American Journal of Kidney Diseases (Am J Kidney Dis)

Publisher: National Kidney Foundation, Elsevier

Journal description

American Journal of Kidney Diseases not only publishes a broad range of clinical and basic investigations in human renal function but also describes the impact of the advances on clinical practice. Coverage encompasses applied physiology, dialysis/chronic uremia, hypertension, urology, pathology, and transplantation. In addition to peer-reviewed original articles and case reports, the Journal includes regular features such as in-depth reviews of relevant clinical topics; presentation and discussion of renal biopsy teaching cases; discussion and analysis of important recent articles; and forum discussions of ethical, moral, and legal issues related to kidney disease. The Journal's website includes such exclusive features as "Atlas of Renal Pathology," CME exercises, clinical nephrology teaching cases, and web-only case reports.

Current impact factor: 5.90

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 5.9
2013 Impact Factor 5.756
2012 Impact Factor 5.294
2011 Impact Factor 5.434
2010 Impact Factor 5.242
2009 Impact Factor 5.152
2008 Impact Factor 4.822
2007 Impact Factor 3.981
2006 Impact Factor 4.072
2005 Impact Factor 4.412
2004 Impact Factor 4.038
2003 Impact Factor 3.897
2002 Impact Factor 3.688
2001 Impact Factor 3.614
2000 Impact Factor 3.646
1999 Impact Factor 3.501
1998 Impact Factor 3.084
1997 Impact Factor 2.813
1996 Impact Factor 2.759
1995 Impact Factor 2.048
1994 Impact Factor 2.09
1993 Impact Factor 1.964
1992 Impact Factor 1.841

Impact factor over time

Impact factor

Additional details

5-year impact 5.56
Cited half-life 9.10
Immediacy index 1.95
Eigenfactor 0.03
Article influence 1.86
Website American Journal of Kidney Diseases website
Other titles American journal of kidney diseases (Online), American journal of kidney diseases, AJKD
ISSN 1523-6838
OCLC 40756717
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Family caregivers of patients with chronic kidney failure have increased burden, as reflected by their high frequency of physical and mental disturbances. The impact of enhanced psychosocial support to caregivers of patients with chronic kidney failure remains unclear. Study design: Open-label randomized controlled trial. Setting & participants: All new patients referred to the renal palliative clinic were screened. Caregivers of patients who met the following criteria were recruited: (1) chronic kidney failure as defined by creatinine clearance < 15mL/min, (2) opted for conservative management by nephrology team or patient, (3) never treated with dialysis or transplantation, and (4) able to provide informed consent. Interventions: Random assignment to treatment with enhanced psychosocial support or standard renal care (control). Enhanced psychosocial support included counseling and psychosocial interventions by an on-site palliative care nurse and designated social worker. Each caregiver was followed up at 2- to 4-week intervals for up to 6 months. Outcomes: Zarit Burden Inventory (ZBI) and Hospital Anxiety and Depression Scale (HADS) in caregivers and McGill Quality of Life scores in patients of both groups were compared. Results: 29 pairs of family caregivers/patients with chronic kidney failure were randomly assigned (intervention, n=14; control, n=15). Mean ages of patients and caregivers were 81.6±5.1 and 59.8±14.2 (SD) years, respectively. The intervention group showed significantly lower ZBI scores than the control group at 1 and 3 months (22.0±5.3 vs 31.6±9.5 and 21.3±6.6 vs 33.4±7.2; P=0.006 and P=0.009, respectively). HADS anxiety scores of caregivers who received the intervention were significantly lower than those of controls at 1 and 3 months (7.1±3.2 vs 10.1±2.2 and 6.5±4.5 vs 11.0±3.1; P=0.01 and P=0.03, respectively). Insignificant reductions in ZBI and HADS scores were found at 6 months. 19 patients died (intervention, n=10; control, n=9) during the study period. Limitations: The study is limited by a relatively small sample size and short duration. Conclusions: Enhanced psychosocial support program in patients with chronic kidney failure and caregivers resulted in an early significant reduction in caregiver burden and anxiety.
    American Journal of Kidney Diseases 11/2015; DOI:10.1053/j.ajkd.2015.09.021

