American Journal of Kidney Diseases (AM J KIDNEY DIS )

Publisher: National Kidney Foundation

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.

  • Impact factor
    5.29
    Show impact factor history
     
    Impact factor
  • 5-year impact
    5.42
  • Cited half-life
    8.60
  • Immediacy index
    1.72
  • Eigenfactor
    0.04
  • Article influence
    1.93
  • Website
    American Journal of Kidney Diseases website
  • Other titles
    American journal of kidney diseases, AJKD
  • ISSN
    0272-6386
  • OCLC
    6887399
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publications in this journal

  • American Journal of Kidney Diseases 12/2014; 64(6).
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    ABSTRACT: Background There is increased interest in using alternative end points for trials of kidney disease progression. The currently established end points of end-stage renal disease and doubling of serum creatinine level, equivalent to a 57% decline in estimated glomerular filtration rate (eGFR), are late events in chronic kidney disease (CKD), requiring large clinical trials with long follow-up. As part of a comprehensive evaluation of lesser declines in eGFR as alternative end points, we describe the consistency of treatment effects of intervention on the alternative and established end points in past trials. Study Design Diagnostic test study. Setting & Population 9,488 participants from 37 randomized controlled trials of CKD progression across 5 intervention types. Index Test Alternative end points including percentage change in eGFR from baseline (20%, 30%, 40%, and 57%) throughout study duration and to 12, 18, and 24 months. eGFR change confirmed versus nonconfirmed at the next visit. Reference Test The historically established end point of time to composite of treated kidney failure (end-stage renal disease), untreated kidney failure (GFR < 15 mL/min/1.73 m2), or doubling of serum creatinine level throughout study duration. Results Over a median of 3.62 years’ follow-up, there were 3,070 established end points. Compared to the established end point, the number of alternative end points was greater for smaller versus larger declines in eGFR and longer versus shorter follow-up intervals. There was a general trend toward attenuation of the treatment effect with end points defined by a lesser eGFR decline, with greater attenuation with nonconfirmed end points, except for the low-protein-diet intervention, for which a stronger treatment effect was observed. The ratio (95% credible interval) of the HR for the alternative to established end point for the 5 intervention types ranged from 0.91 (0.64-1.43) to 1.12 (0.89-1.40) for 40% decline and from 0.88 (0.63-1.39) to 1.15 (0.88-1.54) for 30% decline for the overall study duration, indicating consistency of treatment effects. Limitations Limited variety of interventions tested and low statistical power for many CKD clinical trials. Conclusions These results provide some support for the use of lesser eGFR declines as a surrogate end point, with stronger support for the 40% than 30% decline.
    American Journal of Kidney Diseases 12/2014;
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    ABSTRACT: Background The currently established end points for clinical trials of progression of chronic kidney disease (CKD) are end-stage renal disease and doubling of serum creatinine level, which approximates a 57% decline in estimated glomerular filtration rate (eGFR). There is increased interest in using alternative end points in clinical trials to shorten trial duration and reduce sample size. As part of an evaluation of using lesser declines in GFR as alternative end points, we examined the associations of various levels of eGFR decline with the subsequent development of established end points and assess the consistency of alternate levels of eGFR decline across varying clinical manifestations of kidney disease and interventions. Study Design Observational analysis of randomized controlled trials. Setting & Participants 9,488 participants in 37 randomized controlled trials in CKD. Predictor Alternative end points, defined as 30% and 40% declines in eGFR from baseline to month 12. Effect modification by baseline eGFR, proteinuria, cause of disease, and interventions. Outcomes Established end point, defined as end-stage renal disease, eGFR < 15 mL/min/1.73 m2, or doubling of serum creatinine level. Results From baseline to 12 months, 16.1% and 7.8% of participants had eGFR declines of ≥30% or ≥40%, respectively. Over a median follow-up of 2.0 (IQR, 1.2-3.1) years after the 12-month baseline period, 2,661 established end points were observed. A strong linear association was observed between eGFR decline and subsequent established end points. HRs for the established end point for 30% and 40% decreases in eGFR compared to a 0% decline were 9.6 (95% CI, 7.3-12.6) and 20.3 (95% CI, 14.1-29.3), respectively. The associations were consistent regardless of baseline eGFR, proteinuria, causes of disease, and interventions. Limitations Observational study subject to residual confounding. Conclusions The strong associations between lesser declines in eGFR and the subsequent development of established end points were consistent across different clinical characteristics of kidney disease and interventions and support implementation of alternative end points in clinical trials of CKD progression.
