June 2009 Volume 5 Number 6
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=========================== ADVERTISEMENT ===========================
ISN Nexus Symposium: The Kidney and the Vascular System: Emerging Culprits
in Pathogenesis and Advances in Therapy.
April 15-18, 2010; Kyoto (Japan)
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=========================== ADVERTISEMENT ===========================
AJH Reader's Choice: Higher heart rate may predispose to obesity and
diabetes mellitus: 20-year prospective study in a general population.
Online at
http://links.ealert.nature.com/ctt?kn=16&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Is a higher bpm a cause, consequence or epiphenomenon in metabolic
syndrome?
This study from AJH is available online FREE of charge and re-examines
participants 20 years later for cardiometabolic factors.
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EDITORIAL
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Putting clinical trials on trial
Chloe Harman
p301 | doi:10.1038/nrneph.2009.89
http://links.ealert.nature.com/ctt?kn=58&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
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RESEARCH HIGHLIGHTS
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Glomerular Disease: Lupus nephritis trials end in disappointment
p303 | doi:10.1038/nrneph.2009.64
http://links.ealert.nature.com/ctt?kn=11&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Dialysis: Periodontitis and cardiovascular mortality in ESRD
p304 | doi:10.1038/nrneph.2009.57
http://links.ealert.nature.com/ctt?kn=81&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
IN BRIEF
Genetics | Pathology | Mineral metabolism | Chronic kidney disease
p304 | doi:10.1038/nrneph.2009.63
http://links.ealert.nature.com/ctt?kn=44&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Hypertension: Nicorandil: a useful adjunct for proteinuria?
p305 | doi:10.1038/nrneph.2009.59
http://links.ealert.nature.com/ctt?kn=89&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Diagnosis: Cystatin C is not an unbiased marker of GFR
p305 | doi:10.1038/nrneph.2009.60
http://links.ealert.nature.com/ctt?kn=93&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Debating the source of hypertension
p305 | doi:10.1038/nrneph.2009.61
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Chronic kidney disease: Warfarin bleeding risk increased in CKD
p306 | doi:10.1038/nrneph.2009.58
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IN BRIEF
Genetics | Anemia | Mineral metabolism | Transplantation
p306 | doi:10.1038/nrneph.2009.62
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NEWS AND VIEWS
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Mineral metabolism: Should cinacalcet be used in patients who are not
on dialysis?
Jorge B. Cannata-Andia and Jose L. Fernandez-Martin
p307 | doi:10.1038/nrneph.2009.54
Cinacalcet is an effective treatment for secondary hyperparathyroidism
in patients on dialysis. Until now, no randomized, placebo-controlled,
long-term trial has tested this drug in individuals with chronic kidney
disease who are not receiving dialysis.
http://links.ealert.nature.com/ctt?kn=82&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Transplantation: Tackling inactivity on the waiting list for transplantation
Francois C. Berthoux
p308 | doi:10.1038/nrneph.2009.53
An analysis of the US kidney transplant waiting list suggests that
recording a potential recipient as 'inactive', during which time he or
she cannot be offered a donor organ, is becoming increasingly common
and is not in patients' best interests.
http://links.ealert.nature.com/ctt?kn=98&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Pediatric nephrology: Estimating GFR in children: Schwartz redux
Kevin V. Lemley
p310 | doi:10.1038/nrneph.2009.56
One of the early products of the Chronic Kidney Disease in Children (CKiD)
study has been an updated equation for estimating GFR in children on the
basis of demographic and laboratory parameters. This formula is comparable
in form and performance to the MDRD equations for adults in clinical
trials first published a decade ago.
http://links.ealert.nature.com/ctt?kn=47&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Polycystic kidney disease: The cadence of kidney growth in ADPKD
Arlene Chapman
p311 | doi:10.1038/nrneph.2009.75
Autosomal-dominant polycystic kidney disease is characterized by the
development and expansion of cysts, which ultimately results in kidney
failure. The rate of this expansion can now be quantified within a
short period of time, which has implications for assessing the risk of
renal failure in affected patients.
http://links.ealert.nature.com/ctt?kn=76&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
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REVIEWS
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ANCA-negative pauci-immune crescentic glomerulonephritis
Min Chen, Cees G. M. Kallenberg and Ming-Hui Zhao
Published online: 28 April 2009
p313 | doi:10.1038/nrneph.2009.67
Pauci-immune crescentic glomerulonephritis is usually a manifestation of
antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
However, some patients with pauci-immune crescentic glomerulonephritis
lack ANCA. This Review compares the prevalence, clinical manifestations,
histopathology, and outcomes of ANCA-negative pauci-immune crescentic
glomerulonephritis with that of ANCA-positive disease. The authors also
discuss the possible pathogenesis of ANCA-negative pauci-immune crescentic
glomerulonephritis, paying particular attention to the mechanisms and
role of neutrophil activation.
