ArticleSeminars in nephrology2010
Genetic basis of nondiabetic end-stage renal disease.
Article in Seminars in nephrology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Past Decline Versus Current eGFR and Subsequent ESRD Risk.Journal of the American Society of Nephrology : JASN · 2016Pooled it
- Non-diabetic end-stage renal disease in Saudis associated with polymorphism of MYH9 gene but not UMOD gene.Medicine · 2020Observational
- Risk Adjustment and the Assessment of Disparities in Dialysis Mortality Outcomes.Journal of the American Society of Nephrology : JASN · 2015Article
- Association of coronary artery disease and chronic kidney disease in Lebanese population.International journal of clinical and experimental medicine · 2015Article
- Survival advantage in black versus white men with CKD: effect of estimated GFR and case mix.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2013Article
- Arrest of the true culprit and acquittal of the innocent? Genetic revelations charge APOL1 variants with kidney disease susceptibility.International urology and nephrology · 2010Review
- Poverty and racial disparities in kidney disease: the REGARDS study.American journal of nephrology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Recent breakthroughs in genomics have led to a critical reappraisal of factors once thought to initiate common complex forms of kidney disease. The tenet that diabetes mellitus and hypertension routinely initiate kidney disease whenever blood glucose concentrations or systemic blood pressures reach critical levels for prolonged periods is falling from favor, although it remains important to control hypertension and hyperglycemia to slow nephropathy progression and to prevent cardiovascular disease. Many patients with systemic diseases that potentially may involve their kidneys never develop nephropathy. In addition, severe forms of several common kidney diseases cluster tightly in families. This article discusses the existence of differential nephropathy susceptibility based on an individual's genetic make-up, in the context of environmental exposures. Novel genetic analysis methods and recently identified major kidney disease susceptibility genes are discussed, including novel perspectives for categorizing complex forms of nephropathy based on the expanding spectrum of non-muscle myosin heavy chain 9 gene-associated disease. Genetic screening, gene-environment, and gene-gene interactions are also addressed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.