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113 papers 100 to 500 followers
By Isabel Acosta-Ochoa Nephrology senior staff. Valladolid. Spain
Qing-Ya Zeng, Zhi-Yin Xia, Yan-Shan Tong, Liang Sun, Hong-Bin Mou, Rui Chen, Guang-Yu Bi, Chang-Hua Liu
BACKGROUND: Klotho G-395-A gene polymorphism is associated with several diseases; however, its association with calcium-phosphate metabolism disorders in end-stage renal disease (ESRD) is unknown. METHODS: 137 patients with ESRD and 80 healthy adults (control) were enrolled in the study. Patients with ESRD were divided into three subgroups: hemodialysis (A1, n=52), peritoneal dialysis (A2, n=30), and non-dialysis (A3, n=55). The Klotho G-395-A genotype was detected by TaqMan PCR assay, and ELISA was used to detect the soluble Klotho protein (sKL) and fibroblast growth factor (FGF23)...
December 8, 2018: Nephrology
Chien-Lin Lu, Dong-Feng Yeih, Yi-Chou Hou, Guey-Mei Jow, Zong-Yu Li, Wen-Chih Liu, Cai-Mei Zheng, Yuh-Feng Lin, Jia-Fwu Shyu, Remy Chen, Chung-Yu Huang, Kuo-Cheng Lu
In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status...
December 3, 2018: Nutrients
Florian Lang, Christina Leibrock, Aleksandra A Pandyra, Christos Stournaras, Carsten A Wagner, Michael Föller
Fibroblast growth factor 23 (FGF23) is released primarily from osteoblasts/osteocytes in bone. In cooperation with the transmembrane protein Klotho, FGF23 is a powerful inhibitor of 1α 25OH Vitamin D Hydroxylase (Cyp27b1) and thus of the formation of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). As 1,25(OH)2D3 up-regulates intestinal calcium and phosphate absorption, the downregulation of 1,25(OH)2D3 synthesis counteracts phosphate excess and tissue calcification. FGF23 also directly inhibits renal phosphate reabsorption...
November 30, 2018: Kidney & Blood Pressure Research
Ming Chang Hu, Mingjun Shi, Orson W Moe
Alpha-Klotho is a member of the Klotho family consisting of two other single-pass transmembrane proteins: βKlotho and γKlotho; αKlotho has been shown to circulate in the blood. Fibroblast growth factor (FGF)23 is a member of the FGF superfamily of 22 genes/proteins. αKlotho serves as a co-receptor with FGF receptors (FGFRs) to provide a receptacle for physiological FGF23 signaling including regulation of phosphate metabolism. The extracellular domain of transmembrane αKlotho is shed by secretases and released into blood circulation (soluble αKlotho)...
December 1, 2018: Pflügers Archiv: European Journal of Physiology
Yosuke Nakagawa, Hirotaka Komaba
In patients with chronic kidney disease(CKD), mineral metabolism abnormalities such as hyperphosphatemia, decreased 1,25-dihydroxyvitamin D, and elevated parathyroid hormone develop as kidney function declines, which lead to vascular calcification and a variety of skeletal abnormalities, collectively termed renal osteodystrophy. Because CKD patients have increased risk of bone fractures, it is important to assess fracture risk by measuring bone mineral density and bone metabolism markers. In addition to management of secondary hyperparathyroidism, medications for osteoporosis could be a reasonable option for preventing fracture...
2018: Clinical Calcium
Thierry Hannedouche, Denis Fouque, Dominique Joly
Metabolic complications of chronic kidney disease (CKD) are frequent; the aims of this review are to present a 2018 update for hyperkalemia, hyperphosphatemia and anemia. Hyperkalemia is defined by a plasma level above 5.0 mmol/L, after ruling out pre-analytical problems such as hemolysis. It is frequent in CKD, most often due to drugs and notably renin/ angiotensin blockers. Chronic hyperkalemia is deleterious, with an increased risk of mortality. Therapeutic strategies to decrease the incidence and severity of hyperkalemia are therefore crucial in nephrology: experts recommend to maintain the renin/angiotensin blockers as long as possible, whilst associating diuretics and potassium binders...
November 2018: Néphrologie & Thérapeutique
Matthew J Damasiewicz, Thomas L Nickolas
Renal osteodystrophy (ROD) is the bone component of chronic kidney disease mineral and bone disorder (CKD-MBD). ROD affects bone quality and strength through the numerous hormonal and metabolic disturbances that occur in patients with kidney disease. Collectively these disorders in bone quality increase fracture risk in CKD patients compared with the general population. Fractures are a serious complication of kidney disease and are associated with higher morbidity and mortality compared with the general population...