Abstract: http://links.ealert.nature.com/ctt?kn=9&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=18&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Fibroblast activation and myofibroblast generation in obstructive
nephropathy
Maria T. Grande and Jose M. Lopez-Novoa
p319 | doi:10.1038/nrneph.2009.74
Activation of local resident fibroblasts and generation of myofibroblasts
via epithelial-mesenchymal transition are key processes in the development
of the interstitial fibrosis that characterizes obstructive nephropathy.
Authors from the University of Salamanca examine the molecular mechanisms
of these processes, focusing mainly on data from in vivo models of
unilateral ureteral obstruction. In the final section of the Review,
they highlight possibilities for future therapeutic intervention to
prevent or even reverse obstructive nephropathy.
Abstract: http://links.ealert.nature.com/ctt?kn=84&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=14&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
What nephrologists need to know about hemophagocytic syndrome
Alexandre Karras
Published online: 05 May 2009
p329 | doi:10.1038/nrneph.2009.73
Hemophagocytic syndrome (HPS), which was first described in 1939, is a
heterogeneous disorder characterized by excessive activation and
proliferation of non-malignant macrophages. HPS can cause acute kidney
injury and nephrotic syndrome; in addition, renal transplant recipients
are at risk of developing HPS as a result of their immunocompromised
state. This Review summarizes the presentation, causes, pathophysiology
and renal features of HPS for the benefit of the practicing nephrologist.
Abstract: http://links.ealert.nature.com/ctt?kn=101&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=4&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Monoclonal antibodies for podocytopathies: rationale and clinical responses
Maddalena Marasa and Jeffrey B. Kopp
p337 | doi:10.1038/nrneph.2009.70
The podocytopathies-minimal-change nephropathy, focal segmental
glomerulosclerosis, collapsing glomerulopathy and diffuse mesangial
sclerosis-involve diverse types of injury to podocytes. Although the
precise pathologic mechanisms are unclear, evidence has emerged linking
the immune system with podocyte injury. Current immunosuppressive
treatments have limited efficacy and exert considerable toxicity, but
here, Marasa and Kopp discuss how new therapeutic monoclonal antibodies
and other biologic therapies have the potential to define pathogenetic
pathways and contribute to new therapies.
Abstract: http://links.ealert.nature.com/ctt?kn=43&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=95&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
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CASE STUDY
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Unusual renal presentation of Fabry disease in a female patient
Cataldo Abaterusso, Vincenzo De Biase, Alessandro Salviati, Antonia Fabris,
Deborah Millardi, Paola Tomei, Patrizia Bernich, Antonio Lupo and
Giovanni Gambaro
Published online: 28 April 2009
p349 | doi:10.1038/nrneph.2009.71
Fabry disease, a rare lysosomal storage disorder, predominantly affects
males due to its X-linked inheritance pattern. Here, Abaterusso and
colleagues describe a heterozygous female who developed severe Fabry
disease-related renal disease with neither proteinuria nor microalbuminuria.
This case highlights the importance of considering heterozygous females
not merely as 'carriers' of Fabry disease, and emphasizes that the absence
of microalbuminuria and proteinuria does not rule out chronic kidney
disease in Fabry disease.
Abstract: http://links.ealert.nature.com/ctt?kn=5&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=3&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
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PERSPECTIVES
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Opinion: Ocular features aid the diagnosis of Alport syndrome
Judy Savige and Deb Colville
p356 | doi:10.1038/nrneph.2009.65
Alport syndrome is the most common inherited cause of renal failure after
nephronophthisis and reflux nephropathy in children, and after polycystic
kidney disease in adults, but often goes unrecognized. In this article,
Savige and Colville describe the ocular features of Alport syndrome, and
suggest that imaging of the central and peripheral retina might be a
rapid, noninvasive and inexpensive test to aid diagnosis of Alport
syndrome, particularly in males with early-onset renal failure.
Abstract: http://links.ealert.nature.com/ctt?kn=55&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=53&m=33342533&r=MTc2NDE4ODIzOQS2&b=2&j=NTA3MzgzNTQS1&mt=1&rt=0
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