2,717 results match your criteria Kidney international. Supplement[Journal]


Effect of kidney disease on glucose handling (including genetic defects).

Kidney Int Suppl 2011 Mar(120):S7-13

Department of Genetics, Faculty of Medical Sciences, New University of Lisbon, Lisbon, Portugal.

Reabsorption of glucose in the proximal renal tubule involves the Na(+)-coupled glucose cotransporter (SGLT) and the facilitative glucose transport (GLUT) multigene glucose transport families. Mutations in SLC5A2, the SGLT2 coding gene, are responsible for familial renal glucosuria (FRG), a genetic disorder characterized by glucosuria in the absence of both hyperglycemia and generalized proximal tubular dysfunction. In this paper we focus on FRG and describe other inherited and acquired clinical conditions associated with glucosuria. Read More

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http://dx.doi.org/10.1038/ki.2010.510DOI Listing
March 2011
7 Reads
9 Citations

Need for better diabetes treatment for improved renal outcome.

Kidney Int Suppl 2011 Mar(120):S28-32

Steno Diabetes Center, Gentofte, Denmark.

Diabetic nephropathy has become a worldwide epidemic accounting for approximately one-third of all cases of end-stage renal disease. The problem is expected to grow, as the prevalence of diabetes is expected to increase from 285 million patients at present to 438 million patients in the year 2030, with increasing prevalence of diabetes particularly in Asia, and a global prevalence of microalbuminuria of ∼ 40%. This will have a major societal impact because of the enormous financial burden of renal replacement therapy and the invalidating character of this disease. Read More

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http://dx.doi.org/10.1038/ki.2010.513DOI Listing
March 2011
4 Reads

Glucose dynamics and mechanistic implications of SGLT2 inhibitors in animals and humans.

Kidney Int Suppl 2011 Mar(120):S20-7

Global Clinical Research, Bristol-Myers Squibb, Princeton, New Jersey, USA.

Glucose is freely filtered in the glomeruli before being almost entirely reabsorbed into circulation from the proximal renal tubules. The sodium-glucose cotransporter 2 (SGLT2), present in the S1 segment of the proximal tubule, is responsible for the majority of glucose reabsorption. SGLT2 inhibitors reduce glucose reabsorption and increase urinary glucose excretion. Read More

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http://dx.doi.org/10.1038/ki.2010.512DOI Listing
March 2011
4 Reads

SGLT2 inhibitors: molecular design and potential differences in effect.

Authors:
Masayuki Isaji

Kidney Int Suppl 2011 Mar(120):S14-9

Kissei Pharmaceutical Co. Ltd, Central Research Laboratory, Nagano, Japan.

The physiological and pathological handling of glucose via sodium-glucose cotransporter-2 (SGLT2) in the kidneys has been evolving, and SGLT2 inhibitors have been focused upon as a novel drug for treating diabetes. SGLT2 inhibitors enhance renal glucose excretion by inhibiting renal glucose reabsorption. Consequently, SGLT2 inhibitors reduce plasma glucose insulin independently and improve insulin resistance in diabetes. Read More

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http://dx.doi.org/10.1038/ki.2010.511DOI Listing
March 2011
10 Reads

Glucose handling by the kidney.

Kidney Int Suppl 2011 Mar(120):S1-6

Department of Medicine, Kolling Institute of Medical Research, University of Sydney, Sydney, NSW, Australia.

The kidney contributes to glucose homeostasis through processes of gluconeogenesis, glucose filtration, glucose reabsorption, and glucose consumption. Each of these processes can be altered in patients with type-2 diabetes (T2DM), providing potential targets for novel therapies. Recent studies have indicated that the kidney is responsible for up to 20% of all glucose production via gluconeogenesis. Read More

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http://dx.doi.org/10.1038/ki.2010.509DOI Listing
March 2011
7 Reads

Bone: from a reservoir of minerals to a regulator of energy metabolism.

Kidney Int Suppl 2011 Apr 23(121):S14-9. Epub 2011 Feb 23.

INSERM U 1033-Université de Lyon, Department of Rheumatology, Hôpital Edouard Herriot, Hospices Civils de Lyon, Lyon, France.