November 2018: JBMR plus
Makoto Kuro-O
The Klotho proteins, αKlotho and βKlotho, are essential components of endocrine fibroblast growth factor (FGF) receptor complexes, as they are required for the high-affinity binding of FGF19, FGF21 and FGF23 to their cognate FGF receptors (FGFRs). Collectively, these proteins form a unique endocrine system that governs multiple metabolic processes in mammals. FGF19 is a satiety hormone that is secreted from the intestine on ingestion of food and binds the βKlotho-FGFR4 complex in hepatocytes to promote metabolic responses to feeding...
November 19, 2018: Nature Reviews. Nephrology
Varvara Chatzipetrou, Maude Gerbaix, Serge Ferrari, Andrea Trombetti
The management of osteoporosis in patients with mild to moderate chronic kidney disease (CKD) can be established as in general population. In severe or terminal CKD, bone densitometry is indicated. Bone-specific alkaline phosphatase is considered a useful marker for distinguishing among the histologic types of renal osteodystrophy. In ambiguous cases, bone biopsy together with quantitative histomorphometry will be necessary. As far as the treatment is concerned, the bisphosphonates, which had been avoided due to their renal excretion as well as the official warnings against using them in case of renal clearance lower than 30 ml/min, seem to be effective even in advanced stages of renal disease...
November 7, 2018: Revue Médicale Suisse
Joseph Lunyera, Julia J Scialla
Chronic kidney disease mineral and bone disorder (MBD) encompasses changes in mineral ion and vitamin D metabolism that are widespread in the setting of chronic kidney disease and end-stage renal disease. MBD components associate with cardiovascular disease in many epidemiologic studies. Through impacts on hypertension, activation of the renin-angiotensin-aldosterone system, vascular calcification, endothelial function, and cardiac remodeling and conduction, MBD may be a direct and targetable cause of cardiovascular disease...
November 2018: Seminars in Nephrology
David A Bushinsky, David M Spiegel, Jinwei Yuan, Suzette Warren, Jeanene Fogli, Pablo E Pergola
BACKGROUND AND OBJECTIVES: Patiromer is a sodium-free, nonabsorbed, potassium-binding polymer that uses calcium as the counter-exchange ion and is approved for treatment of hyperkalemia. The 4-week TOURMALINE study in patients with hyperkalemia previously demonstrated that patiromer administered once daily reduces serum potassium similarly when given with or without food. We report a prespecified exploratory efficacy analysis as well as a post hoc efficacy and safety analysis of the TOURMALINE study on circulating markers of mineral metabolism...
October 31, 2018: Clinical Journal of the American Society of Nephrology: CJASN
Yan Yang, Shi Qiu, Linghui Deng, Xi Tang, Xinrui Li, Qiang Wei, Ping Fu
BACKGROUND: Mineral bone disease constitutes a common complication of post-kidney transplantation, leading to great disability. As there is no consensus on the optimal treatment for post-kidney transplant recipients (KTRs), we aimed to evaluate the efficacy and safety of bisphosphonate and its combined therapies. METHODS: We incorporated relevant trials to perform a network meta-analysis from direct and indirect comparisons. We searched PubMed, Embase and the CENTRAL and the reference lists of relevant articles up to August 1, 2017, for randomized controlled trials...
October 19, 2018: BMC Nephrology
J Aleksova, K W Ng, C Jung, H Zeimer, K M Dwyer, F Milat, R J MacIsaac
The metabolic abnormalities affecting bone in the setting of chronic kidney disease (CKD) are complex with over-lapping and inter-acting aetiologies and have challenging diagnostic and management strategies. Disturbances in calcium, phosphate, fibroblast growth factor 23, parathyroid hormone (PTH) concentrations and vitamin D deficiency are commonly encountered and contribute to the clinical syndromes of bone disorders in CKD including hyperparathyroidism, osteomalacia, osteoporosis and adynamic bone disease...
October 9, 2018: Internal Medicine Journal
Yi-Chou Hou, Chien-Lin Lu, Kuo-Cheng Lu
As the GFR loss aggravates, the disturbed mineral metabolism worsens the bone microstructure and remodelling - scenario, which is known as CKD-mineral bone disease (MBD). CKD-MBD is characterized by : (i) abnormal metabolism of calcium, phosphorus, parathyroid hormone (PTH), or vitamin D; (ii) abnormalities in bone turnover, mineralization, volume linear growth or strength; (iii) soft-tissue calcifications, either vascular or extra-osseous. Uremic vascular calcification and osteoporosis are the most common complications related to CKD-MBD...