  • American Journal of Kidney Diseases 11/2015; DOI:10.1053/j.ajkd.2015.10.002
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: The KDIGO (Kidney Disease: Improving Global Outcomes) clinical practice guidelines establish international recommendations for the definition and treatment of kidney disease. Our objective was to characterize the strength of evidence supporting the KDIGO guidelines, the class of recommendations made, and the relationship between these. Study design: We reviewed and abstracted the level of evidence and strength of recommendations in the currently available KDIGO guidelines. Setting & population: KDIGO clinical practice guidelines target care of patients with kidney disease to improve outcomes. Selection criteria for studies: All KDIGO guidelines published on the KDIGO website as of November 2013 were included. Predictor: Recommendations pertaining to disease, diagnosis, or treatment. Outcomes: Levels of evidence and strength of recommendations. Results: Of 853 recommendations in 9 guidelines, 5% were supported by level A quality evidence; 17%, level B; 31%, level C; 18%, level D; and 20%, ungraded evidence. The strength of recommendations was class 1 for 25%, class 2 for 54%, and ungraded for 20%. Only 3% of recommendations were class 1 in strength and supported by level A evidence. Of the recommendations, 2% concerned disease definition and classification; 29%, diagnosis; and 69%, treatment. Limitations: Our study included only the KDIGO guidelines. We did not assess historical changes in nephrology guidelines recommendations. Conclusions: KDIGO recommendations were based largely on weak evidence, reflecting expert opinion. Few recommendations were both strong and supported by high-level evidence.
    American Journal of Kidney Diseases 11/2015; DOI:10.1053/j.ajkd.2015.09.016
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Levosimendan has been shown to confer direct renoprotection in renal endotoxemic and ischemia-reperfusion injury and could increase renal blood flow in patients with low-cardiac-output heart failure. Results from clinical trials of levosimendan on acute kidney injury (AKI) following cardiac surgery are controversial. Study design: A random-effect meta-analysis was conducted based on evidence from PubMed, EMBASE, and Cochrane Library. Settings & population: Adult patients undergoing cardiac surgery. Selection criteria for studies: Randomized controlled trials comparing the renal effect of levosimendan versus placebo or other inotropic drugs during cardiac surgery. Intervention: Perioperative levosimendan continuous infusion at a rate of 0.1 to 0.2μg/kg/min following a loading dose (6-24μg/kg) for 24 hours or only 1 loading dose (24μg/kg) within 1 hour. Outcomes: AKI, need for renal replacement therapy, mechanical ventilation duration, intensive care unit stay during hospitalization, and postoperative mortality (in-hospital or within 30 days). Results: 13 trials with a total of 1,345 study patients were selected. Compared with controls, levosimendan reduced the incidence of postoperative AKI (40/460 vs 78/499; OR, 0.51; 95% CI, 0.34-0.76; P=0.001; I(2)=0.0%), renal replacement therapy (22/492 vs 49/491; OR, 0.43; 95% CI, 0.25-0.76; P=0.002; I(2)=0.0%), postoperative mortality (35/658 vs 94/657; OR, 0.41; 95% CI, 0.27-0.62; P<0.001; I(2)=0.0%), mechanical ventilation duration (in days; n=235; weighted mean difference, -0.34; 95% CI, -0.58 to -0.09; P=0.007], and intensive care unit stay (in days; n=500; weighted mean difference, -2.2; 95% CI, -4.21 to -0.13; P=0.04). Limitations: Different definitions for AKI among studies. Small sample size for some trials. Conclusions: Perioperative administration of levosimendan in patients undergoing cardiac surgery may reduce complications. Future trials are needed to determine the dose effect of levosimendan in improving outcomes, especially in patients with decreased baseline kidney function.
    American Journal of Kidney Diseases 10/2015; DOI:10.1053/j.ajkd.2015.09.015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: The potential effects of iron-dosing strategies and erythropoiesis-stimulating agents (ESAs) on health-related quality of life (HRQoL) in the dialysis population are unclear. We examined the independent associations of bolus versus maintenance iron dosing and high versus low ESA dosing on HRQoL. Study design: Retrospective cohort design. Setting & participants: Clinical data (2008-2010) from a large dialysis organization merged with data from the US Renal Data System. 13,039 patients receiving center-based hemodialysis were included. Predictor: Iron and ESA dosing were assessed during 1-month (n=14,901) and 2-week (n=15,296) exposure periods. Outcomes: HRQoL was measured by the Kidney Disease Quality of Life (KDQOL) instrument (0-100 scale) during a 3-month follow-up period. Measurements: Generalized linear mixed models, adjusting for several covariates, were used to estimate associations between iron and ESA dosing and HRQoL overall and for clinically relevant subgroups. Results: For the 1-month exposure period, patients with lower baseline hemoglobin levels who received higher ESA dosing had higher physical health and kidney disease symptom scores (by 2.4 [95% CI, 0.6-4.2] and 5.6 [95% CI, 2.8-8.4] points, respectively) in follow-up than patients who received lower ESA dosing. For the 2-week exposure period, patients with low baseline hemoglobin levels who received bolus dosing had higher mental health scores (by 1.9 [95% CI, 0.0-3.8] points) in follow-up. Within the low-baseline-hemoglobin subgroup, individuals with a catheter or dialysis vintage less than 1 year who received higher ESA dosing had higher HRQoL scores in follow-up (by 5.0-9.9 points) and individuals with low baseline transferrin saturations who received bolus dosing had higher HRQoL scores in follow-up (by 2.6-5.8 points). Limitations: Observational design; short duration of observation. Conclusions: For individuals with low baseline hemoglobin levels, higher ESA dosing and bolus iron dosing were associated with slightly higher HRQoL scores in follow-up. These differences became more pronounced and clinically relevant for specific subgroups.
    American Journal of Kidney Diseases 10/2015; DOI:10.1053/j.ajkd.2015.09.011
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Levocarnitine deficiency in hemodialysis patients is common. Although the effect of levocarnitine therapy on uremic anemia has been studied in small trials, its effects on cardiac function remain unclear. Study design: Multicenter, prospective, open-label, parallel, randomized, controlled trial. Setting & participants: Patients undergoing maintenance hemodialysis with carnitine deficiency (free carnitine plasma concentration < 40μmol/L) enrolled in 3 hemodialysis centers. Intervention: Random assignment to treatment for 12 months with oral levocarnitine therapy at a dose of 20mg/kg/d or control group (no levocarnitine therapy). Outcomes & measurements: Cardiac function was assessed by echocardiography. The primary end point was change in ejection fraction from baseline at the end of the study. Secondary end points included changes in left ventricular mass index and clinical parameters from baseline at the end of the study. Results: 222 patients were randomly assigned, of whom 148 patients (levocarnitine group, n=75; control group, n=73) were analyzed. Ejection fraction increased from baseline to the end of the study in the levocarnitine group by 5.43% (95% CI, 4.53%-6.32%), but not in the control group (change, -0.14%; between-group difference, 5.57% [95% CI, 4.48%-6.66%]; P<0.001). Left ventricular mass index decreased from baseline to the end of the study in the levocarnitine group (change of -8.89 [95% CI, -11.7 to -6.09] g/m(2)), but not in the control group (change of 1.62g/m(2); between-group difference, 10.50 [95% CI, 7.51 to 13.60] g/m(2); P<0.001). Levocarnitine therapy reduced N-terminal pro-brain natriuretic peptide (NT-proBNP) levels and improved the erythropoietin responsiveness index, whereas no such effects were observed in the control group. Limitations: Not a double-blinded study. Conclusions: Levocarnitine therapy is useful for hemodialysis patients with carnitine deficiency; these patients may benefit from such therapy, with amelioration of cardiac function and reduction of left ventricular mass index.
    American Journal of Kidney Diseases 10/2015; DOI:10.1053/j.ajkd.2015.09.010
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hyperphosphatemia in dialysis patients is routinely attributed to nonadherence to diet, prescribed phosphate binders, or both. The role of individual patient variability in other determinants of phosphate control is not widely recognized. In a manner that cannot be explained by dialysis parameters or serum phosphate levels, dialytic removal of phosphate may vary by >400mg per treatment. Similarly, enteral phosphate absorption, unexplained by diet or vitamin D intake, may differ by ≥250mg/d among patients. Binder efficacy also varies among patients, with 2-fold differences reported. One or more elements of this triple threat-varying dialytic removal, phosphate absorption, and phosphate binding-may account for hyperphosphatemia in dialysis patients rather than nonadherence to therapy. Just as the cause(s) of hyperphosphatemia may vary, so too may an individual patient's response to different therapeutic interventions.
    American Journal of Kidney Diseases 10/2015; DOI:10.1053/j.ajkd.2015.07.035

