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

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.

Author(s):  
Giuseppe Cianciolo ◽  
Gaetano La Manna ◽  
Irene Capelli ◽  
Lorenzo Gasperoni ◽  
Andrea Galassi ◽  
...  

Abstract Chronic kidney disease–mineral bone disorder (CKD-MBD) plays a pivotal role in the excess of cardiovascular morbidity and mortality associated with CKD. There is now a growing awareness that pathways involved in CKD-MBD, like canonical Wnt signalling, are activated from the earliest stages of CKD, playing a role in the development of adynamic bone disease with unknown consequences on vasculature. These changes occur before the classic changes in mineral metabolism: secondary hyperparathyroidism, calcitriol deficiency and hyperphosphataemia. Furthermore, vascular calcification is frequently associated and evolves with decreased bone mineral density and deranged bone turnover, while bone and arterial mineralization share common pathways. Therefore, results of clinical trials focused on mineral bone disorder, aimed at preserving bone and cardiovascular health, are considered unsatisfactory. In order to identify more effective therapeutic strategies, it is necessary to clarify the pathways modulating the cross-talk between bone and vasculature and identify new mediators involved in the pathogenesis of CKD-MBD. Much attention has been paid recently to the role of the transforming growth factor-beta superfamily members in renal disease, and in particular of activin A (ActA). Preclinical studies demonstrate an upgrade of ActA signalling in kidney, skeleton, vasculature and heart during CKD. This supports the idea that an endocrine factor produced in the kidney during renal disease, in addition to promoting the progression of kidney damage, deranges other organs’ homoeostasis and participates in CKD-MBD. In this review, we analyse the contribution of ActA to kidney fibrosis and inflammation as well as its role in the development of CKD-MBD.


Author(s):  
Sharjeel Usmani ◽  
Najeeb Ahmed ◽  
Gopinath Gnanasegaran ◽  
Fahad Marafi ◽  
Tim van den Wyngaert

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