Nature Reviews Nephrology Journal Impact Factor & Information

Publisher: Nature Publishing Group

Journal description

Current impact factor: 8.54

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 8.542
2013 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

Additional details

5-year impact 7.79
Cited half-life 3.10
Immediacy index 1.62
Eigenfactor 0.01
Article influence 2.76
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

  • [Show abstract] [Hide abstract]
    ABSTRACT: Acute kidney injury (AKI) is a common complication in hospitalized patients, associated with >50% mortality in those in intensive care who require renal replacement therapy. Data suggest that AKI is a systemic disease that adversely affects the immune system and organ function, and in this way contributes to the high mortality observed in affected patients. Data from patients and animal models indicate that AKI adversely affects the lungs. Respiratory complications are common in patients with AKI and include pulmonary oedema, respiratory failure requiring mechanical ventilation, prolonged duration of mechanical ventilation, and prolonged weaning from mechanical ventilation. The development of respiratory failure in patients with AKI greatly increases the risk of death. Data from animal models support the notion that cardiogenic pulmonary oedema (from volume overload) and non-cardiogenic pulmonary oedema (from endothelial injury due to inflammation and apoptosis) can occur in AKI. In this Review we discuss the clinical, epidemiologic, and animal data that provide insights into the mechanisms by which AKI can lead to lung injury and respiratory complications. Elucidation of the mechanisms of lung injury and respiratory complications after AKI is essential to develop effective therapies and reduce the high mortality associated with AKI and respiratory failure.
    Nature Reviews Nephrology 10/2015; DOI:10.1038/nrneph.2015.158
  • Nature Reviews Nephrology 10/2015; DOI:10.1038/nrneph.2015.165
  • Nature Reviews Nephrology 10/2015; DOI:10.1038/nrneph.2015.166
  • Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.160
  • [Show abstract] [Hide abstract]
    ABSTRACT: Important advances have been made in basic and clinical nephrology research over the past decade, with improved pathological insights into various disease processes and the introduction of new treatments for diseases such as atypical haemolytic uraemic syndrome. However, many challenges remain. In this Viewpoint, we asked five Nature Reviews Nephrology Advisory Board members, who have been associated with the journal since its launch in November 2005, to reflect on the progress and roadblocks of the past 10 years. They also comment on areas where effort and money should be invested and how they expect the field to progress in the next 10 years.
    Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.152
  • Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.161
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dysregulated phosphate metabolism is a common consequence of chronic kidney disease, and is characterized by a high circulating level of fibroblast growth factor (FGF)-23, hyperparathyroidism, and hyperphosphataemia. Kidney transplantation can elicit specific alterations to phosphate metabolism that evolve over time, ranging from severe hypophosphataemia (<0.5 mmol/l) to hyperphosphataemia (>1.50 mmol/l) and high FGF-23 levels. The majority of renal transplant recipients develop hypophosphataemia during the first 3 months after transplantation as a consequence of relatively slow adaptation of FGF-23 and parathyroid hormone levels to restored renal function, and the influence of immunosuppressive drugs. By 3-12 months after transplantation, phosphate homeostasis is at least partially restored in the majority of recipients, which is paralleled by a substantially reduced risk of cardiovascular-associated morbidity and mortality compared with the pre-transplantation setting. Many renal transplant recipients, however, exhibit persistent abnormalities in phosphate homeostasis, which is often due to multifactorial causes, and may contribute to adverse outcomes on the cardiovascular system, kidney, and bone. Dietary and pharmacologic interventions might improve phosphate homeostasis in renal transplant recipients, but additional insight into the pathophysiology of transplantation-associated abnormalities in phosphate homeostasis is needed to further optimize disease management and improve prognosis for renal transplant recipients.
    Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.153
  • Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.149
  • Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.147
  • Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.150
  • Nature Reviews Nephrology 09/2015; DOI:10.1038/nrneph.2015.151
  • Nature Reviews Nephrology 08/2015; 11(10). DOI:10.1038/nrneph.2015.145
  • [Show abstract] [Hide abstract]
    ABSTRACT: Patients with kidney disease often exhibit multiple organ dysfunction that is caused, in part, by marked connectivity between the kidney and other organs and tissues. Substantial crosstalk occurs between the kidney and the brain, as indicated by the frequent presentation of neurological disorders, such as cerebrovascular disease, cognitive impairment, and neuropathy during the natural history of chronic kidney disease. The underlying pathophysiology of such comorbid neurological disorders in kidney disease is governed by shared anatomic and vasoregulatory systems and humoral and non-humoral bidirectional pathways that affect both the kidney and the brain. During acute kidney injury, the brain and kidney might interact through the amplification of cytokine-induced damage, extravasation of leukocytes, oxidative stress, and dysregulation of sodium, potassium, and water channels. The advent of dialysis and renal transplantation programmes has led to a reduction in the rate of neurological complications associated with uraemia, but a new set of complications have arisen as a consequence of the effects of dialysis on the central nervous system over the short and long term. This Review discusses the clinical complications of acute and chronic renal failure from a neurologic perspective, and highlights current understanding of the underlying pathophysiologies.
    Nature Reviews Nephrology 08/2015; DOI:10.1038/nrneph.2015.131
  • Nature Reviews Nephrology 08/2015; DOI:10.1038/nrneph.2015.143
  • Nature Reviews Nephrology 08/2015; DOI:10.1038/nrneph.2015.142
  • Nature Reviews Nephrology 08/2015; DOI:10.1038/nrneph.2015.141
  • Nature Reviews Nephrology 08/2015; DOI:10.1038/nrneph.2015.134
  • [Show abstract] [Hide abstract]
    ABSTRACT: Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease. Relentless cyst growth substantially enlarges both kidneys and culminates in renal failure. Patients with ADPKD also have vascular abnormalities; intracranial aneurysms (IAs) are found in ∼10% of asymptomatic patients during screening and in up to 25% of those with a family history of IA or subarachnoid haemorrhage. As the genes responsible for ADPKD-PKD1 and PKD2-have complex integrative roles in mechanotransduction and intracellular calcium signalling, the molecular basis of IA formation might involve focal haemodynamic conditions exacerbated by hypertension and altered flow sensing. IA rupture results in substantial mortality, morbidity and poor long-term outcomes. In this Review, we focus mainly on strategies for screening, diagnosis and treatment of IAs in patients with ADPKD. Other vascular aneurysms and anomalies-including aneurysms of the aorta and coronary arteries, cervicocephalic and thoracic aortic dissections, aortic root dilatation and cerebral dolichoectasia-are less common in this population, and the available data are insufficient to recommend screening strategies. Treatment decisions should be made with expert consultation and be based on a risk-benefit analysis that takes into account aneurysm location and morphology as well as patient age and comorbidities.
    Nature Reviews Nephrology 08/2015; DOI:10.1038/nrneph.2015.128