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Johan Svensson Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Åsa Tivesten Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Klara Sjögren Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Olle Isaksson Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Göran Bergström Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Subburaman Mohan Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Johan Mölne Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Jörgen Isgaard Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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Claes Ohlsson Department of Internal Medicine, Sahlgrenska University Hospital, Gröna Stråket 8, SE-413 45 Göteborg, Sweden
Department of Clinical Physiology, Göteborg University, Göteborg, Sweden
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California, USA
Department of Pathology, Sahlgrenska University Hospital, Göteborg, Sweden

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). In diabetic as well as non diabetic end-stage renal failure, there are marked abnormalities in the GH/IGF-I system ( Jain et al. 1998 , Rabkin & Schaefer 2004 ). In humans with diabetes mellitus (DM) type I, circulating IGF-I is low and

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0024
Volume/Issue:
Volume 193: Issue 3
Free access
Alaa E S Abdel-Razik Faculty of Life Sciences, University of Manchester, 1.124 Stopford Building, Oxford Road, Manchester M13 9PT, UK

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Ellen J Forty Faculty of Life Sciences, University of Manchester, 1.124 Stopford Building, Oxford Road, Manchester M13 9PT, UK

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Richard J Balment Faculty of Life Sciences, University of Manchester, 1.124 Stopford Building, Oxford Road, Manchester M13 9PT, UK

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Nick Ashton Faculty of Life Sciences, University of Manchester, 1.124 Stopford Building, Oxford Road, Manchester M13 9PT, UK

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. 2002 ). Furthermore, recent evidence now suggests that UTS may play a role in regulating renal function in mammals. The kidney is a major source of UTS in humans ( Nothacker et al . 1999 ), primates, mice ( Elshourbagy et al . 2002 ) and rats ( Song

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0260
Volume/Issue:
Volume 198: Issue 3
Free access
Kayte A Jenkin College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia

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Lannie O'Keefe College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia

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Anna C Simcocks College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia

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Esther Grinfeld College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia

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Michael L Mathai College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia
College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia

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Andrew J McAinch College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia

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Deanne H Hryciw College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia

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, it is important to identify physiological targets, which may ameliorate the progression of obesity and the subsequent decline in renal function. The endocannabinoid system has been characterised as an important endogenous lipid signalling system

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0004
Volume/Issue:
Volume 225: Issue 2
Free access
Emily G Farrow
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Lelia J Summers
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Susan C Schiavi Department of Medical and Molecular Genetics, Genzyme, Oregon Health and Science University, Indiana University School of Medicine, 975 West Walnut Street, IB130, Indianapolis, Indiana 46202, USA

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James A McCormick Department of Medical and Molecular Genetics, Genzyme, Oregon Health and Science University, Indiana University School of Medicine, 975 West Walnut Street, IB130, Indianapolis, Indiana 46202, USA

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David H Ellison Department of Medical and Molecular Genetics, Genzyme, Oregon Health and Science University, Indiana University School of Medicine, 975 West Walnut Street, IB130, Indianapolis, Indiana 46202, USA

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Kenneth E White
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hyperphosphatemic tumoral calcinosis (TC). In situations of elevated FGF23, renal phosphate wasting occurs through down-regulation of the proximal tubule (PT) membrane type-IIa (Npt2a) and type-IIc (Npt2c) sodium phosphate co-transporters ( Larsson et al . 2004

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-10-0181
Volume/Issue:
Volume 207: Issue 1
Free access
Georgios A Christou Laboratory of Physiology, Medical School, University of Ioannina, 45110 Ioannina, Greece

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Dimitrios N Kiortsis Laboratory of Physiology, Medical School, University of Ioannina, 45110 Ioannina, Greece

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cardiovascular disease (CVD) in obese or overweight patients ( Hotta et al . 2000 ). Adiponectin is currently considered to be eliminated through renal biodegradation/excretion, but this mechanism has been proposed mostly on the basis of indirect data ( von

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-13-0578
Volume/Issue:
Volume 221: Issue 2
Free access
Li Juan He Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, People's Republic of China

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Min Liang Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, People's Republic of China

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Fan Fan Hou Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, People's Republic of China

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Zhi Jian Guo Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, People's Republic of China

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Di Xie Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, People's Republic of China

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Xun Zhang Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, People's Republic of China

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Introduction Diabetic nephropathy is a major complication of diabetes and a leading cause of end-stage renal failure in many countries. Although hyperglycemia is the underlying metabolic abnormality, many other mechanisms have also been proposed for

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0481
Volume/Issue:
Volume 200: Issue 3
Free access
Claire E Hills Department of Biological Sciences, Department of Infection, Biomedical Research Institute, The University of Warwick, Coventry CV4 7AL, UK

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Paul E Squires
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Rosemary Bland
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Introduction Diabetic nephropathy is a leading cause of chronic kidney disease and end-stage renal disease in the US and Europe (reviewed in Ritz 1999 ). This condition includes both structural and functional alterations in the kidney of the

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0295
Volume/Issue:
Volume 199: Issue 3
Free access
Youichi Sato Department of Pharmaceutical Information Science, Institute of Health Biosciences, The University of Tokushima Graduate School, 1-78-1 Sho-machi, Tokushima City 770-8505 Japan

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Takanobu Kamada Department of Pharmaceutical Information Science, Institute of Health Biosciences, The University of Tokushima Graduate School, 1-78-1 Sho-machi, Tokushima City 770-8505 Japan

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Aiko Yamauchi Department of Pharmaceutical Information Science, Institute of Health Biosciences, The University of Tokushima Graduate School, 1-78-1 Sho-machi, Tokushima City 770-8505 Japan

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inhibitors and the role of DPP4 in various tissues are not fully understood. We previously showed that DPP4-deficient rats developed renal dysfunction when compared with WT rats following streptozotocin (STZ) treatment to induce diabetes. Creatinine clearance

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0016
Volume/Issue:
Volume 223: Issue 2
Free access
Shun-Neng Hsu The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, UK
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan

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Louise A Stephen The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, UK

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Scott Dillon The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, UK

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Elspeth Milne The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, UK

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Behzad Javaheri Comparative Biomedical Sciences, The Royal Veterinary College, London, UK

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Andrew A Pitsillides Comparative Biomedical Sciences, The Royal Veterinary College, London, UK

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Amanda Novak The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, UK

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Jose Luis Millán Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA

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Vicky E MacRae The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, UK

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Katherine A Staines Centre for Stress and Age-Related Disease, University of Brighton, Brighton, UK

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Colin Farquharson The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, UK

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of CKD–mineral bone disorder (CKD–MBD) which develops in the early stages of CKD and disease progression can result in cardiovascular disease and renal osteodystrophy (ROD) – the skeletal pathology component of the CKD-MBD syndrome ( Fang et al

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-22-0097
Volume/Issue:
Volume 254: Issue 3
Open access
Shigeru Shibata Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan
Division of Clinical Epigenetics, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan

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body mainly by acting on the distal part of the renal nephron (which normally includes distal convoluted tubules (DCTs), connecting tubules and collecting duct). Although NaCl reabsorbed in the distal segment represents only a fraction of that handled

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-16-0669
Volume/Issue:
Volume 234: Issue 1
Free access