Secondary hyperparathyroidism is a difficult complication of chronic kidney disease (CKD) patients. Its prevalence increases in parallel with the worsening of renal function, reaching 90% in CKD patients stage 5/5D. Its genesis is multifactorial, with dysregulation of Vitamin D and FGF-23 playing a major role. In patients affected by hyperparathyroidism, the skeleton loses its natural strength becoming extremely frail. The incidence of fractures is approximately 3-4 times higher than in the general population, as compared for age and gender. Other complications including bone pain, pruritus and worsening of anemia, are also common in this condition. In addition, valve and vascular calcifications, vascular stiffness and calciphylaxis are dreadful consequences of hyperparathyroidism. Taken together, all these comorbidities related to hyperparathyroidism contribute to reduce the quality of life in these patients, increasing the risk of cardiovascular morbidity and mortality.
Guidelines represent a valid aid to clinical practice; however, the transition from the KDOQI to KDIGO guidelines, has not been completely accepted by the whole nephrological community. Furthermore, the patient’s awareness of hyperparathyroidism and its complications are not sufficiently emphasized. During the last 20 years, pharmaceutical companies has developed at least 20 new drugs that can be pave the way to personalized medicine. Among them, active vitamin D compounds, such as calcitriol, newer vitamin D analogues, associated with modulation of calcium and phosphorous balance by dietary intake and dialysis, phosphate binders, and the most recent calcimimetics are the most used therapeutic strategies. In particular, calcimimetics are effective in controlling hyperparathyroidism; studies are also underway to evaluate the effect on extra-skeletal complications, such as cardiovascular comorbidities. Another very promising category of drugs are antisclerostin antibodies; a short formal indication is awaited for their use also in CKD patients. The current focus is thus to identify new molecules involved in physiopathology of bone metabolism (interleukins, sclerostin, ect.) and to develop new drugs able to help the patients reach the guidelines targets.
In this Research Topic, we invite researchers to contribute original articles, case reports and review articles that offer insight into secondary hyperparathyroidism in CKD patients. Articles may address various aspect of mineral metabolism, and in particular of secondary hyperparathyroidism and its impact in cardiovascular comorbidities and fractures. Potential topics include but are not limited to the following:
• Epidemiology of secondary hyperparathyroidism
• Physiopathology of secondary hyperparathyroidism
• Molecular mechanisms shared between bone and other organs and/or diseases
• Recent discoveries in animal/in-vitro models to unravel molecular mechanisms involved in mineral metabolism in CKD and/or ESRD patients
• Alterations in mineral bone metabolism and complications
• Secondary hyperparathyroidism and quality of life
• Targets in mineral bone metabolism (different guidelines)
• Therapeutic approach in secondary hyperparathyroidism
• Patients awareness in secondary hyperparathyroidism
Secondary hyperparathyroidism is a difficult complication of chronic kidney disease (CKD) patients. Its prevalence increases in parallel with the worsening of renal function, reaching 90% in CKD patients stage 5/5D. Its genesis is multifactorial, with dysregulation of Vitamin D and FGF-23 playing a major role. In patients affected by hyperparathyroidism, the skeleton loses its natural strength becoming extremely frail. The incidence of fractures is approximately 3-4 times higher than in the general population, as compared for age and gender. Other complications including bone pain, pruritus and worsening of anemia, are also common in this condition. In addition, valve and vascular calcifications, vascular stiffness and calciphylaxis are dreadful consequences of hyperparathyroidism. Taken together, all these comorbidities related to hyperparathyroidism contribute to reduce the quality of life in these patients, increasing the risk of cardiovascular morbidity and mortality.
Guidelines represent a valid aid to clinical practice; however, the transition from the KDOQI to KDIGO guidelines, has not been completely accepted by the whole nephrological community. Furthermore, the patient’s awareness of hyperparathyroidism and its complications are not sufficiently emphasized. During the last 20 years, pharmaceutical companies has developed at least 20 new drugs that can be pave the way to personalized medicine. Among them, active vitamin D compounds, such as calcitriol, newer vitamin D analogues, associated with modulation of calcium and phosphorous balance by dietary intake and dialysis, phosphate binders, and the most recent calcimimetics are the most used therapeutic strategies. In particular, calcimimetics are effective in controlling hyperparathyroidism; studies are also underway to evaluate the effect on extra-skeletal complications, such as cardiovascular comorbidities. Another very promising category of drugs are antisclerostin antibodies; a short formal indication is awaited for their use also in CKD patients. The current focus is thus to identify new molecules involved in physiopathology of bone metabolism (interleukins, sclerostin, ect.) and to develop new drugs able to help the patients reach the guidelines targets.
In this Research Topic, we invite researchers to contribute original articles, case reports and review articles that offer insight into secondary hyperparathyroidism in CKD patients. Articles may address various aspect of mineral metabolism, and in particular of secondary hyperparathyroidism and its impact in cardiovascular comorbidities and fractures. Potential topics include but are not limited to the following:
• Epidemiology of secondary hyperparathyroidism
• Physiopathology of secondary hyperparathyroidism
• Molecular mechanisms shared between bone and other organs and/or diseases
• Recent discoveries in animal/in-vitro models to unravel molecular mechanisms involved in mineral metabolism in CKD and/or ESRD patients
• Alterations in mineral bone metabolism and complications
• Secondary hyperparathyroidism and quality of life
• Targets in mineral bone metabolism (different guidelines)
• Therapeutic approach in secondary hyperparathyroidism
• Patients awareness in secondary hyperparathyroidism
