Nature Reviews Nephrology Journal Impact Factor & Information

Publisher: Nature Publishing Group

Journal description

Current impact factor: 8.37

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 8.368
2012 Impact Factor 7.943
2011 Impact Factor 7.092
2010 Impact Factor 4.75

Impact factor over time

Impact factor
Year

Additional details

5-year impact 7.41
Cited half-life 2.30
Immediacy index 1.21
Eigenfactor 0.01
Article influence 2.63
ISSN 1759-507X

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Author's pre-print on arXiv or bioRXiv
    • Author's post-print on author's personal website, institutional repository, PubMed Central or funding body's archive
    • Published source must be acknowledged
    • Must link to publisher version with DOI
    • Publisher's version/PDF cannot be used
  • Classification
    ​ yellow

Publications in this journal

  • Chirag R Parikh, Jennifer A Schaub
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.106
  • Ellen F Carney
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.107
  • Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.98
  • Anglina Kataria, Leonardo Trasande, Howard Trachtman
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    ABSTRACT: The global incidence of chronic kidney disease (CKD) is increasing among individuals of all ages. Despite advances in proteomics, genomics and metabolomics, there remains a lack of safe and effective drugs to reverse or stabilize renal function in patients with glomerular or tubulointerstitial causes of CKD. Consequently, modifiable risk factors that are associated with a progressive decline in kidney function need to be identified. Numerous reports have documented the adverse effects that occur in response to graded exposure to a wide range of environmental chemicals. This Review summarizes the effects of such chemicals on four aspects of cardiorenal function: albuminuria, glomerular filtration rate, blood pressure and serum uric acid concentration. We focus on compounds that individuals are likely to be exposed to as a consequence of normal consumer activities or medical treatment, namely phthalates, bisphenol A, polyfluorinated alkyl acids, dioxins and furans, polycyclic aromatic hydrocarbons and polychlorinated biphenyls. Environmental exposure to these chemicals during everyday life could have adverse consequences on renal function and might contribute to progressive cumulative renal injury over a lifetime. Regulatory efforts should be made to limit individual exposure to environmental chemicals in an attempt to reduce the incidence of cardiorenal disease.
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.94
  • Susan J Allison
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.99
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    ABSTRACT: Healthy kidneys maintain fluid and electrolyte homoeostasis by adjusting urine volume and composition according to physiological needs. The final urine composition is determined in the last tubular segment: the collecting duct. Water permeability in the collecting duct is regulated by arginine vasopressin (AVP). Secretion of AVP from the neurohypophysis is regulated by a complex signalling network that involves osmosensors, barosensors and volume sensors. AVP facilitates aquaporin (AQP)-mediated water reabsorption via activation of the vasopressin V2 receptor (AVPR2) in the collecting duct, thus enabling concentration of urine. In nephrogenic diabetes insipidus (NDI), inability of the kidneys to respond to AVP results in functional AQP deficiency. Consequently, affected patients have constant diuresis, resulting in large volumes of dilute urine. Primary forms of NDI result from mutations in the genes that encode the key proteins AVPR2 and AQP2, whereas secondary forms are associated with biochemical abnormalities, obstructive uropathy or the use of certain medications, particularly lithium. Treatment of the disease is informed by identification of the underlying cause. Here we review the clinical aspects and diagnosis of NDI, the various aetiologies, current treatment options and potential future developments.
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.89
  • Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.96
  • Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.97
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    ABSTRACT: Podocytes are unique, highly specialized, terminally differentiated cells that are integral components of the kidney glomerular filtration barrier. Podocytes are vulnerable to a variety of injuries and in response they undergo a series of changes ranging from hypertrophy, autophagy, dedifferentiation, mesenchymal transition and detachment to apoptosis, depending on the nature and extent of the insult. Emerging evidence indicates that Wnt/β-catenin signalling has a central role in mediating podocyte dysfunction and proteinuria. Wnts are induced and β-catenin is activated in podocytes in various proteinuric kidney diseases. Genetic or pharmacologic activation of β-catenin is sufficient to impair podocyte integrity and causes proteinuria in healthy mice, whereas podocyte-specific ablation of β-catenin protects against proteinuria after kidney injury. Mechanistically, Wnt/β-catenin controls the expression of several key mediators implicated in podocytopathies, including Snail1, the renin-angiotensin system and matrix metalloproteinase 7. Wnt/β-catenin also negatively regulates Wilms tumour protein, a crucial transcription factor that safeguards podocyte integrity. Targeted inhibition of Wnt/β-catenin signalling preserves podocyte integrity and ameliorates proteinuria in animal models. This Review highlights advances in our understanding of the pathomechanisms of Wnt/β-catenin signalling in mediating podocyte injury, and describes the therapeutic potential of targeting this pathway for the treatment of proteinuric kidney disease.