October 2018: Nephrology
Allison B Reiss, Nobuyuki Miyawaki, Jane Moon, Lora J Kasselman, Iryna Voloshyna, Robert D'Avino, Joshua De Leon
Mineral bone disease (MBD) is a common complication of chronic kidney disease (CKD) characterized by disruption of normal mineral homeostasis within the body. One or more of the following may occur: hypocalcemia, hyperphosphatemia, secondary hyperparathyroidism (SHPT), decreased vitamin D and vascular calcification (VC). The greater the decrease in renal function, the worse the progression of CKD-MBD. These abnormalities may lead to bone loss, osteoporosis and fractures. CKD-MBD is a major contributor to the high morbidity and mortality among patients with CKD...
November 2018: Atherosclerosis
Camiel L M de Roij van Zuijdewijn, Dinky E de Haseth, Bastiaan van Dam, Willem A Bax, Muriel P C Grooteman, Michiel L Bots, Peter J Blankestijn, Menso J Nubé, Marinus A van den Dorpel, Pieter M Ter Wee, Erik L Penne
BACKGROUND/AIMS: In hemodialysis (HD) patients, the bromcresol green (BCG) assay overestimates, whereas the bromcresol purple (BCP) assay underestimates albumin concentration. Since corrected calcium concentrations depend on albumin, the albumin assay may have implications for the management of bone mineral disorders. METHODS: A subset of patients from CONTRAST, a cohort of prevalent HD patients, was analyzed. Bone mineral parameters and prescription of medication were compared between patients in whom albumin was assessed by BCP versus BCG...
2018: Nephron
Judith Beto, Nisha Bhatt, Teresa Gerbeling, Chhaya Patel, Debra Drayer
Renal dietitians play a pivotal role in the ongoing management of chronic kidney disease in patients on hemodialysis. Awareness of changes to clinical practice guidelines that may impact laboratory parameters associated with chronic kidney disease-mineral and bone disorder is important for optimal patient care. In this article, the Kidney Disease: Improving Global Outcomes 2017 Clinical Practice Guideline Update recommendations related to the treatment of secondary hyperparathyroidism in adults on hemodialysis are reviewed and treatment implications for renal dietitians discussed...
August 24, 2018: Journal of Renal Nutrition
Marinella Ruospo, Suetonia C Palmer, Patrizia Natale, Jonathan C Craig, Mariacristina Vecchio, Grahame J Elder, Giovanni Fm Strippoli
BACKGROUND: Phosphate binders are used to reduce positive phosphate balance and to lower serum phosphate levels for people with chronic kidney disease (CKD) with the aim to prevent progression of chronic kidney disease-mineral and bone disorder (CKD-MBD). This is an update of a review first published in 2011. OBJECTIVES: The aim of this review was to assess the benefits and harms of phosphate binders for people with CKD with particular reference to relevant biochemical end-points, musculoskeletal and cardiovascular morbidity, hospitalisation, and death...
August 22, 2018: Cochrane Database of Systematic Reviews
Chandan Vangala, Jenny Pan, Ronald T Cotton, Venkat Ramanathan
The risk of mineral and bone disorders among patients with chronic kidney disease is substantially elevated, owing largely to alterations in calcium, phosphorus, vitamin D, parathyroid hormone, and fibroblast growth factor 23. The interwoven relationship among these minerals and hormones results in maladaptive responses that are differentially affected by the process of kidney transplantation. Interpretation of conventional labs, imaging, and other fracture risk assessment tools are not standardized in the post-transplant setting...
2018: Frontiers in Medicine
Anna Jovanovich, Jessica Kendrick
Chronic kidney disease mineral bone disorder (CKD-MBD) is common in end-stage renal disease and is associated with an increased risk of cardiovascular morbidity and mortality. Mainstays of treatment include decreasing serum phosphorus level toward the normal range with dietary interventions and phosphate binders and treating increased parathyroid hormone levels with activated vitamin D and/or calcimimetics. There is significant variation in serum levels of mineral metabolism markers, intestinal absorption of phosphorus, and therapeutic response among individual patients and subgroups of patients with end-stage renal disease...
July 2018: Seminars in Nephrology
2018-08-09 07:37:11
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