scholarly journals Treatment of secondary hyperparathyroidism in patients on hemodialysis using a novel synthetic peptide calcimimetic, etelcalcetide: a short-term clinical study

2018 ◽  
Vol 46 (11) ◽  
pp. 4578-4585 ◽  
Author(s):  
Akira Mima ◽  
Kosuke Tansho ◽  
Dai Nagahara ◽  
Kenji Watase
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Major Complication ◽  
Therapeutic Effects ◽  
Serum Parathyroid Hormone ◽  
Short Term ◽  
Mineral Bone Disorder ◽  
Gastrointestinal Adverse Events ◽  
Observation Period

Objective Secondary hyperparathyroidism (SHPT) is a major complication in patients with chronic kidney disease (CKD). SHPT is related to chronic kidney disease-mineral bone disorder, leading to increased morbidity and mortality. Etelcalcetide is intravenously administered at the end of hemodialysis (HD). Etelcalcetide differs from the oral calcimimetic cinacalcet because it reduces gastrointestinal adverse events, thereby improving therapeutic effects. Etelcalcetide has only been approved by the U.S. Food and Drug Administration for several months. Therefore, there have only been a few reports regarding treatment of SHPT using etelcalcetide. This study aimed to evaluate the efficacy of etelcalcetide in patients on HD with SHPT. Methods Nine patients on HD (four men and five women, aged 58 ± 10 years) were enrolled in this study. All of the patients received etelcalcetide (5–10 mg, three times a week after HD). The observation period was 4.4 ± 1.0 months. Results All of the patients showed a significant reduction in serum parathyroid hormone levels during the observation period (−59% ± 20%). No significant adverse effects were observed. Conclusions Although this study had an uncontrolled small group and a short observation period, our results suggest that etelcalcetide could be a promising agent for SHPT treatment.

scholarly journals Generalised osteitis fibrosa cystica due to secondary hyperparathyroidism in chronic kidney disease

2014 ◽  
Vol 9 (1) ◽  
pp. 60-66
Author(s):  
Sundar K Shrestha ◽  
A Tayal
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Osteitis Fibrosa ◽  
Screening Methods ◽  
Medical Sciences ◽  
Serum Parathyroid Hormone ◽  
Mortality And Morbidity ◽  
Osteitis Fibrosa Cystica ◽  
High Bone

Secondary hyperparathyroidism is a frequent complication of patients with chronic kidney disease and is characterized by excessive serum parathyroid hormone levels and an imbalance in calcium and phosphorus metabolism. Secondary hyperparathyroidism is the leading cause of renal osteodystrophy and bone disease. Osteitis fibrosa cystica, the classic and former most common osteodystrophy, is mainly caused by high bone turnover secondary to high levels of circulating PTH. Its pathophysiology is mainly due to hyperphosphatemia and vitamin D deficiency and resistance. This condition has a high impact on the mortality and morbidity of dialysis patients Hyperparathyroidism develops early in the course of CKD and becomes more prominent as kidney function declines. However recently, with the technical development of imaging and laboratory screening methods, hypercalcemia due to primary or secondary hyperparathyroidism can often be detected early; as a result the frequency of osteitis fibrosa cystica has declined. Journal of College of Medical Sciences-Nepal, 2013, Vol-9, No-1, 60-66 DOI: http://dx.doi.org/10.3126/jcmsn.v9i1.9676

scholarly journals Cinacalcet Administration by Gastrostomy Tube in a Child Receiving Peritoneal Dialysis

2014 ◽  
Vol 19 (3) ◽  
pp. 202-205
Author(s):  
Kristen R. Nichols ◽  
Chad A. Knoderer ◽  
Bethanne Johnston ◽  
Amy C. Wilson
Keyword(s):  
Chronic Kidney Disease ◽  
Peritoneal Dialysis ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Gastrostomy Tube ◽  
Hormone Concentration ◽  
Serum Parathyroid Hormone ◽  
Laboratory Parameters ◽  
Prescribing Information

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.