  • American Journal of Kidney Diseases 10/2015; 66(5):e39-e40. DOI:10.1053/j.ajkd.2015.08.009
  • [Show abstract] [Hide abstract]
    ABSTRACT: Patients with cirrhosis are prone to develop acute kidney injury (AKI) due to a number of causes, including bacterial infections with or without septic shock, hypovolemia, administration of nephrotoxic drugs, and intrinsic kidney diseases, among others. Most importantly, patients with advanced cirrhosis develop a distinctive cause of AKI, characterized by rapidly progressive glomerular filtration rate loss associated with marked disturbances in circulatory function in the absence of obvious pathologic abnormalities in the kidneys, known as hepatorenal syndrome (HRS). Decreased kidney function results from intense renal vasoconstriction secondary to the complex circulatory changes of cirrhosis with splanchnic vasodilatation and effective hypovolemia. Beyond activation of vasoactive systems, factors including impaired renal blood flow autoregulation and systemic inflammation may play a role in the development of HRS. Most patients improve with albumin and vasopressors; however, the prognosis of HRS remains very poor. Novel biomarkers may be helpful in distinguishing HRS from other causes of AKI in patients with cirrhosis.
    American Journal of Kidney Diseases 10/2015; DOI:10.1053/j.ajkd.2015.09.013