Besides locomotion, organ protection, and calcium-phosphorus homeostasis, the three classical functions of the skeleton, bone remodeling affects energy metabolism through uncarboxylated osteocalcin, a recently discovered hormone secreted by osteoblasts. This review traces how energy metabolism affects osteoblasts through the central control of bone mass involving leptin, serotoninergic neurons, the hypothalamus, and the sympathetic nervous system. Next, the role of osteocalcin (insulin secretion, insulin sensitivity, and pancreas β-cell proliferation) in the regulation of energy metabolism is described. Read More

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http://dx.doi.org/10.1038/ki.2011.25DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257050PMC
April 2011
5 Reads

Phosphate and FGF-23.

Authors:
Harald Jüppner

Kidney Int Suppl 2011 Apr 23(121):S24-7. Epub 2011 Feb 23.

Endocrine Unit and Pediatric Nephrology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.

Fibroblast growth factor (FGF)-23 is probably the most important regulator of serum phosphate and calcitriol (1,25(OH)₂D₃) levels. It is secreted by osteocytes and osteoblasts in response to oral phosphate loading or increased serum 1,25(OH)₂D₃ levels. In human chronic kidney disease (CKD), plasma FGF-23 appears to be a sensitive biomarker of abnormal renal phosphate handling, as FGF-23 levels increase during early stages of kidney malfunction. Read More

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http://dx.doi.org/10.1038/ki.2011.27DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257051PMC
April 2011
4 Reads

Phosphate and Klotho.

Authors:
Makoto Kuro-O

Kidney Int Suppl 2011 Apr 23(121):S20-3. Epub 2011 Feb 23.

Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9072, USA.

Klotho is a putative aging suppressor gene encoding a single-pass transmembrane co-receptor that makes the fibroblast growth factor (FGF) receptor specific for FGF-23. In addition to multiple endocrine organs, Klotho is expressed in kidney distal convoluted tubules and parathyroid cells, mediating the role of FGF-23 in bone-kidney-parathyroid control of phosphate and calcium. Klotho⁻/⁻ mice display premature aging and chronic kidney disease-associated mineral and bone disorder (CKD-MBD)-like phenotypes mediated by hyperphosphatemia and remediated by phosphate-lowering interventions (diets low in phosphate or vitamin D; knockouts of 1α-hydroxylase, vitamin D receptor, or NaPi cotransporter). Read More

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http://dx.doi.org/10.1038/ki.2011.26DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3260960PMC
April 2011
4 Reads

The intact nephron hypothesis: the concept and its implications for phosphate management in CKD-related mineral and bone disorder.

Kidney Int Suppl 2011 Apr 23(121):S3-8. Epub 2011 Feb 23.

Renal Division, Department of Internal Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA.

Mechanistic understanding of secondary hyperparathyroidism, vascular calcification, and regulation of phosphate metabolism in chronic kidney disease (CKD) has advanced significantly in the past five decades. In 1960, Bricker developed the 'intact nephron hypothesis', opening the door for hundreds of investigations. He emphasized that 'as the number of functioning nephrons decreases, each remaining nephron must perform a greater fraction of total renal excretion'. Read More

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http://dx.doi.org/10.1038/ki.2011.23DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3260962PMC
April 2011
11 Reads

Cardiovascular risk factors in chronic kidney disease: does phosphate qualify?

Kidney Int Suppl 2011 Apr 23(121):S9-13. Epub 2011 Feb 23.

Renal Division, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

Risk factors for disease states are rigorously defined. This analysis considers the definition of a risk factor as applied to the question of whether the serum phosphorus level is a risk factor for cardiovascular disease. Observational studies strongly suggest that phosphorus is associated with cardiovascular risk, and definitive prospective animal studies are supportive. Read More

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http://dx.doi.org/10.1038/ki.2011.24DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3260961PMC
April 2011
5 Reads

Non-immune interventions to protect kidney allografts in the long term.

Kidney Int Suppl 2010 Dec(119):S71-5

Department of Medicine and Transplantation, Ospedali Riuniti-Mario Negri Institute for Pharmacological Research, Bergamo, Italy.

