BMC Nephrology (BMC Nephrol)

Publisher: BioMed Central

Journal description

BMC Nephrology publishes original research articles in all aspects of the prevention, diagnosis and management of kidney and associated disorders, as well as related molecular genetics, pathophysiology, and epidemiology.

Current impact factor: 1.69

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 1.69
2013 Impact Factor 1.52
2012 Impact Factor 1.644
2011 Impact Factor 2.176
2010 Impact Factor 2.136

Impact factor over time

Impact factor
Year

Additional details

5-year impact 1.81
Cited half-life 2.50
Immediacy index 0.26
Eigenfactor 0.01
Article influence 0.58
Website BMC Nephrology website
Other titles BioMed Central nephrology, Nephrology
ISSN 1471-2369
OCLC 45259909
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

BioMed Central

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Publisher's version/PDF may be used
    • Eligible UK authors may deposit in OpenDepot
    • Creative Commons Attribution License
    • Copy of License must accompany any deposit.
    • All titles are open access journals
    • 'BioMed Central' is an imprint of 'Springer Verlag (Germany)'
  • Classification
    green

Publications in this journal

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    ABSTRACT: Background Anemia is common among patients with chronic kidney disease (CKD) but its health consequences are poorly defined. The aim of this study was to determine the relationship between anemia and cognitive decline in older adults with CKD. Methods We studied a subgroup of 762 adults age ≥55 years with CKD participating in the Chronic Renal Insufficiency Cohort (CRIC) study. Anemia was defined according to the World Health Organization criteria (hemoglobin <13 g/dL for men and <12 g/dL for women). Cognitive function was assessed annually with a battery of six tests. We used logistic regression to determine the association between anemia and baseline cognitive impairment on each test, defined as a cognitive score more than one standard deviation from the mean, and mixed effects models to determine the relation between anemia and change in cognitive function during follow-up after adjustment for demographic and clinical characteristics. Results Of 762 participants with mean estimated glomerular filtration rate of 42.7 ± 16.4 ml/min/1.73 m2, 349 (46 %) had anemia. Anemia was not independently associated with baseline cognitive impairment on any test after adjustment for demographic and clinical characteristics. Over a median 2.9 (IQR 2.6–3.0) years of follow-up, there was no independent association between anemia and change in cognitive function on any of the six cognitive tests. Conclusions Among older adults with CKD, anemia was not independently associated with baseline cognitive function or decline.
    Full-text · Article · Dec 2016 · BMC Nephrology
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    ABSTRACT: Background: Although dysnatremia has been reported to be correlated with mortality risk, this issue remains unresolved in patients undergoing continuous renal replacement therapy (CRRT). Furthermore, it has not been determined whether change in or correction of sodium is related to mortality risk in this subset. Methods: A total of 569 patients were prospectively enrolled at the start of CRRT between May 2010 and September 2013. The patients were divided into 5 groups: normonatremia (135-145 mmol/L), mild hyponatremia (131.1-134.9 mmol/L), moderate to severe hyponatremia (115.4-131.0 mmol/L), mild hypernatremia (145.1-148.4 mmol/L), and moderate to severe hypernatremia (148.5-166.0 mmol/L). The non-linear relationship between sodium and mortality was initially explored. Subsequently, the odds ratios (ORs) for 30-day mortality were calculated after adjustment of multiple covariates. Results: The relationship between baseline sodium and mortality was U-shaped. The mild hyponatremia, moderate to severe hyponatremia, and moderate to severe hypernatremia groups had greater ORs for mortality (1.65, 1.91, and 2.32, respectively) than the normonatremia group (all P values < 0.05). However, later sodium levels (24 and 72 h after CRRT) did not predict 30-day mortality. Furthermore, the changes in sodium over 24 or 72 h, including the appropriate correction of dysnatremia, did not show any relationships with mortality, irrespective of baseline sodium level. Conclusions: Sodium level at the start of CRRT was a strong predictor of mortality. However, changes in sodium level and the degree of sodium correction were not associated with the mortality risk in the patients with CRRT.
    Preview · Article · Dec 2016 · BMC Nephrology
