosis in Haemodialysis Patients

Author(s):  
Haiting Huang ◽  
Jun Lu ◽  
Pengwei Guo ◽  
Jun Pang ◽  
Jing Ma ◽  
...  

AbstractFew cases of uraemic tumoral calcinosis (UTC) have been reported. This study aimed to investigate the clinical efficacy of parathyroidectomy for UTC. Historical clinical data of patients with end-stage renal disease and UTC who underwent parathyroidectomy were analysed. Absorption of metastatic calcification was compared before and after operation. Changes in intact parathyroid hormone, serum calcium, phosphorus, and alkaline phosphatase levels were analysed before parathyroidectomy and at 1 week and 3, 6, and 12 months after parathyroidectomy. Eight patients met the enrolment criteria (men, 6; mean age, 38.6 SD 10.9 years). Uraemic tumoral calcinosis, which developed 2–8 years after dialysis began, was caused by secondary hyperparathyroidism. Massive calcium deposition was found in the shoulder (n = 6), hip (n = 3), and elbow (n = 2). Four patients had > 2 joints affected, and a single joint was involved for four patients. Seven patients had rapid remission (< 6 months) of the masses after parathyroidectomy. In one patient, the mass remained unabsorbed until 6 months postoperatively. Hypocalcaemia occurred in all patients where parathyroidectomy was successful, and calcium supplementation was required 1 year postoperatively. Serum intact parathyroid hormone levels on day 7 and at 3 and 6 months postoperatively decreased significantly from baseline and remained low 1 year postoperatively (22.015 SD33.134 pg/mL). Postoperative phosphorus levels were significantly lower than preoperative levels (p < 0.05), but no significant difference was found in alkaline phosphatase levels (p > 0.05). Parathyroidectomy has promising efficacy for UTC treatment and regulation of serum intact parathyroid hormone and phosphorus. Hypocalcaemia is a common complication after parathyroidectomy. Current Controlled Trials ChiCTR2000041311, date of registration: Dec. 23, 2020.

2019 ◽  
Author(s):  
Takashi Hatano ◽  
Yu Imai ◽  
Kei-ichiro Mori ◽  
Jun Moritake ◽  
Katsuhisa Endo ◽  
...  

Abstract The most common renal symptoms of tuberous sclerosis complex (TSC) are angiomyolipomas (AMLs) and renal cysts; however, some patients with TSC also develop urolithiasis. In this study, we evaluated the incidence, risk factors and clinical courses of TSC-associated urolithiasis. We analyzed a total of 102 patients who met the diagnostic criteria for TSC, of whom 15 (14.7%) had urolithiasis. We compared urinary specific gravity, urine pH, serum calcium, intact parathyroid hormone and the use of antiepileptic agents of the urolithiasis and non-urolithiasis groups. The urine specific gravity and urine pH were higher in the urolithiasis group than in the non-urolithiasis group (P = 0.005, P = 0.042, respectively). No significant difference was found between the two groups with regard to the serum corrected calcium and intact parathyroid hormone levels. The antiepileptic drugs topiramate and zonisamide were more frequently administered to the urolithiasis group than the non-urolithiasis group (P <0.001, P = 0.039, respectively). Four patients in the urolithiasis group underwent surgery. Three patients could not receive extracorporeal shock wave lithotripsy due to the risk of bleeding from the AML, and therefore underwent transurethral lithotripsy. If urolithiasis is comorbid with TSC-associated AML, the treatment options are more limited in cases with multiple AMLs around the stone due to an increased risk of hemorrhage. Prevention and early detection of urolithiasis are beneficial to patients with TSC.


1997 ◽  
Vol 78 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Georg Lietz ◽  
Alison Avenell ◽  
Simon P Robins

The influence of Na load on bone metabolism was investigated in postmenopausal women using urinary deoxypyridinoline (DPD) as a marker of bone resorption. In a cross-over study, fourteen postmenopausal women were divided into two groups of seven. A fixed diet providing 816 mg Ca/d with either 60 or 170 mmol Na/d was consumed. At the end of an 8 d period the groups switched diets for a further 8d period. Urine was collected daily for the last 4d of each period. There was no significant difference in DPD excretion between high-Na and low-Na diets (129 nmol/d v. 132 nmol/d; P = 0·18). There was, however, a significant relationship (P = 0·02) between the changes in DPD excretion and urinary Ca. Plasma Mg fell from 0·83 to 0·81mmol/l on the high Na intake (P<0·001), but there was no significant effect on plasma Ca or intact parathyroid hormone levels. It is concluded that varying dietary Na intake may affect Ca and Mg metabolism, but we were unable to demonstrate an effect on bone resorption at the levels of intake used


2005 ◽  
Vol 101 (3) ◽  
pp. c122-c127 ◽  
Author(s):  
Cristina Jorge ◽  
Célia Gil ◽  
Marília Possante ◽  
Eugénia Silva ◽  
Rui Andrade ◽  
...  