Chronic rejection, the primary cause of late renal allograft loss, results from a complex interplay between immunological and non-immunological factors. During the past few decades, transplant research has focused almost exclusively on identifying more powerful and minimally toxic immunosuppressive strategies to prevent acute rejection and alloimmune response toward the graft, whereas poor attention has been paid to non-immunological factors. However, the discrepancy between remarkable improvements in the prevention of acute rejection and failure to ameliorate long-term graft outcomes suggests that non-immunological injuries may have an important role in the progressive loss of graft function. Read More

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http://dx.doi.org/10.1038/ki.2010.427DOI Listing
December 2010
4 Reads

Optimal immunosuppression to prevent chronic allograft dysfunction.

Kidney Int Suppl 2010 Dec(119):S66-70

Department of Nephrology, Hospital Universitari de Bellvitge, University of Barcelona, IDIBELL, Barcelona, Spain.

Prevention of chronic allograft dysfunction is currently one of the main goals in renal transplantation for the improvement of kidney graft survival. For this purpose, refinements in immunosuppressive regimens, both controlling alloimmune responses and avoiding calcineurin inhibitor (CNI)-derived nephrotoxicity, are mandatory. The majority of trials aiming to avoid CNI-related nephrotoxicity have only reported short-term data, with different rates of acute rejection depending on the strategy performed. Read More

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http://dx.doi.org/10.1038/ki.2010.426DOI Listing
December 2010
6 Reads

Immune monitoring and biomarkers to predict chronic allograft dysfunction.

Authors:
Roslyn B Mannon

Kidney Int Suppl 2010 Dec(119):S59-65

Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.

Late failure of a kidney transplant continues to be a major problem after transplantation, in spite of more potent immunosuppressive strategies and the focus of clinical management shifting toward prolonging long-term graft survival. It is now recognized that graft failure occurs because of two major complications: death with a functioning graft and intrinsic allograft failure. Recent studies of late kidney graft loss have indicated a complexity of findings, including etiologies that are both immune and non-immune. Read More

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http://dx.doi.org/10.1038/ki.2010.425DOI Listing
December 2010
4 Reads

Consequences of transplant quality on chronic allograft nephropathy.

Kidney Int Suppl 2010 Dec(119):S54-8

Division of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Using kidneys from expanded-criteria donors to alleviate organ shortage has raised concern on reduced transplant outcomes. In this paper, we review how critical donor-related factors such as donor age, brain death, and consequences of ischemia-reperfusion injury (IRI) determine graft quality and impact chronic allograft nephropathy. We propose that combinatorial effects of organ-intrinsic features associated with increasing age and unspecific injuries related to brain death and IRI will impact innate and adaptive immune responses. Read More

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http://dx.doi.org/10.1038/ki.2010.424DOI Listing
December 2010
9 Reads

Infection and chronic allograft dysfunction.

Kidney Int Suppl 2010 Dec(119):S47-53

Department of Nephrology and Transplantation, Royal Free Hospital, London, UK.

With the advent of more potent immunosuppressive regimens, the incidence of acute rejection following renal transplantation has declined sharply in recent years. In spite of this, long-term graft outcomes remain suboptimal because of relentless attrition by cumulated insults to the allograft. As acute rejection rates have declined, other causes of graft injury and loss have recently emerged. Read More

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http://dx.doi.org/10.1038/ki.2010.423DOI Listing
December 2010
4 Reads

Metabolic syndrome, insulin resistance, and chronic allograft dysfunction.

Kidney Int Suppl 2010 Dec(119):S42-6

Nephrology Section and Research Unit, Hospital Universitario de Canarias, University of La Laguna, Tenerife, Canary Islands, Spain.

Metabolic syndrome (MS) is a cluster of cardiovascular (CV) risk factors (hypertension, dyslipidemia, obesity, and glucose homeostasis alterations), and insulin resistance (IR) is suggested to be a common pathogenic background. In the general population, MS and IR have been proven to be risk factors for diabetes, CV disease, and chronic kidney disease. In the renal transplant setting, few studies have analyzed the relevance of MS and IR. Read More

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http://dx.doi.org/10.1038/ki.2010.422DOI Listing
December 2010
4 Reads

Rejection and function and chronic allograft dysfunction.

Kidney Int Suppl 2010 Dec(119):S38-41

Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.