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    ABSTRACT: Background: The patterns, performance characteristics, and yield of diagnostic tests ordered for the evaluation of acute kidney injury (AKI) have not been rigorously evaluated. Methods: We characterized the frequency of AKI diagnostic testing for urine, blood, radiology, and pathology tests in all adult inpatients who were admitted with or developed AKI (N = 4903 patients with 5731 AKI episodes) during a single calendar year. We assessed the frequency of abnormal test results overall and by AKI stage. We manually reviewed electronic medical records to evaluate the diagnostic yield of selected urine, blood, and radiology tests. Diagnostic yield of urine and blood tests was determined based on whether an abnormal test affected AKI diagnosis or management, whereas diagnostic yield of radiology tests was based on whether an abnormal test resulted in a procedural intervention. In sensitivity analyses we also evaluated appropriateness of testing using prespecified criteria. Results: Frequency of testing increased with higher AKI stage for nearly all diagnostic tests, whereas frequency of detecting an abnormal result increased for some, but not all, tests. Frequency of detecting an abnormal result was highly variable across tests, ranging from 0 % for anti-glomerular basement membrane testing to 71 % for urine protein testing. Many of the tests evaluated had low diagnostic yield. In particular, selected urine and blood tests were unlikely to impact AKI diagnosis or management, whereas radiology tests had greater clinical utility. Conclusions: In patients with AKI, many of the diagnostic tests performed, even when positive or abnormal, may have limited clinical utility.
    No preview · Article · Dec 2016 · BMC Nephrology
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    ABSTRACT: Background: Recent studies indicate that mural cells of the preglomerular vessels, known as cells of renin lineage (CoRL), contribute to repair and regeneration of injured kidney glomeruli. However, their potential roles in tubulointerstitial disease are less understood. The aim of this study was to better understand CoRL number and distribution following UUO so that future mechanistic studies could be undertaken. Methods: We mapped the fate of CoRL in adult Ren1cCreER x Rs-tdTomato-R reporter mice that underwent UUO. Kidney biopsies from sham and UUO-subjected mice on days 3, 7, and 14 were evaluated by immunohistochemistry. Results: In sham animals, CoRL were restricted to juxtaglomerular location. At day 7 following UUO, CoRL increased two-fold, were perivascular in location, and co-expressed pericyte markers (PDGFßR, NG2), but did not express renin. At day 14 post UUO, labeled CoRL detached from vessels and were present in the interstitium, in areas of fibrosis, where they now expressed the myofibroblast marker alpha-smooth muscle actin. The increase in CoRL was likely due to proliferation as marked by BrdU labeling, and migration from the cortex. Following UUO starting from day 3, active hypoxia inducible factor-2α was detected in nuclei in labeled CoRL, in the cortex, but not those cells found in medulla. Conclusions: We have demonstrated that arteriolar CoRL are potential kidney progenitors that may contribute to the initial vascular regeneration. However, in chronic kidney injury (≥14 days post UUO), perivascular CoRL transition to myofibroblast-like cells.
    Preview · Article · Dec 2016 · BMC Nephrology
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    ABSTRACT: Background Encapsulating peritoneal sclerosis (EPS) is classically described as progressive sclerosis and cocooning of the entire peritoneum; however, there has been limited number of reported cases of localized fibrosis as a variant form. Case presentation We describe two cases of acute bowel obstruction with isolated transition points in the setting of long-term peritoneal dialysis. Conclusion We postulate that some of the cases of small bowel obstruction with an obvious transition point in long-term peritoneal dialysis patients may represent a unique and localized form of EPS. We aim to emphasize the presence of macroscopic variations in presentation of EPS.
    Preview · Article · Dec 2016 · BMC Nephrology
  • C. Vaughan Tuohy · Maria E. Montez-Rath · Mintu Turakhia · Tara I. Chang · John W. Winkelman · Wolfgang C. Winkelmayer
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    ABSTRACT: Background Sleep disordered breathing (SDB) such as sleep apnea is associated with cardiovascular disease in the general population. However, little is known about the cardiovascular risks of SDB in patients with end-stage renal disease (ESRD). Methods We identified Medicare fee-for-service beneficiaries aged ≥67 years initiating dialysis between 2004 and 2009. Outcomes of interest included all-cause mortality, incident myocardial infarction, ischemic stroke, and atrial fibrillation. We compared patients with and without diagnosed SDB using Cox proportional hazards regression. Results Between 2004 and 2009, 184,217 older patients developed ESRD, of whom 15,121 (8.2 %) were previously diagnosed with SDB. Patients diagnosed with SDB were younger, more likely to be male and Caucasian, less Medicaid eligible, had more non-Nephrology clinic visits, higher body mass index, and more comorbidity. In analyses adjusting for demographics and BMI, diagnosed SDB was associated with higher risk of death and atrial fibrillation, but not associated with myocardial infarction or ischemic stroke risk. After further adjustment for all baseline characteristics, diagnosed SDB was associated with slightly lower risks of death (hazard ratio [HR]: 0.93, 95 % confidence interval [CI]: 0.91–0.96), myocardial infarction (HR: 0.92, CI: 0.87–0.98), and ischemic stroke (HR: 0.90, 95 % CI: 0.82–0.98), and not associated with atrial fibrillation (HR: 1.02, CI: 0.98–1.07). Conclusions In older patients initiating dialysis in the U.S., diagnosed SDB was weakly associated with lower risks of death and important cardiovascular outcomes, thus adding to the list of established risk factors that are paradoxically associated with cardiovascular outcomes in the ESRD population.