  • American Journal of Kidney Diseases 10/2015; 66(5):e37-e38. DOI:10.1053/j.ajkd.2015.08.010

  • American Journal of Kidney Diseases 10/2015; 66(5):A18-A21. DOI:10.1053/j.ajkd.2015.06.029
  • [Show abstract] [Hide abstract]
    ABSTRACT: In this article, we review approaches for decreasing uremic solute concentrations in chronic kidney disease and in particular, in end-stage renal disease (ESRD). The rationale to do so is the straightforward relation between concentration and biological (toxic) effect for most toxins. The first section is devoted to extracorporeal strategies (kidney replacement therapy). In the context of high-flux hemodialysis and hemodiafiltration, we discuss increasing dialyzer blood and dialysate flows, frequent and/or extended dialysis, adsorption, bioartificial kidney, and changing physical conditions within the dialyzer (especially for protein-bound toxins). The next section focuses on the intestinal generation of uremic toxins, which in return is stimulated by uremic conditions. Therapeutic options are probiotics, prebiotics, synbiotics, and intestinal sorbents. Current data are conflicting, and these issues need further study before useful therapeutic concepts are developed. The following section is devoted to preservation of (residual) kidney function. Although many therapeutic options may overlap with therapies provided before ESRD, we focus on specific aspects of ESRD treatment, such as the risks of too-strict blood pressure and glycemic regulation and hemodynamic changes during dialysis. Finally, some recommendations are given on how research might be organized with regard to uremic toxins and their effects, removal, and impact on outcomes of uremic patients.
    American Journal of Kidney Diseases 10/2015; DOI:10.1053/j.ajkd.2015.08.029

  • American Journal of Kidney Diseases 10/2015; 66(5):e41-e42. DOI:10.1053/j.ajkd.2015.08.008

  • American Journal of Kidney Diseases 10/2015; 66(5):A15-A16. DOI:10.1053/j.ajkd.2015.08.012

  • American Journal of Kidney Diseases 10/2015; 66(5):742-744. DOI:10.1053/j.ajkd.2015.08.019