Despite the impressive reduction in early acute rejection rates over the past decades, chronic allograft dysfunction remains a key issue after renal transplantation. A number of factors, such as the quality of the original organ, ischemia/reperfusion injury, and/or (treated) acute rejection, will adversely affect renal structure, causing early (but often mild) tubular atrophy and interstitial fibrosis. It remains, however, controversial whether subclinical acute rejection or borderline changes imply a different functional prognosis with longer times of follow-up, if cases with late clinical acute rejection, inadequate dosing, and/or incompliance with drug prescription are excluded. Read More

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http://dx.doi.org/10.1038/ki.2010.421DOI Listing
December 2010
11 Reads

Genomics of chronic allograft injury.

Kidney Int Suppl 2010 Dec(119):S33-7

Renal Division and Abdominal Transplant Program, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, USA.

Chronic allograft injury (CAI) is common after kidney transplantation in which immunological (e.g., acute and chronic cellular and antibody-mediated rejection) and nonimmunological factors (e. Read More

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http://dx.doi.org/10.1038/ki.2010.420DOI Listing
December 2010
4 Reads

The pathology of chronic allograft dysfunction.

Kidney Int Suppl 2010 Dec(119):S27-32

Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Chronic allograft dysfunction is associated with a variety of fibrosing/sclerosing changes in the allograft. Fibrosis is multifactorial, a final pathway following varying types of injury. Using a range of diagnostic criteria, the pathologist can and should define specific lesions enabling identification of pathogenic processes affecting the allograft. Read More

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http://dx.doi.org/10.1038/ki.2010.419DOI Listing
December 2010
3 Reads

Mechanistic connection between inflammation and fibrosis.

Kidney Int Suppl 2010 Dec(119):S22-6

Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.

Fibrosis of the kidney is caused by the prolonged injury and deregulation of normal wound healing and repair processes, and by an excess deposition of extracellular matrices. Despite intensive research, our current understanding of the precise mechanism of fibrosis is limited. There is a connection between fibrotic events involving inflammatory and non-inflammatory glomerulonephritis, inflammatory cell infiltration, and podocyte loss. Read More

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http://dx.doi.org/10.1038/ki.2010.418DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067095PMC
December 2010
4 Reads

T-cell alloimmunity and chronic allograft dysfunction.

Kidney Int Suppl 2010 Dec(119):S2-12

Medical Research Council Centre for Transplantation, King's College London, King's Health Partners, Guy's Hospital, London, UK.

Solid organ transplantation is the standard treatment to improve both the quality of life and survival in patients with various end-stage organ diseases. The primary barrier against successful transplantation is recipient alloimmunity and the need to be maintained on immunosuppressive therapies with associated side effects. Despite such treatments in renal transplantation, after death with a functioning graft, chronic allograft dysfunction (CAD) is the most common cause of late allograft loss. Read More

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http://dx.doi.org/10.1038/ki.2010.416DOI Listing
December 2010
9 Reads

Innate immunity and cardiac allograft rejection.

Kidney Int Suppl 2010 Dec(119):S18-21

MGH Transplant Center and Division of Cardiac Surgery, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

The development of immunosuppressive drugs to control adaptive immune responses has led to the success of heart transplantation as a therapy for end-stage heart failure. However, these agents are largely ineffective in suppressing components of the innate immune system. This distinction has gained clinical significance as mounting evidence now indicates that innate immune responses have important roles in the acute and chronic rejection of cardiac allografts including cardiac allograft vasculopathy (CAV). Read More

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http://dx.doi.org/10.1038/ki.2010.417DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261228PMC
December 2010
3 Reads

Emerging role of B cells in chronic allograft dysfunction.

Kidney Int Suppl 2010 Dec(119):S13-7

Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.

B cells have many possible mechanisms by which they can affect allograft survival, including antigen presentation, cytokine production, immune regulation, and differentiation into alloantibody-producing plasma cells. This report reviews the last mechanism, which the authors regard as most critical for the long-term survival of allografts, namely, the promotion of chronic rejection by alloantibodies. Chronic humoral rejection characteristically arises late after transplantation and causes transplant glomerulopathy, multilamination of peritubular capillary basement membranes, and C4d deposition in PTCs and glomeruli. Read More

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http://dx.doi.org/10.1038/ki.2010.436DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4341830PMC
December 2010
4 Reads

Chronic renal allograft dysfunction (CAD): new frontiers. Introduction.