    American Journal of Kidney Diseases 12/2014;
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    ABSTRACT: The US Food and Drug Administration currently accepts halving of glomerular filtration rate (GFR), assessed as doubling of serum creatinine level, as a surrogate end point for the development of kidney failure in clinical trials of kidney disease progression. A doubling of serum creatinine level generally is a late event in chronic kidney disease (CKD); thus, there is great interest in considering alternative end points for clinical trials to shorten their duration, reduce sample size, and extend their conduct to patients with earlier stages of CKD. However, the relationship between lesser declines in GFR and the subsequent development of kidney failure has not been well characterized. The National Kidney Foundation and Food and Drug Administration sponsored a scientific workshop to critically examine available data to determine whether alternative GFR-based end points have sufficiently strong relationships with important clinical outcomes of CKD to be used in clinical trials. Based on a series of meta-analyses of cohorts and clinical trials and simulations of trial designs and analytic methods, the workshop concluded that a confirmed decline in estimated GFR of 30% over 2 to 3 years may be an acceptable surrogate end point in some circumstances, but the pattern of treatment effects on GFR must be examined, specifically acute effects on estimated GFR. An estimated GFR decline of 40% may be more broadly acceptable than a 30% decline across a wider range of baseline GFRs and patterns of treatment effects on GFR. However, there are other circumstances in which these end points could lead to a reduction in statistical power or erroneous conclusions regarding benefits or harms of interventions. We encourage careful consideration of these alternative end points in the design of future clinical trials.
    American Journal of Kidney Diseases 12/2014;
  • American Journal of Kidney Diseases 12/2014; 64(6).
  • NKF; 11/2014
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    ABSTRACT: Patients with kidney disease frequently experience adverse effects from medication exposure, even when drugs are cleared by nonrenal pathways. Although many studies suggest that nonrenal drug clearance is decreased in chronic kidney disease (CKD), there remains a paucity of in vivo studies in patients with varying degrees of decreased kidney function and those comparing the impact of dialysis modality (eg, hemodialysis [HD] and peritoneal dialysis [PD]). We performed in vivo clinical pharmacokinetic studies of midazolam, a nonrenally cleared specific probe for CYP3A4, and fexofenadine, a nonspecific probe for hepatic and intestinal transporters. Healthy controls (n=8), patients with non-dialysis-dependent (NDD)-CKD (n=8), and patients receiving HD (n=10) or PD (n=8). Exposure to midazolam and fexofenadine were quantified using area under the curve (AUC). Comprehensive pharmacokinetic parameters also were calculated for both probes. Midazolam AUC was significantly higher in the HD group (382.8 h·ng/mL) than in the healthy-control (63.0 h·ng/mL; P<0.001), NDD-CKD (84.5 h·ng/mL; P=0.002), and PD (47.4 h·ng/mL; P<0.001) groups. Fexofenadine AUC was significantly higher in each of the NDD-CKD (2,950 h·ng/mL; P=0.003), HD (2,327 h·ng/mL; P=0.01), and PD (2,095 h·ng/mL; P=0.04) groups compared with healthy controls (1,008 h·ng/mL). Small study groups had different proportions of diabetic patients, early stages of CKD not available. Our data suggest that selection of dialysis modality is a major determinant of exposure to the CYP3A4 probe midazolam. Exposure to the intestinal and hepatic transporter probe fexofenadine is altered in patients with NDD-CKD and PD and HD patients. Thus, drug development and licensing of nonrenally cleared drugs should include evaluation in these 3 patient groups, with these results included in approved product information labeling. This reinforces the critical need for more in vivo studies of humans that evaluate the exposure to drugs cleared by these pathways. Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 11/2014;
