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

  • [Show abstract] [Hide abstract]
    ABSTRACT: A growing number of monoclonal gammopathy–associated kidney diseases recently have been recognized. We present the case of a 54-year-old man who presented with acute kidney injury and hypocomplementemia. Kidney biopsy confirmed the presence of immunoglobulin G κ pseudothrombi with intracytoplasmic crystals in glomeruli and tubules. Levels of κ free light chains were elevated without a detectable monoclonal gammopathy, and bone marrow biopsy results were normal. After the first course of rituximab, cyclophosphamide, and dexamethasone in addition to daily plasmapheresis, kidney function recovered within 2 weeks and dialysis therapy was discontinued. Treatment for monoclonal protein–induced kidney disease should be considered in the setting of progressive decreased kidney function, even in the absence of a circulating monoclonal protein or cellular clone of origin.
    American Journal of Kidney Diseases 10/2014;
  • American Journal of Kidney Diseases 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Proteinuria has been associated with transplant loss and mortality in kidney transplant recipients. Both spot samples (albumin-creatinine ratio [ACR] and protein-creatinine ratio [PCR]) and 24-hour collections (albumin excretion rate [AER] and protein excretion rate [PER]) have been used to quantify protein excretion, but which measurement is a better predictor of outcomes in kidney transplantation remains uncertain. Study Design Observational cohort study. Setting & Participants Tertiary care center, 207 kidney transplant recipients who were enrolled in a prospective study to measure glomerular filtration rate. Consecutive patients who met inclusion criteria were approached. Predictors ACR and PCR in spot urine samples, AER and PER in 24-hour urine collections. Outcomes Primary outcome included transplant loss, doubling of serum creatinine level, or death. Measurements Urine and serum creatinine were measured using a modified Jaffé reaction that had not been standardized by isotope-dilution mass spectrometry. Urine albumin was measured by immunoturbidimetry. Urine protein was measured by pyrogallol red molybdate complex formation using a timed end point method. Results Mean follow-up was 6.4 years and 22% developed the primary end point. Multivariable-adjusted areas under the receiver operating characteristic curves were similar for the different protein measurements: ACR (0.85; 95% CI, 0.79-0.89), PCR (0.84; 95% CI, 0.79-0.89), PER (0.86; 95% CI, 0.80-0.90), and AER (0.83; 95% CI, 0.78-0.88). C Index values also were similar for the different proteinuria measurements: 0.87 (95% CI, 0.79-0.95), 0.86 (95% CI, 0.79-0.94), 0.88 (95% CI, 0.82-0.94), and 0.86 (95% CI, 0.77-0.95) for log(ACR), log(PCR), log(PER), and log(AER), respectively. Limitations Single-center study. Measurement of proteinuria was at variable times posttransplantation. Conclusions Spot and 24-hour measurements of albumin and protein excretion are similar predictors of doubling of serum creatinine level, transplant loss, and death. Thus, spot urine samples are a suitable alternative to 24-hour urine collection for measuring protein excretion in this population.
    American Journal of Kidney Diseases 10/2014;
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    ABSTRACT: Glomerulopathy is an uncommon but increasingly recognized complication of hematopoietic cell transplantation. It typically manifests as membranous nephropathy, less commonly as minimal change disease, and rarely as proliferative glomerulonephritis. There is evidence to suggest that these glomerulopathies might represent manifestations of chronic graft-versus-host disease. In this report, we focus on membranous nephropathy as the most common form of glomerulopathy after hematopoietic cell transplantation. We present a case of membranous nephropathy that developed 483 days post–allogeneic hematopoietic stem cell transplantation in a patient with a history of acute graft-versus-host disease. We also share our experience with 4 other cases of membranous nephropathy occurring after allogeneic hematopoietic stem cell transplantation. Clinicopathologic correlates, including the association with graft-versus-host-disease, HLA antigen typing, glomerular deposition of immunoglobulin G (IgG) subclasses, subepithelial colocalization of IgG deposits with phospholipase A2 receptor staining, C4d deposition along the peritubular capillaries, and treatment, are discussed with references to the literature.
    American Journal of Kidney Diseases 10/2014;
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    ABSTRACT: We report a case of multiorgan failure resulting from treatment with the antiviral foscarnet in a kidney transplant recipient. Precipitation of foscarnet crystals was confirmed histologically from a biopsy of the transplant using optical and infrared microscopy. In addition to kidney damage resulting from foscarnet crystal precipitation in the tubular lumen and glomerular capillaries, the patient presented with pancreatitis, pancolitis, and myocarditis with shock. Interruption of the treatment led to rapid improvement in her general condition, but did not prevent permanent loss of the kidney transplant. When faced with unexplained multiorgan failure in a patient treated with foscarnet, one should assume this substance to be toxic. A kidney biopsy can confirm this diagnosis.