Authors:
Mohamed H Sayegh

Kidney Int Suppl 2010 Dec(119):S1

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http://dx.doi.org/10.1038/ki.2010.415DOI Listing
December 2010
4 Reads

Serum fructosamine versus glycosylated hemoglobin as an index of glycemic control, hospitalization, and infection in diabetic hemodialysis patients.

Kidney Int Suppl 2010 Aug(117):S41-5

Avram Division of Nephrology, Long Island College Hospital, Brooklyn, New York 11201, USA.

Diabetes is the most common cause of end-stage renal disease and an important risk factor for morbidity and mortality in dialysis patients. Glycemic control, utilizing serial measurement of glycosylated hemoglobin (HbA1c), is generally recommended to limit end-organ damage, including cardiovascular morbidity and mortality. We, along with others, have previously suggested that HbA1c may not be a reliable measure of glycemic control in dialysis patients, and have therefore explored the use of serum fructosamine (SF) as an alternative marker. Read More

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http://dx.doi.org/10.1038/ki.2010.193DOI Listing
August 2010
16 Reads

Extracellular mass/body cell mass ratio is an independent predictor of survival in peritoneal dialysis patients.

Kidney Int Suppl 2010 Aug(117):S37-40

Avram Division of Nephrology, Long Island College Hospital, Brooklyn, New York 11201, USA.

Malnutrition is a strong predictor of mortality in peritoneal dialysis (PD) patients. Extracellular mass (ECM) contains all the metabolically inactive, whereas body cell mass (BCM) contains all the metabolically active, tissues of the body. ECM/BCM ratio is a highly sensitive index of malnutrition. Read More

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http://linkinghub.elsevier.com/retrieve/pii/S008525381554467
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http://dx.doi.org/10.1038/ki.2010.192DOI Listing
August 2010
7 Reads

Treatment of secondary hyperparathyroidism in ESRD: a 2-year, single-center crossover study.

Kidney Int Suppl 2010 Aug(117):S33-6

Avram Division of Nephrology, Long Island College Hospital, Brooklyn, New York 11201, USA.

Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease. The management of SHPT commonly involves vitamin D, either calcitriol or newer analogs (paricalcitol or doxercalciferol), along with dietary phosphorus restriction and phosphate binding agents. Published reports have suggested that treatment with paricalcitol in hemodialyzed (HD) patients offers a morbidity or mortality advantage in comparison with treatment with calcitriol. Read More

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http://dx.doi.org/10.1038/ki.2010.191DOI Listing
August 2010
8 Reads

Anemia management in chronic kidney disease.

Kidney Int Suppl 2010 Aug(117):S3-9

Department of Nephrology, Winthrop-University Hospital, Mineola, New York 11501, USA.

Anemia is one of the most common and morbid complications of chronic kidney disease, causing unpleasant symptoms and reducing the quality of life. The availability of recombinant human erythropoietin (rHuEPO) in 1989 has been one of the most important developments in the care of this population in the past several decades. Treatment with erythropoiesis-stimulating agents (ESAs) has improved patients' lives, but recent studies have found that higher hemoglobin (Hgb) targets cause harm, resulting in more cautious treatment. Read More

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http://dx.doi.org/10.1038/ki.2010.188DOI Listing
August 2010
6 Reads

Stressful ethical issues in uremia therapy.

Authors:
Eli A Friedman

Kidney Int Suppl 2010 Aug(117):S22-32

Downstate Medical Center, Brooklyn, New York 11203, USA.

The objectives of this review are to introduce and explore the following representative ethical problems generated by modern renal replacement therapy: (1) reviewing the historical origin of medical ethics with specific reference to nephrology; (2) recognizing the complex stresses surrounding assignment of a deceased donor renal transplant to a geriatric patient while young patients continue waiting for a donor kidney; and (3) appreciating the concept of futility and support for a uremic patient opting for death rather than further uremia therapy as the best in choice in coping with renal failure. Read More

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http://dx.doi.org/10.1038/ki.2010.190DOI Listing
August 2010
3 Reads

Kidney bone disease and mortality in CKD: revisiting the role of vitamin D, calcimimetics, alkaline phosphatase, and minerals.

Kidney Int Suppl 2010 Aug(117):S10-21

Harold Simmons Center for Chronic Disease Research and Epidemiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California 90509-2910, USA.

