scholarly journals Correlation of serum parathyroid hormone with mineral bone disease in chronic kidney disease patients

2015 ◽  
Vol 8 (6) ◽  
pp. 708
Author(s):  
RajeshwariS Vhora ◽  
Avinash Munde ◽  
Charan Bale ◽  
ArjunLal Kakrani
Nephrology ◽  
2006 ◽  
Vol 11 (6) ◽  
pp. 555-559 ◽  
Author(s):  
JASON DEVILLE ◽  
MICAH L THORP ◽  
LOIS TOBIN ◽  
EEVA GRAY ◽  
ERIC S JOHNSON ◽  
...  

2005 ◽  
Vol 123 (2) ◽  
pp. 83-87 ◽  
Author(s):  
Carlos Perez Gomes ◽  
Maria Inês Barreto Silva ◽  
Maria Eugênia Leite Duarte ◽  
David Dorigo ◽  
Carla Cavalheiro da Silva Lemos ◽  
...  

CONTEXT AND OBJECTIVE: Few studies have focused on bone disease in patients with chronic kidney disease under conservative treatment. The objective was to evaluate bone disease in patients with chronic kidney disease. DESIGN AND SETTING: Case series, at the Nephrology Division, Hospital Universitário Pedro Ernesto. METHODS: 131 patients with creatinine clearance from 10 to 60 ml/min/1.73 m² were followed up for at least one year. Serum creatinine, albumin, calcium, phosphorus, alkaline phosphatase, total CO2 (tCO2), intact parathyroid hormone (iPTH), and alkaline phosphatase were measured. Creatinine clearance was calculated from 24-hour urine creatinine measurements and protein ingestion estimates from urea assays. RESULTS: Patients presenting creatinine clearance < 30 ml/min/1.73 m² had higher iPTH values, but normal serum levels for calcium, phosphorus, alkaline phosphatase and tCO2. Patients presenting iPTH values of twice the normal upper limit (144 pg/ml) showed lower tCO2 values. Bone alkaline phosphatase was evaluated in 37 patients with creatinine clearance < 30 ml/min/1.73 m², showing correlation with alkaline phosphatase but not with parathyroid hormone. Bone biopsy on nine patients with creatinine clearance < 30 ml/min/1.73 m² and iPTH > 144 pg/ml showed osteitis fibrosa (4), mild lesion (4) and high turnover (1). CONCLUSION: The present data suggest the importance of early control for iPTH and metabolic acidosis, among patients under conservative management for chronic kidney disease, in order to prevent complications related to bone disease.


2014 ◽  
Vol 19 (3) ◽  
pp. 202-205
Author(s):  
Kristen R. Nichols ◽  
Chad A. Knoderer ◽  
Bethanne Johnston ◽  
Amy C. Wilson

A 2-year-old male with chronic kidney disease with secondary hyperparathyroidism developed hypercalcemia while receiving calcitriol, without achieving a serum parathyroid hormone concentration within the goal range. Cinacalcet 15 mg (1.2 mg/kg), crushed and administered via gastrostomy tube, was added to the patient’s therapy. This therapy was effective in achieving targeted laboratory parameters in our patient despite instructions in the prescribing information that cinacalcet should always be taken whole.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Canlin Yang ◽  
Xiaotong Xie ◽  
Jie Xing ◽  
Xin Yang ◽  
Xiao liang Zhang

Abstract Background and Aims Vascular calcification is an independent predict factor of cardiovascular mortality and all-cause mortality in chronic kidney disease (CKD) patients. Animals experiments and clinical studies showed the inhibition effect of diphosphonates in vascular calcification, but the results of the studies remains controversial. This meta-analysis aims to evaluate the effects of diphosphonates on vascular calcification in patients with CKD. Method Randomized controlled trials (RCT) and non-RCTs of diphosphonates for the treatment of vascular calcification in CKD patients until September 2020 were searched in the database of PubMed, Embase, Cochrane library, CNKI and Wanfang. Literatures were screened according to the inclusion and exclusion criteria and quality was evaluated by two investigators independently. The standard deviation from mean (SMD) and 95% confidence interval (CI) were used to representthe counting data. Data extracted from the literatures were analyzed with Stata software (version 15.0). Results A total of 6 RCTs and 1 non-RCT with 272 patients were included, characteristics of the studies included are shown in Table 1. Meta-analysis indicated that diphosphonates inhibit vascular calcification in CKD [SMD =-0.297, 95% CI = (-0.591, -0.002), P = 0.049] (Figure 1). Etidronate is the most effective one in treating with vascular calcification (P = 0.020) (Figure 2). But there isn’t significant difference in aortic artery calcification and coronary artery calcification compared with the control group (P&gt;0.05). There was no statistically significant difference in the change of blood calcium, blood phosphate, and serum parathyroid hormone between two groups (all P&gt;0.05). Conclusion Diphosphonates can inhibit the progression of vascular calcification in CKD patients, and it hasn’t obvious effect on blood calcium, blood phosphate, and serum parathyroid hormone. Etidronate is the most promising therapeutic agent.


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