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    ABSTRACT: In general populations, healthy lifestyle is associated with fewer adverse outcomes. We estimated the degree to which adherence to a healthy lifestyle decreases the risk of renal and cardiovascular events among adults with chronic kidney disease (CKD). Prospective cohort. 3,006 adults enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study. 4 lifestyle factors (regular physical activity, body mass index [BMI] of 20-<25kg/m(2), nonsmoking, and "healthy diet"), individually and in combination. CKD progression (50% decrease in estimated glomerular filtration rate or end-stage renal disease), atherosclerotic events (myocardial infarction, stroke, or peripheral arterial disease), and all-cause mortality. Multivariable-adjusted Cox proportional hazards. During a median follow-up of 4 years, we observed 726 CKD progression events, 355 atherosclerotic events, and 437 deaths. BMI≥25kg/m(2) and nonsmoking were associated with reduced risk of CKD progression (HRs of 0.75 [95% CI, 0.58-0.97] and 0.61 [95% CI, 0.45-0.82] for BMIs of 25 to <30 and ≥30kg/m(2), respectively, versus 20 to <25kg/m(2); HR for nonsmoking of 0.68 [95% CI, 0.55-0.84] compared to the current smoker reference group) and reduced risk of atherosclerotic events (HRs of 0.67 [95% CI, 0.46-0.96] for BMI of 25-<30 vs 20-<25kg/m(2) and 0.55 [95% CI, 0.40-0.75] vs current smoker). Factors associated with reduced all-cause mortality were regular physical activity (HR, 0.64 [95% CI, 0.52-0.79] vs inactive), BMI≥30kg/m(2) (HR, 0.64 [95% CI, 0.43-0.96] vs 20-<25kg/m(2)), and nonsmoking (HR, 0.45 [95% CI, 0.34-0.60] vs current smoker). BMI<20kg/m(2) was associated with increased all-cause mortality risk (HR, 2.11 [95% CI, 1.13-3.93] vs 20-<25kg/m(2)). Adherence to all 4 lifestyle factors was associated with a 68% lower risk of all-cause mortality compared to adherence to no lifestyle factors (HR, 0.32; 95% CI, 0.11-0.89). Lifestyle factors were measured only once. Regular physical activity, nonsmoking, and BMI≥25kg/m(2) were associated with lower risk of adverse outcomes in this cohort of individuals with CKD. Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 11/2014;
  • American Journal of Kidney Diseases 11/2014;
  • American Journal of Kidney Diseases 11/2014;
  • American Journal of Kidney Diseases 11/2014;
  • American Journal of Kidney Diseases 11/2014;
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    ABSTRACT: The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative (NKF-KDOQI) guideline for management of dyslipidemia in chronic kidney disease (CKD) was published in 2003. Since then, considerable evidence, including randomized controlled trials of statin therapy in adults with CKD, has helped better define medical treatments for dyslipidemia. In light of the new evidence, KDIGO (Kidney Disease: Improving Global Outcomes) formed a work group for the management of dyslipidemia in patients with CKD. This work group developed a new guideline that contains substantial changes from the prior KDOQI guideline. KDIGO recommends treatment of dyslipidemia in patients with CKD primarily based on risk for coronary heart disease, which is driven in large part by age. The KDIGO guideline does not recommend using low-density lipoprotein cholesterol level as a guide for identifying individuals with CKD to be treated or as treatment targets. Initiation of statin treatment is no longer recommended in dialysis patients. To assist US practitioners in interpreting and applying the KDIGO guideline, NKF-KDOQI convened a work group to write a commentary on this guideline. For the most part, our work group agreed with the recommendations of the KDIGO guideline, although we describe several areas in which we believe the guideline statements are either too strong or need to be more nuanced, areas of uncertainty and inconsistency, as well as additional research recommendations. The target audience for the KDIGO guideline includes nephrologists, primary care practitioners, and non-nephrology specialists such as cardiologists and endocrinologists. As such, we also put the current recommendations into the context of other clinical practice recommendations for cholesterol treatment. Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 11/2014;