Recent evidence suggests that the traditional syndromes known as renal osteodystrophy, secondary hyperparathyroidism, and vitamin D deficiency are related to mortality in persons with moderate to advanced chronic kidney disease (CKD). The so-called 'kidney bone disease', also known as 'mineral and bone disorders', is defined to include bone disorders, mineral disarrays, and vascular calcification. We have identified 14 common and clinically relevant conditions of contemporary nature that are related to the kidney bone disease, including calcitriol (active vitamin D) deficiency, 25(OH)-vitamin D deficiency, biochemical hyperparathyroidism, relatively low parathyroid hormone (PTH) level, increased serum alkaline phosphatase (hyperphosphatasemia), elevated fibroblast growth factor (FGF)-23, high turnover bone disease, adynamic bone disease, uremic osteoporosis, vascular calcification, hyper- and hypophosphatemia, and hyper- and hypocalcemia. Read More

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http://dx.doi.org/10.1038/ki.2010.189DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494176PMC
August 2010
7 Reads

Symposium proceedings. Perspective: irreversible progressive chronic kidney disease -- an overview.

Authors:
Morrell M Avram

Kidney Int Suppl 2010 Aug(117):S1-2

Avram Division of Nephrology, Long Island College Hospital, Brooklyn, New York 11201, USA.

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http://dx.doi.org/10.1038/ki.2010.187DOI Listing
August 2010
5 Reads

The metabolic syndrome following kidney transplantation.

Kidney Int Suppl 2010 Sep(118):S8-14

Renal and Transplantation Department, Guy's and St Thomas' Hospital, Great Maze Pond, London, UK.

The metabolic syndrome is a constellation of defined cardiovascular risk factors occurring simultaneously in a single individual. The result of dysregulated glucose and vascular metabolism, the syndrome has been identified as a significant risk factor for cardiovascular morbidity in the general population. More recently, a relatively high prevalence of the metabolic syndrome has been recognized among kidney transplant recipients. Read More

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http://dx.doi.org/10.1038/ki.2010.210DOI Listing
September 2010
4 Reads

Potential of emerging immunosuppressive strategies to improve the posttransplant cardiovascular risk profile.

Kidney Int Suppl 2010 Sep(118):S15-21

Department of Medicine, University of Wisconsin, Madison, Wisconsin 53793, USA.

Currently used immunosuppressants exacerbate cardiovascular risk. However, attempts to limit the use of these agents increase the risk of allograft rejection. Immunosuppressants targeting signal 2 and signal 3 lymphocyte activation pathways are under clinical development. Read More

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http://dx.doi.org/10.1038/ki.2010.211DOI Listing
September 2010
8 Reads

Pretransplant cardiovascular evaluation and posttransplant cardiovascular risk.

Kidney Int Suppl 2010 Sep(118):S1-7

Cleveland Clinic, Lerner College of Medicine, Cleveland, Ohio, USA.

Modern immunosuppression has expanded access to kidney transplantation by limiting the risk of rejection. However, cardiovascular disease (CVD) remains the principal cause of death with a functioning graft, threatening the long-term survival of transplant recipients. The article reviews the leading risk factors for cardiovascular morbidity both before and after kidney transplantation. Read More

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http://dx.doi.org/10.1038/ki.2010.209DOI Listing
September 2010
3 Reads

Screening for chronic kidney disease in Australia: a pilot study in the community and workplace.

Kidney Int Suppl 2010 Mar(116):S9-16

Kidney Health Australia, Adelaide, South Australia, Australia.

The pilot program Kidney Evaluation for You (KEY) was conducted in Australia to screen for chronic kidney disease (CKD). Targeting people at high risk (those with diabetes, hypertension, a first-degree relative with kidney failure, or age >50 years), KEY aimed to establish community-based screening protocols, assess efficacy in promoting changes in risk-factor management, and explore participant CKD awareness. KEY offered free cardiovascular and kidney checks using point-of-care testing for on-site pathology measurements (estimated glomerular filtration rate, hemoglobin A1c, cholesterol, hemoglobin, albuminuria), lifestyle assessment, and exit interviews. Read More

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http://dx.doi.org/10.1038/ki.2009.538DOI Listing
March 2010
4 Reads

Prevalence of chronic kidney disease in the Kidney Early Evaluation Program (KEEP) México and comparison with KEEP US.