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.88
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    ABSTRACT: Chronic kidney disease (CKD) is prevalent in many countries, and the costs associated with the care of patients with end-stage renal disease (ESRD) are estimated to exceed US$1 trillion globally. The clinical and economic rationale for the design of timely and appropriate health system responses to limit the progression of CKD to ESRD is clear. Clinical care might improve if early-stage CKD with risk of progression to ESRD is differentiated from early-stage CKD that is unlikely to advance. The diagnostic tests that are currently used for CKD exhibit key limitations; therefore, additional research is required to increase awareness of the risk factors for CKD progression. Systems modelling can be used to evaluate the impact of different care models on CKD outcomes and costs. The US Indian Health Service has demonstrated that an integrated, system-wide approach can produce notable benefits on cardiovascular and renal health outcomes. Economic and clinical improvements might, therefore, be possible if CKD is reconceptualized as a part of primary care. This Review discusses which early CKD interventions are appropriate, the optimum time to provide clinical care, and the most suitable model of care to adopt.
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.85
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    ABSTRACT: Improved understanding of the oxygen-dependent regulation of erythropoiesis has provided new insights into the pathogenesis of anaemia associated with renal failure and has led to the development of novel therapeutic agents for its treatment. Hypoxia-inducible factor (HIF)-2 is a key regulator of erythropoiesis and iron metabolism. HIF-2 is activated by hypoxic conditions and controls the production of erythropoietin by renal peritubular interstitial fibroblast-like cells and hepatocytes. In anaemia associated with renal disease, erythropoiesis is suppressed due to inadequate erythropoietin production in the kidney, inflammation and iron deficiency; however, pharmacologic agents that activate the HIF axis could provide a physiologic approach to the treatment of renal anaemia by mimicking hypoxia responses that coordinate erythropoiesis with iron metabolism. This Review discusses the functional inter-relationships between erythropoietin, iron and inflammatory mediators under physiologic conditions and in relation to the pathogenesis of renal anaemia, as well as recent insights into the molecular and cellular basis of erythropoietin production in the kidney. It furthermore provides a detailed overview of current clinical experience with pharmacologic activators of HIF signalling as a novel comprehensive and physiologic approach to the treatment of anaemia.
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.82
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    ABSTRACT: Advances in chemotherapy for haematological malignancies, resulting from a greater understanding of the complex pathophysiology of these diseases, have improved the survival of patients with these disorders. Clinicians must now, therefore, be more aware of the issues related to fluid, electrolyte, and acid-base disorders, as well as acute and chronic kidney injuries that can develop in such patients as a result of the underlying malignancy and its treatment. Patients with acute kidney injury associated with haematological malignancy have a worse prognosis than do other patients with acute kidney injury. Glomerular diseases associated with haematological malignancies are thought to be paraneoplastic syndromes with variable histological presentations. Some of the newest therapeutic agents used to treat haematological malignancies have adverse renal effects that can preclude continuation of treatment, often leading to difficult clinical decisions when patients have advanced disease and alternative treatment options are limited. Haematopoietic stem cell transplantation has an expanding role as a therapy for haematological malignancies but is also associated with important renal complications. Here, we review the literature that examines the incidences, aetiologies, mechanisms and treatment options for renal disorders associated with haematological malignancies.
    Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.81
  • Nature Reviews Nephrology 06/2015; DOI:10.1038/nrneph.2015.86
  • Nature Reviews Nephrology 05/2015; DOI:10.1038/nrneph.2015.84
  • Nature Reviews Nephrology 05/2015; DOI:10.1038/nrneph.2015.83
  • Nature Reviews Nephrology 05/2015; DOI:10.1038/nrneph.2015.80
  • Nature Reviews Nephrology 05/2015; DOI:10.1038/nrneph.2015.78
  • Nature Reviews Nephrology 05/2015; 11(7). DOI:10.1038/nrneph.2015.79
  • Nature Reviews Nephrology 05/2015; DOI:10.1038/nrneph.2015.77
  • Nature Reviews Nephrology 05/2015; DOI:10.1038/nrneph.2015.75