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    ABSTRACT: Prior to conducting genome-wide association studies (GWAS) of renal traits and diseases, systematic checks to ensure data integrity and analytical work flow should be conducted. Using positive controls (ie, known associations between a single-nucleotide polymorphism [SNP] and a corresponding trait) allows for identifying errors that are not apparent solely from global evaluation of summary statistics. Strong genetic control associations of chronic kidney disease (CKD), as derived from GWAS, are lacking in the non-African ancestry CKD population; thus, in this perspective, we provide examples of and considerations for using positive controls among patients with CKD. Using data from individuals with CKD who participated in the CRIC (Chronic Renal Insufficiency Cohort) Study or PediGFR (Pediatric Investigation for Genetic Factors Linked to Renal Progression) Consortium, we evaluated 2 kinds of positive control traits: traits unrelated to kidney function (bilirubin level and body height) and those related to kidney function (cystatin C and urate levels). For the former, the proportion of variance in the control trait that is explained by the control SNP is the main determinant of the strength of the observable association, irrespective of adjustment for kidney function. For the latter, adjustment for kidney function can be effective in uncovering known associations among patients with CKD. For instance, in 1,092 participants in the PediGFR Consortium, the P value for the association of cystatin C concentrations and rs911119 in the CST3 gene decreased from 2.7 × 10-3 to 2.4 × 10-8 upon adjustment for serum creatinine–based estimated glomerular filtration rate. In this perspective, we give recommendations for the appropriate selection of control traits and SNPs that can be used for data checks prior to conducting GWAS among patients with CKD.
    American Journal of Kidney Diseases 11/2014;
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    ABSTRACT: Thrombotic microangiopathy (TMA) is a severe disorder with poor outcomes. The cause is unknown for many patients, although TMA is associated with connective tissue disorders, including systemic lupus erythematosus (SLE). While uncommon, TMA is one of the most serious complications of SLE and in many cases may be resistant to therapy. We report a patient with SLE complicated by TMA that was refractory to standard therapy but responded well to eculizumab, with continued remission after 1 year of follow-up. Eculizumab might be useful in the management of resistant cases of TMA caused by SLE. Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 11/2014;
  • American Journal of Kidney Diseases 11/2014;
  • American Journal of Kidney Diseases 11/2014;
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    ABSTRACT: Exercise training increasingly is recommended as an important part of the management of cardiovascular disease. However, few studies have evaluated the effectiveness of exercise training in patients with chronic kidney disease (CKD), and those that have included very selective populations. Analysis of secondary outcomes of a randomized controlled trial, with participants randomly assigned to either lifestyle intervention or usual care (control). Patients with CKD stages 3 to 4 and one or more uncontrolled cardiovascular risk factor were recruited from an outpatient clinic at a large tertiary hospital. Lifestyle intervention included access to multidisciplinary care through a nurse practitioner-led CKD clinic, exercise training, and a lifestyle program. The exercise training was a 2-phased program in which participants received 8 weeks of supervised training before commencing 10 months of home-based training. Efficacy, as assessed by metabolic equivalent tasks (METs), 6-minute walk distance, Timed Get-Up-and-Go test, grip strength, and anthropomorphic measures; adherence, as assessed by self-reported physical activity; and safety, as assessed by reported serious adverse events, were recorded. 83 patients were randomly assigned and 72 patients completed follow-up testing (intervention, n=36; control, n=36). The intervention resulted in a significant improvement in METs (pre, 7.2±3.3; post, 9.7±3.6), 6-minute walk distance (pre, 485±110m; post, 539±82m), and body mass index (pre, 32.5±6.7kg/m(2); post, 31.9±7.3kg/m(2)). Reported physical activity levels significantly increased in the intervention group at 6 months, but decreased at 12 months. There were no serious adverse events related to the exercise training. This study was not powered to evaluate the safety of exercise training on serious adverse events. The findings from the present study suggest that an exercise program that includes a supervised and home-based training phase is effective, adhered to, and safe in patients with CKD. Crown Copyright © 2014. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 11/2014;
  • American Journal of Kidney Diseases 11/2014;