Kidney Int Suppl 2010 Mar(116):S2-8

Universidad Panamericana School of Medicine, México City, México.

The National Kidney Foundation Kidney Early Evaluation Program (KEEP) is a free community screening program aimed at early detection of kidney disease among high-risk individuals. A pilot phase of KEEP México began in 2008 in México City and Jalisco State. Adults with diabetes, hypertension, or family history of diabetes, hypertension, or chronic kidney disease (CKD) were invited to participate through advertising campaigns. Read More

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http://dx.doi.org/10.1038/ki.2009.540DOI Listing
March 2010
13 Reads

The Kidney Early Evaluation Program (KEEP) of Japan: results from the initial screening period.

Kidney Int Suppl 2010 Mar(116):S17-23

International Kidney Evaluation Association Japan, Tokyo, Japan.

The International Kidney Evaluation Association Japan evaluated chronic kidney disease (CKD) in Japan, using a Japanese version of the US National Kidney Foundation's Kidney Early Evaluation Program (KEEP). The screening criteria for the first 1065 participants were presence of diabetes or hypertension, or family history of diabetes, hypertension, or kidney disease. Mean age was 59. Read More

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http://dx.doi.org/10.1038/ki.2009.539DOI Listing
March 2010
6 Reads

Overview of the KEEP international articles.

Authors:
George L Bakris

Kidney Int Suppl 2010 Mar(116):S1

Hypertensive Disease Unit, University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA.

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http://dx.doi.org/10.1038/ki.2009.537DOI Listing
March 2010
4 Reads

Maintenance immunosuppressive therapy and generic cyclosporine A use in adult renal transplantation: a single center analysis.

Kidney Int Suppl 2010 Mar(115):S8-11

Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

At present, solid organ transplantation relies on chronic immunosuppression. Calcineurin inhibitors (CNIs) still remain one of the most important components in current immunosuppressive regimens. However, life-long immunosuppression of transplant recipients is associated with high costs for the individual, health-care systems, and society. Read More

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http://dx.doi.org/10.1038/ki.2009.505DOI Listing
March 2010
7 Reads

Interchangeability of ciclosporin formulations in stable adult renal transplant recipients: comparison of Equoral and Neoral capsules in an international, multicenter, randomized, open-label trial.

Kidney Int Suppl 2010 Mar(115):S12-6

Institute for Clinical and Experimental Medicine, Prague, Czech Republic.

The cost of immunosuppression following transplantation can be reduced by using generic ciclosporin (for example, Equoral) rather than innovator ciclosporin drugs such as Neoral. Thus, this study aims to evaluate the interchangeability, safety, and tolerability of Equoral, a generic ciclosporin, with Neoral in stable adult renal transplant recipients. This was a multicenter, randomized, open-label, parallel-group clinical trial in stable renal transplant patients, comparing 6 months of treatment with Equoral with the same treatment period on Neoral. Read More

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http://dx.doi.org/10.1038/ki.2009.506DOI Listing
March 2010
11 Reads

Bioequivalence testing of immunosuppressants: concepts and misconceptions.

Kidney Int Suppl 2010 Mar(115):S1-7

Clinical Research and Development, Department of Anesthesiology, University of Colorado Denver, Aurora, Colorado 80045-7503, USA.

Immunosuppressants are considered critical dose/narrow therapeutic index drugs and there is the lingering suspicion among physicians and patients that generic versions may differ in quality and therapeutic efficacy from the brand name drug. The innovator's and the generic active drug molecule are exactly the same and are produced following exactly the same tight rules of good manufacturing practice. Upon oral administration, the drug molecule separates from the formulation and passes the membranes of gut mucosa cells; from this point on, the formulation has no influence on the kinetics of a drug and its biological effects. Read More

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http://dx.doi.org/10.1038/ki.2009.504DOI Listing
March 2010
7 Reads

Clinical relevance of FGF-23 in chronic kidney disease.

Kidney Int Suppl 2009 Dec(114):S34-42

Department of Internal Medicine IV-Renal and Hypertensive Disease, Saarland University Medical Centre, Homburg/Saar, Germany.