Potential effect of pharmaceutical care to improve outcomes in patients with chronic kidney disease-mineral bone disorder in Sulaimani dialysis centers

2020 ◽  
pp. 82-94
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Pharmaceutical Care ◽  
Biochemical Parameters ◽  
Positive Impact ◽  
Potential Effect ◽  
Care Group ◽  
Mineral Bone Disorder ◽  
Bone Disorder

Objective: the present study was aimed to evaluate the role of pharmaceutical services in improving the outcome of mineral bone disorder in patients with advanced chronic kidney disease. Methodology: One hundred and twenty patients with chronic kidney disease-mineral bone disorder (CKD-MBD) screened for eligibility, seventy-six patients enrolled in the study and randomly allocated into two groups: pharmaceutical care and usual care, both groups interviewed by the pharmacist using specific questionnaire for assessing the quality of life (QoL). All the drug related problems (DRPs) including drug-drug interactions (DDIs) were recorded by the pharmacist. Blood samples were collected and utilized for analyzing the levels of vitamin D, phosphorous, calcium, albumin and parathyroid hormone at baseline and three months after. The pharmaceutical care group received all the educations about their medications and how to minimize DRPs; improve the QoL. Additionally, the pharmaceutical intervention included correcting the biochemical parameters. Results: Pharmaceutical care significantly improved patients QoL and minimized DRPs and DDIs. It was also effective in improving the biochemical parameters. Conclusion: Pharmaceutical care has a positive impact on improving the outcome of patients with CKD-MBD through attenuating DRPs, improving the biochemical parameters and the QoL.

Effect of parathyroidectomy on bone tissue biomarkers and body composition in patients with chronic kidney disease and secondary hyperparathyroidism

2021 ◽  
Author(s):  
Flavia Ramos de Siqueira ◽  
Karin Carneiro de Oliveira ◽  
Wagner Vasques Dominguez ◽  
César Augusto Madid Truyts ◽  
Rosa Maria Affonso Moysés ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Body Composition ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Bone Tissue ◽  
Tissue Biomarkers

scholarly journals Enteropeptidase inhibitor SCO-792 effectively prevents kidney function decline and fibrosis in a rat model of chronic kidney disease

2020 ◽  
Author(s):  
Yuko Katayama ◽  
Jun Sugama ◽  
Tomohisa Suzuki ◽  
Yoshimasa Ishimura ◽  
Akihiro Kobayashi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Function ◽  
Therapeutic Potential ◽  
Renal Plasma Flow ◽  
Production Capacity ◽  
Therapeutic Effects ◽  
Kidney Fibrosis ◽  
Obesity And Diabetes ◽  
Gfr Decline

Abstract Background Inhibiting enteropeptidase, a gut serine protease regulating protein digestion, suppresses food intake and ameliorates obesity and diabetes in mice. However, the effects of enteropeptidase inhibition on the kidney parameters are largely unknown. Here, we evaluated the chronic effects of an enteropeptidase inhibitor, SCO-792, on kidney function, albuminuria, and kidney pathology in spontaneously hypercholesterolaemic (SHC) rats, a rat chronic kidney disease (CKD) model. Methods SCO-792, an orally available enteropeptidase inhibitor, was administered (0.03% and 0.06% (w/w) in the diet) for five weeks to 20-week-old SHC rats showing albuminuria and progressive decline in glomerular filtration rate (GFR). The effects of SCO-792 and the contribution of amino acids to these effects were evaluated. Results SCO-792 increased the faecal protein content, indicating that SCO-792 inhibited enteropeptidase in SHC rats. Chronic treatment with SCO-792 prevented GFR decline and suppressed albuminuria. Moreover, SCO-792 improved glomerulosclerosis and kidney fibrosis. Pair feeding with SCO-792 (0.06%) was less effective in preventing GFR decline, albuminuria, and renal histological damage than SCO-792 treatment, indicating the enteropeptidase-inhibition-dependent therapeutic effects of SCO-792. SCO-792 did not affect the renal plasma flow, suggesting that its effect on GFR was mediated by an improvement in filtration fraction. Moreover, SCO-792 increased hydrogen sulphide production capacity, which has a role in tissue protection. Finally, methionine and cysteine supplementation to the diet abrogated SCO-792-induced therapeutic effects on albuminuria. Conclusions SCO-792-mediated inhibition of enteropeptidase potently prevented GFR decline, albuminuria, and kidney fibrosis; hence, it may have therapeutic potential against CKD.

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