    American Journal of Kidney Diseases 10/2014;
  • American Journal of Kidney Diseases 10/2014;
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    ABSTRACT: Background Residual proteinuria during renin-angiotensin-aldosterone system (RAAS) blockade is a major renal and cardiovascular risk factor in chronic kidney disease. Dietary sodium restriction potentiates the antiproteinuric effect of RAAS blockade, but residual proteinuria remains in many patients. Previous studies linked high fibroblast growth factor 23 (FGF-23) levels with volume overload; others linked higher serum phosphate levels with impaired RAAS-blockade efficacy. We hypothesized that FGF-23 reduces the capacity of dietary sodium restriction to potentiate RAAS blockade, impairing the antiproteinuric effect. Study Design Post hoc analysis of cohort data from a randomized crossover trial with two 6-week study periods comparing proteinuria after a regular-sodium diet with proteinuria after a low-sodium diet, both during background angiotensin-converting enzyme inhibition. Setting & Participants 47 nondiabetic patients with CKD with residual proteinuria (median protein excretion, 1.9 [IQR, 0.8-3.1] g/d; mean age, 50 ± 13 [SD] years; creatinine clearance, 69 [IQR, 50-110] mL/min). Predictor Plasma carboxy-terminal FGF-23 levels. Outcomes Difference in residual proteinuria at the end of the regular-sodium versus low-sodium study period. Residual proteinuria during the low-sodium diet period adjusted for proteinuria during the regular-sodium diet period. Results Higher baseline FGF-23 level was associated with reduced antiproteinuric response to dietary sodium restriction (standardized β = −0.46; P = 0.001; model R2 = 0.71). For every 100-RU/mL increase in FGF-23 level, the antiproteinuric response to dietary sodium restriction was reduced by 10.6%. Higher baseline FGF-23 level was a determinant of more residual proteinuria during the low-sodium diet (standardized β = 0.27; P = 0.003) in linear regression analysis adjusted for baseline proteinuria (model R2 = 0.71). There was no interaction with creatinine clearance (P interaction = 0.5). Baseline FGF-23 level did not predict changes in systolic or diastolic blood pressure upon intensified antiproteinuric treatment. Limitations Observational study, limited sample size. Conclusions FGF-23 levels are associated independently with impaired antiproteinuric response to sodium restriction in addition to RAAS blockade. Future studies should address whether FGF-23−lowering strategies may further optimize proteinuria reduction by RAAS blockade combined with dietary sodium restriction.
    American Journal of Kidney Diseases 09/2014;
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    ABSTRACT: Low ankle-brachial index (ABI) is a reflection of atherosclerotic disease, and high ABI is an indicator of calcified vessels. The associations of albuminuria and cystatin C level with incidence of either low or high ABI are unknown.
    American Journal of Kidney Diseases 07/2014;
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    ABSTRACT: Objectively structured clinical examinations (OSCEs) are widely used in medical education, but we know of none described that are specifically for nephrology fellowship training. OSCEs use simulation to educate and evaluate. We describe a technically simple, multidisciplinary, low-cost OSCE developed by our program that contains both examination and training features and focuses on management and clinical knowledge of rare hemodialysis emergencies. The emergencies tested are venous air embolism, blood leak, dialysis membrane reaction, and hemolysis. Fifteen fellows have participated in the OSCE as examinees and/or preceptors since June 2010. All have passed the exercise. Thirteen responded to an anonymous survey in July 2013 that inquired about their confidence in managing each of the 4 tested emergencies pre- and post-OSCE. Fellows were significantly more confident in their ability to respond to the emergencies after the OSCE. Those who subsequently saw such an emergency reported that the OSCE experience was somewhat or very helpful in managing the event. The OSCE tested and trained fellows in the recognition and management of rare hemodialysis emergencies. OSCEs and simulation generally deserve greater use in nephrology subspecialty training; however, collaboration between training programs would be necessary to validate such exercises.
    American Journal of Kidney Diseases 01/2014;
  • American Journal of Kidney Diseases 01/2014; 63(5):736–738.