Fibroblast growth factor (FGF)-23 is a recently discovered regulator of calcium-phosphate metabolism. Whereas other known FGFs mainly act in a paracrine manner, FGF-23 has significant systemic effects. Together with its cofactor Klotho, FGF-23 enhances renal phosphate excretion in order to maintain serum phosphate levels within the normal range. Read More

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http://dx.doi.org/10.1038/ki.2009.405DOI Listing
December 2009
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Role of oxidants/inflammation in declining renal function in chronic kidney disease and normal aging.

Kidney Int Suppl 2009 Dec(114):S3-11

Division of Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, New York 10029, USA.

Oxidant stress (OS) and inflammation increase in normal aging and in chronic kidney disease (CKD), as observed in human and animal studies. In cross-sectional studies of the US population, these changes are associated with a decrease in renal function, which is exhibited by a significant proportion of the population. However, since many normal adults have intact renal function, and longitudinal studies show that some persons maintain normal renal function with age, the link between OS, inflammation, and renal decline is not clear. Read More

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http://dx.doi.org/10.1038/ki.2009.401DOI Listing
December 2009
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Sevelamer and the bone-vascular axis in chronic kidney disease: bone turnover, inflammation, and calcification regulation.

Kidney Int Suppl 2009 Dec(114):S26-33

Department of Nephrology and Clinical Immunology, University Hospital, Rheinisch-Westfälische Technische Hochschule Aachen University, Aachen, Germany.

Hyperphosphatemia is a central characteristic feature of chronic kidney disease-mineral and bone disorder (CKD-MBD). Phosphorus excess is an independent cardiovascular risk factor for morbidity and mortality in patients with advanced CKD. Over the past 40 years, hyperphosphatemia has been a central therapeutic issue in advanced CKD. Read More

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http://dx.doi.org/10.1038/ki.2009.404DOI Listing
December 2009
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Endotoxin-binding affinity of sevelamer: a potential novel anti-inflammatory mechanism.

Kidney Int Suppl 2009 Dec(114):S20-5

Kidney and Dialysis Research Laboratory, Division of Nephrology, Department of Medicine, St Elizabeth's Medical Center, Boston, Massachusetts 02135, USA.

Chronic inflammation is highly prevalent in patients with chronic kidney disease (CKD), and is associated with increased cardiovascular morbidity and mortality. There are numerous causes of inflammation in CKD, including the potential exposure to bacterial lipopolysaccharide (LPS) in the bloodstream from the intestinal tract as a result of uremia-related increases in intestinal permeability. Sevelamer, a commonly prescribed non-calcium, non-metal-based phosphate binder in CKD, also possesses putative anti-inflammatory properties, as its use has been associated with a reduction in systemic markers of inflammation. Read More

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http://dx.doi.org/10.1038/ki.2009.403DOI Listing
December 2009
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Uremic toxins originating from colonic microbial metabolism.

Kidney Int Suppl 2009 Dec(114):S12-9

Department of Nephrology, University Hospitals Leuven, Leuven, Belgium.

Numerous molecules, which are either excreted or metabolized by the kidney, accumulate in patients with chronic kidney disease (CKD). These uremic retention molecules (URMs), contributing to the syndrome of uremia, may be classified according to their site of origin, that is, endogenous metabolism, microbial metabolism, or exogenous intake. It is increasingly recognized that bacterial metabolites, such as phenols, indoles, and amines, may contribute to uremic toxicity. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00852538155390
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http://dx.doi.org/10.1038/ki.2009.402DOI Listing
December 2009
26 Reads

Beyond phosphate binding: the effect of binder therapy on novel biomarkers may have clinical implications for the management of chronic kidney disease patients.

Authors:
Gary E Striker

Kidney Int Suppl 2009 Dec(114):S1-2

Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.

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http://dx.doi.org/10.1038/ki.2009.400DOI Listing
December 2009
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KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD).

Authors:

Kidney Int Suppl 2009 Aug(113):S1-130

The 2009 Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline on the management of chronic kidney disease-mineral and bone disorder (CKD-MBD) is intended to assist the practitioner caring for adults and children with CKD stages 3-5, on chronic dialysis therapy, or with a kidney transplant. The guideline contains recommendations on evaluation and treatment for abnormalities of CKD-MBD. This disease concept of CKD-MBD is based on a prior KDIGO consensus conference. Read More

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http://linkinghub.elsevier.com/retrieve/pii/S008525381553893
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http://dx.doi.org/10.1038/ki.2009.188DOI Listing
August 2009
142 Reads