    No preview · Article · Dec 2016 · BMC Nephrology
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    ABSTRACT: Background Hemophagocytic lymphohistiocytosis (HLH) is a fatal clinical syndrome characterized by excessive immune activation and inflammation. It is frequently complicated by acute kidney injury (AKI) that often develops as acute tubular necrosis (ATN). Meanwhile, renal thrombotic microangiopathy (TMA) is a rare pathologic finding that mostly occurs in hemolytic uremic syndrome or thrombotic thrombocytopenic purpura. There are only few reports on TMA developing in patients with HLH. We present here a rare case of TMA associated HLH. Case presentation A 60-year-old woman was admitted for a fever of unknown origin that had persisted for several weeks. She presented with AKI and pancytopenia. Clinical, laboratory and bone marrow biopsy findings met the criteria of HLH. Kidney biopsy showed TMA and minimal ATN, which suggested that the primary cause of AKI was TMA in this case. Because of sustained oliguria, we initiated hemodialysis (HD) and also decided to use chemotherapy composed of dexamethasone, etoposide and cyclosporine for treatment of HLH. Six months after the initiation of chemotherapy, pancytopenia was completely resolved, indicating the resolution of HLH. At the same time, serum creatinine decreased to a normal range without the need for HD, suggesting the resolution of TMA. Conclusion We report a case of renal TMA associated HLH. This case suggests that renal TMA should be considered as a primary cause of AKI in patients with underlying HLH.
    Preview · Article · Dec 2016 · BMC Nephrology
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    ABSTRACT: Background Warfarin related nephropathy is one of the potential complications of warfarin therapy. Despite the well described histological entity, the clinical course and approach to warfarin related nephropathy in patients requiring life-long anticoagulation is however not well described in the literature. Case presentation We report the clinical course of a 56 years old Chinese lady who presented with over anti-coagulation and acute kidney injury while on warfarin therapy for permanent atrial fibrillation and mechanical valve replacement. Renal biopsy was performed as the acute kidney injury was persistent despite normalization of the International Normalized Ratio and the diagnosis of warfarin related nephropathy was made. Temporary interruption of anti-coagulation, in combination with oral N-acetylcysteine resulted in subsequent stabilization of renal function. Conclusion The diagnosis of warfarin induced nephropathy should be considered in patients presenting with unexplained acute kidney injury and over anti-coagulation. Awareness of this clinical entity is important for clinician managing anti-coagulation therapy and renal function should be monitored regularly in patients who are on warfarin therapy.
    Preview · Article · Feb 2016 · BMC Nephrology
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    ABSTRACT: In a recent study published by the National Project Team on chronic kidney diseases of unknown origin in Sri Lanka, identified cadmium as a major risk factor but strong conclusions were not made as the identified environmental toxins were within the permissible levels.Sri Lankan food consumption pattern is different so that approach of total exposure of cadmium by food and water been calculated. Such calculation point out that total exposure of cadmium exceed the provisional tolerable weekly intake determined by international agencies.
    Preview · Article · Dec 2015 · BMC Nephrology
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    ABSTRACT: Background: Pyrrolidine dithiocarbamate (PDTC) reduces renal cyst growth in a rodent model of polycystic kidney disease (PKD) but the mechanism of action is not clear. Here, we investigated the hypothesis that PDTC reduces the proliferation of cystic epithelial cells in vitro in a nuclear factor (NF)-κB-dependent manner. Methods: Immortalized autosomal dominant PKD (ADPKD) cells that are heterozygous (WT9-7) and homozygous (WT-9-12) for a truncating Pkd1 mutation, and immortalized normal human tubular cells (HK-2), were exposed to NF-κB-inducing agents with or without PDTC. Cell proliferation and apoptosis were assessed by bromodeoxyuridine assay and Annexin V flow cytometry, respectively. NF-κB activity was assessed by luciferase reporter assay and western blotting for nuclear p65, p50, and RelB subunits and cytoplasmic phosphorylated-IκBα. Results: Serum-induced proliferation was similar in all cell lines over 72 h. PDTC demonstrated anti-proliferative effects that were delayed in ADPKD cells compared to HK-2. Basal NF-κB-dependent luciferase reporter activity was lower in ADPKD cells compared to normal cells. Classical NF-κB stimulants, lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α, increased NF-κB luciferase activity in HK-2, whereas in PKD cell lines, NF-κB activity was only induced by TNF-α. However, neither stimulant altered proliferation in any cell line. PDTC reduced TNF-α-stimulated NF-κB activity in HK-2 only. Conclusions: PDTC reduced proliferation in ADPKD cells but did not consistently alter NF-κB activation, suggesting that other signalling pathways are likely to be involved in its ability to attenuate renal cyst growth in vivo.
    Full-text · Article · Dec 2015 · BMC Nephrology