2004 ◽  
Vol 286 (5) ◽  
pp. E686-E696 ◽  
Author(s):  
Radhika Vattikuti ◽  
Dwight A. Towler

Cardiovascular calcification is a common consequence of aging, diabetes, hypercholesterolemia, mechanically abnormal valve function, and chronic renal insufficiency. Although vascular calcification may appear to be a uniform response to vascular insult, it is a heterogenous disorder, with overlapping yet distinct mechanisms of initiation and progression. A minimum of four histoanatomic variants—atherosclerotic (fibrotic) calcification, cardiac valve calcification, medial artery calcification, and vascular calciphylaxis—arise in response to metabolic, mechanical, infectious, and inflammatory injuries. Common to the first three variants is a variable degree of vascular infiltration by T cells and macrophages. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clear; stroke, amputation, ischemic heart disease, and increased mortality are portended by the anatomy and extent of calcific vasculopathy. Along with dystrophic calcium deposition in dying cells and lipoprotein deposits, active endochondral and intramembranous (nonendochondral) ossification processes contribute to vascular calcium load. Thus vascular calcification is subject to regulation by osteotropic hormones and skeletal morphogens in addition to key inhibitors of passive tissue mineralization. In response to oxidized lipids, inflammation, and mechanical injury, the microvascular smooth muscle cell becomes activated. Orthotopically, proliferating stromal myofibroblasts provide osteoprogenitors for skeletal growth and fracture repair; however, in valves and arteries, vascular myofibroblasts contribute to cardiovascular ossification. Current data suggest that paracrine signals are provided by bone morphogenetic protein-2, Wnts, parathyroid hormone-related polypeptide, osteopontin, osteoprotegerin, and matrix Gla protein, all entrained to endocrine, metabolic, inflammatory, and mechanical cues. In end-stage renal disease, a “perfect storm” of vascular calcification often occurs, with hyperglycemia, hyperphosphatemia, hypercholesterolemia, hypertension, parathyroid hormone resistance, and iatrogenic calcitriol excess contributing to severe calcific vasculopathy. This brief review recounts emerging themes in the pathobiology of vascular calcification and highlights some fundamental deficiencies in our understanding of vascular endocrinology and metabolism that are immediately relevant to human health and health care.


2017 ◽  
Vol 34 (12) ◽  
pp. 1199-1204 ◽  
Author(s):  
Erin Tkach ◽  
Ammie White ◽  
Kevin Dysart ◽  
Brenda Waber ◽  
Ursula Nawab ◽  
...  

Objective We compared the accuracy of serum intact parathyroid hormone (iPTH), alkaline phosphatase (ALP), and phosphate (phos) levels for diagnosing severe metabolic bone disease (MBD) in very low-birth-weight (VLBW) infants with severe bronchopulmonary dysplasia (BPD). Study Design Retrospective analysis of VLBW infants with severe BPD admitted between 2010 and 2012 and with ≥ 1 iPTH, ALP, and phos level collected within a similar 72-hour period. MBD severity was classified by serial radiography. Results Laboratory values were available for 65 infants, of whom 24 (36.9%) developed severe MBD. A maximum ALP > 660 IU/L was the most accurate for diagnosing severe MBD (area under the curve: 88.4%; 95% confidence interval [CI]: 77.2–94.5%). Maximum iPTH was the least accurate (optimal cut point > 130 pg/mL; area under the curve: 70.5%; 95% CI: 58.2–81.4). Conclusion Maximum ALP was more accurate than iPTH or phos for diagnosing severe MBD among preterm infants with severe BPD.


2006 ◽  
Vol 52 (9) ◽  
pp. 1771-1776 ◽  
Author(s):  
Tom Cantor ◽  
Zan Yang ◽  
Nicolae Caraiani ◽  
Ekambaram Ilamathi

Abstract Background: Variability among assays used to measure intact parathyroid hormone (iPTH) is of particular concern because of the routine use of iPTH assay results to guide management of osteodystrophy and calcium metabolism in patients with end-stage renal disease (ESRD). The aim of this study was to determine the extent to which results from commercially available iPTH assays diverge from results obtained with the Nichols Allegro® Intact PTH immunoradiometric assay (IRMA), which was used as evidence in the development of the National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative Clinical Practice Guidelines. Methods: We divided EDTA plasma from 46 dialysis patients with ESRD and measured iPTH values with the following commercially available iPTH assays: Nichols’ Allegro iPTH IRMA, Nichols Advantage® iPTH immunochemiluminescent assay (ICMA), Scantibodies’ Total Intact PTH™ IRMA, DiaSorin’s N-tact® iPTH IRMA, DPC’s Coat-A-Count® iPTH IRMA, Roche’s Elecsys® iPTH ICMA, and DSL’s Active® iPTH IRMA. Results: Method comparison showed considerable interassay differences in the measurement of iPTH in ESRD patients. IPTH values assessed by other methods ranged, on average, from 60% to 152% of the Nichols Allegro IRMA values. Of the 6 iPTH assays tested, only the Scantibodies Total Intact PT IRMA (P = 0.7554) and the Roche Elecsys iPTH ICMA (P = 0.1327) resulted in iPTH values not statistically different from those obtained with the Nichols Allegro iPTH IRMA. Conclusions: Noncomparability among iPTH assays remains a distinct problem for the management of ESRD patients. These results should be taken into consideration when determining the course of medical treatment based on measured iPTH concentrations


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