  • American Journal of Kidney Diseases 01/2014;
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    ABSTRACT: Background Exercise capacity, which is predictive of all-cause mortality and cardiovascular disease risk, is reduced significantly in patients with non–dialysis-dependent chronic kidney disease. This pilot study examined the effect of moderate-intensity exercise training on kidney function and indexes of cardiovascular risk in patients with progressive chronic kidney disease stages 3 to 4. Study Design Single-blind, randomized, controlled, parallel trial. Setting & Participants 20 patients (aged 18-80 years; 17 men) randomly assigned to rehabilitation (n = 10) or usual care (n = 10). Participants were included if they were 18 years or older and had evidence of rate of decline in creatinine-based estimated glomerular filtration rate (eGFRcr) ≥ 2.9 mL/min/1.73 m2 per year for 12 months preintervention. Patients were excluded if they had unstable medical conditions or had recently started regular exercise. Intervention The rehabilitation group received resistance and aerobic training (3 days per week) for a 12-month period. The usual care group received standard care. Outcomes Kidney function assessed by comparing mean rate of change in eGFRcr (mL/min/1.73 m2 per year) from a 12-month preintervention period against the 12-month intervention period. Pulse wave velocity (PWV), peak oxygen uptake (Vo2peak), and waist circumference assessed at 0, 6, and 12 months. Measurements eGFR assessed using creatinine, cystatin C (eGFRcys), and a combination of both values (eGFRcr-cys). Results 18 participants (rehabilitation, 8; usual care, 10) completed the study. A significant mean difference in rate of change in eGFRcr (+7.8 ± 3.0 [95% CI, 1.1-13.5] mL/min/1.73 m2 per year; P = 0.02) was observed between the rehabilitation and usual care groups, with the rehabilitation group demonstrating a slower decline. No significant between-group mean differences existed in absolute eGFRcr, eGFRcr-cys, or eGFRcys at 12 months of study intervention. Significant between-group mean differences existed in PWV (−2.30 [95% CI, −3.02 to −1.59] m/s), waist circumference (−7.1 ± 12.8 [95% CI, −12.4 to −3.2] cm), and Vo2peak (5.7 [95% CI, 1.34-10.10] mL/kg/min). Change in eGFRcr was correlated inversely with PWV (r = −0.5; P = 0.04) at 12 months. Limitations Small sample size, inconsistency between primary and secondary measures of kidney function. Conclusions The effect of a 1-year exercise intervention on progression of kidney disease is inconclusive. A larger study with longer follow-up may be necessary.
    American Journal of Kidney Diseases 01/2014;
  • American Journal of Kidney Diseases 01/2014;
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    ABSTRACT: Background Hepatic transcatheter arterial embolization (TAE) has become an accepted treatment option for patients with symptomatic autosomal dominant polycystic kidney disease (ADPKD) who also have polycystic liver disease and who are not good candidates for surgery. However, indications for TAE and long-term outcome with it are still unclear. Study Design Retrospective cohort study. Setting & Participants Symptomatic patients with ADPKD with polycystic liver disease who underwent hepatic TAE, June 2001 to December 2012, at Toranomon Hospital and whose liver volume data were available were studied (N = 244; 56% on dialysis therapy, none with kidney transplants). Mean age was 55 ± 9 (SD) years, and mean liver volumes were 8,353 ± 2,807 and 6,626 ± 2,485 cm3 in men and women, respectively. Target arteries were embolized from the periphery using platinum microcoils. Predictors Sex-specific quartiles (6,433, 8,142, and 9,574 cm3 in men and 4,638, 6,078, and 8,181 cm3 in women) of total liver volume pretreatment. Outcomes All causes of mortality were obtained from medical records, followed up until July 31, 2013. Measurements Laboratory values were measured before TAE and 1, 3, 6, and 12 months after. Organ volumes were measured pretreatment, then 6 and 12 months after, by summing the products of the organ areas traced in each computed tomographic image. Results Liver/cyst volume decreased to 94.7% (95% CI, 93.5%-95.8%) at 6 months and 90.8% (95% CI, 88.7%-92.9%) at 12 months of pretreatment volumes. Serum protein and hematocrit values improved significantly without liver damage. Survival was significantly better for patients with liver volume ≤ 9,574 cm3 (men) and ≤8,181 cm3 (women) than for those with larger livers (5-year survival, 69% and 48%; P = 0.02). Infection and liver failure caused most deaths, especially in patients with larger livers. Limitations Referral bias and lack of control group. Conclusions Hepatic TAE appears to be a safe and less invasive option for patients with symptomatic polycystic liver, especially those contraindicated for surgical treatment (eg, with malnutrition or on dialysis therapy), improving both hepatic volume and nutrition.
    American Journal of Kidney Diseases 01/2014;
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    ABSTRACT: Both chronic kidney disease (CKD) and osteoporosis are major public health problems associated with an aging population. Osteoporosis is characterized by reduced bone mineral density, while CKD results in qualitative changes in bone structure; both conditions increase the predisposition to fragility fractures. There is a significant coprevalence of osteoporotic fractures and CKD, particularly in the elderly population. Not only is the risk of fracture higher in the CKD population, but clinical outcomes are significantly worse, with substantial health care costs. Management of osteoporosis in the CKD population is particularly complex given the impact of renal osteodystrophy on bone quality and the limited safety and hard outcome data for current therapy in patients with severe CKD or on dialysis therapy. In this review, we discuss the pathophysiology of osteoporosis, the impact of CKD on bone strength, and the role of novel imaging techniques and biomarkers in predicting underlying renal osteodystrophy on bone histomorphometry in the context of CKD.
    American Journal of Kidney Diseases 01/2014;
  • American Journal of Kidney Diseases 01/2014;
  • American Journal of Kidney Diseases 01/2014; 64(1):156.
  • American Journal of Kidney Diseases 01/2014; 63(4):549–551.