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3 results on '"chronic kidney disease – mineral bone disorder"'

1. Different Effect of Lanthanum Carbonate and Sevelamer Hydrochloride on Calcium Balance in Patients with Moderate to Advanced Chronic Kidney Disease

Author

Makowka A and Nowicki M

Subjects
calcium, chronic kidney disease – mineral bone disorder, hyperphosphatemia, phosphate-binders, pth, Therapeutics. Pharmacology, RM1-950
Abstract

Agnieszka Makowka, Michal Nowicki Department of Nephrology, Hypertension and Kidney Transplantation, Medical University of Lodz, Lodz, PolandCorrespondence: Michal NowickiDepartment of Nephrology, Hypertension and Kidney Transplantation, Medical University of Lodz, Central University Hospital, Pomorska Str 251, Lodz, 92-213, PolandTel +48 42 2014400Fax +48 42 2014401Email nefro@wp.plObjective: Opposite to lanthanum carbonate (LC), sevelamer hydrochloride (SH) may increase intestinal calcium absorption. The study compared the effects of LC and SH on serum and urine phosphate and calcium, and on hormones regulating mineral-bone metabolism.Patients and Methods: A prospective randomized crossover study included 34 patients with eGFR < 60 mL/min. A single oral dose of LC (1,000 mg) or SH (2,400 mg) was administered in random order 15 minutes after a standardized meal fortified with 5 g calcium carbonate. Serum calcium, phosphate, and parathormone were measured before and 3, 6, 12, and 24 hours after each medication. Bone alkaline phosphatase (BAP), sclerostin, calcitriol, and FGF-23 were measured at baseline and after 12 and 24 hours. A 24-hour calcium and phosphate excretion was measured after each drug.Results: Serum calcium increased 3 and 6 hours after SH then returned to baseline. After LC calcium was unchanged for up to 3 hours then transiently increased and eventually returned to baseline. The area under curve (AUC) of serum calcium for 12 hours after SH was larger than after LC (p=0.04). Serum phosphate decreased after each drug with a nadir 3 hours post-SH and 6 hours post-LC. AUC of serum phosphate was similar after both medications. PTH decreased transiently after both drugs. BAP did not change. FGF-23 was constant for the first 12 hours but later decreased after each drug.Conclusion: A 2,400 mg SH and 1,000 mg LC are similarly effective in lowering serum phosphate in CKD, but LC induce in less intestinal calcium absorption after a meal. The trial was registered on February 23, 2018 in the clinicaltrial.gov database – NCT03451019.Keywords: calcium, chronic kidney disease – mineral bone disorder, hyperphosphatemia, phosphate-binders, PTH

Published
2021

2. Different Effect of Lanthanum Carbonate and Sevelamer Hydrochloride on Calcium Balance in Patients with Moderate to Advanced Chronic Kidney Disease

Author

Agnieszka Makówka and Michał Nowicki

Subjects
medicine.medical_specialty, Therapeutics and Clinical Risk Management, Calcitriol, phosphate-binders, chemistry.chemical_element, Calcium, Excretion, Hyperphosphatemia, chemistry.chemical_compound, Internal medicine, medicine, Pharmacology (medical), General Pharmacology, Toxicology and Pharmaceutics, hyperphosphatemia, Original Research, Calcium metabolism, Chemical Health and Safety, calcium, business.industry, General Medicine, medicine.disease, Phosphate, Crossover study, Lanthanum carbonate, Endocrinology, chemistry, chronic kidney disease – mineral bone disorder, business, Safety Research, medicine.drug, PTH
Abstract

Agnieszka Makowka, Michal Nowicki Department of Nephrology, Hypertension and Kidney Transplantation, Medical University of Lodz, Lodz, PolandCorrespondence: Michal NowickiDepartment of Nephrology, Hypertension and Kidney Transplantation, Medical University of Lodz, Central University Hospital, Pomorska Str 251, Lodz, 92-213, PolandTel +48 42 2014400Fax +48 42 2014401Email nefro@wp.plObjective: Opposite to lanthanum carbonate (LC), sevelamer hydrochloride (SH) may increase intestinal calcium absorption. The study compared the effects of LC and SH on serum and urine phosphate and calcium, and on hormones regulating mineral-bone metabolism.Patients and Methods: A prospective randomized crossover study included 34 patients with eGFR < 60 mL/min. A single oral dose of LC (1,000 mg) or SH (2,400 mg) was administered in random order 15 minutes after a standardized meal fortified with 5 g calcium carbonate. Serum calcium, phosphate, and parathormone were measured before and 3, 6, 12, and 24 hours after each medication. Bone alkaline phosphatase (BAP), sclerostin, calcitriol, and FGF-23 were measured at baseline and after 12 and 24 hours. A 24-hour calcium and phosphate excretion was measured after each drug.Results: Serum calcium increased 3 and 6 hours after SH then returned to baseline. After LC calcium was unchanged for up to 3 hours then transiently increased and eventually returned to baseline. The area under curve (AUC) of serum calcium for 12 hours after SH was larger than after LC (p=0.04). Serum phosphate decreased after each drug with a nadir 3 hours post-SH and 6 hours post-LC. AUC of serum phosphate was similar after both medications. PTH decreased transiently after both drugs. BAP did not change. FGF-23 was constant for the first 12 hours but later decreased after each drug.Conclusion: A 2,400 mg SH and 1,000 mg LC are similarly effective in lowering serum phosphate in CKD, but LC induce in less intestinal calcium absorption after a meal. The trial was registered on February 23, 2018 in the clinicaltrial.gov database – NCT03451019.Keywords: calcium, chronic kidney disease – mineral bone disorder, hyperphosphatemia, phosphate-binders, PTH

Published
2021

3. Novel Aspects in the pathogenesis of Chronic Kidney Disease-Mineral Bone Disorder (CKD-MBD)

Author

Ruderman, Irene and Ruderman, Irene

Abstract

Chronic Kidney Disease – Mineral and Bone Disorder (CKD-MBD) is a clinical entity, broadly defined by (a) disturbances in mineral metabolism, (b) abnormal bone remodeling and (c) accelerated vascular calcification. CKD-MBD is ubiquitous as kidney function deteriorates and contributes significantly to increased fracture risk and excess cardiovascular morbidity and mortality. Due to the complex and multifactorial nature of this condition, there remains many unanswered questions on how to best investigate and manage all aspects of CKD-MBD. The general aim of this thesis was to investigate the pathophysiology, clinical outcomes and novel assessment strategies of the three domains of CKD-MBD. More specifically, this thesis aimed to 1) evaluate the outcomes of calciphylaxis in Australian patients, 2) develop a greater understanding of changes in skin and subcutaneous tissue in patients with kidney disease, 3) demonstrate the consequences of severe secondary hyperparathyroidism (SHPT) in the absence of calcimimetic treatment, 4) understand the temporal relationship between calciprotein particles and biochemical markers of CKD-MBD and 5) evaluate bone microarchitecture in patients with severe SHPT using a novel imaging modality. Although calciphylaxis is a rare disease, it can be considered a form of accelerated vascular calcification. It predominantly affects patients with chronic kidney disease (CKD) and is associated with significant morbidity and mortality due to progressive cutaneous calcification, necrotic ulceration and infection. Clinical registries have been established to better understand risk factors, optimal treatments and disease outcomes of calciphylaxis. To better understand outcomes of Australian patients with calciphylaxis, Chapter 2 investigated the five-year outcomes from the internet-based Australian Calciphylaxis Registry. Data was recorded on patient characteristics, biochemical parameters, treatments and disease outcomes. The Australian Calciphylaxis

Published
2020

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