ReviewNature reviews. Nephrology2016
Insights into kidney diseases from genome-wide association studies.
Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 6 of them syntheses 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
67 citing papers in PubMed, 6 syntheses or guidelines pooled it, 107 citations in OpenAlex.
- Shared genetic effect of kidney function on bipolar and major depressive disorders: a large-scale genome-wide cross-trait analysis.Human genomics · 2024Pooled it
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- A catalog of genetic loci associated with kidney function from analyses of a million individuals.Nature genetics · 2019Pooled it
- An African perspective on the genetic risk of chronic kidney disease: a systematic review.BMC medical genetics · 2018Pooled it
- Fifty Shades of Risk: Population Studies and the Genetic Architecture of Kidney Diseases.Journal of the American Society of Nephrology : JASN · 2026Review
- From GWAS Signals to Causal Genes in Chronic Kidney Disease.Current issues in molecular biology · 2026Review
- Diagnostic utility of whole exome sequencing in pediatric and adult patients with suspected monogenic chronic kidney disease.Molecular biology reports · 2025Article
- A multi-ethnic polygenic risk score for chronic kidney disease is associated with increased risk of hypertension in African American individuals.BMC nephrology · 2025Article
- CRISPR and gene editing for kidney diseases: where are we?Clinical kidney journal · 2025Review
- Genetic Susceptibility to Glomerulonephritis in Children: Analysis of Structural Kidney Genes and Immune System Genes.Journal of clinical medicine · 2025Article
- GWAS scorecard prioritizes kidney genes using coding and regulatory variants.Nature reviews. Nephrology · 2025Article
- Conditional KnockoutInternational journal of molecular sciences · 2025Article
- Review
- Association of Tumor Necrosis Factor-Alpha (TNF-α) rs1800629 Polymorphism in Chronic Kidney Disease.Cureus · 2024Article
- Monogenic Kidney Diseases in Kidney Transplantation.Kidney international reports · 2024Review
- Association of Single Nucleotide Polymorphisms in KCNA10 and SLC13A3 Genes with the Susceptibility to Chronic Kidney Disease of Unknown Etiology in Central Indian Patients.Biochemical genetics · 2023Article
- Influence of variability in the cyclooxygenase pathway on cardiovascular outcomes of nephrosclerosis patients.Scientific reports · 2023Article
- Genetic predisposition may not improve prediction of cardiac surgery-associated acute kidney injury.Frontiers in genetics · 2023Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Over the past decade, genome-wide association studies (GWAS) have considerably improved our understanding of the genetic basis of kidney function and disease. Population-based studies, used to investigate traits that define chronic kidney disease (CKD), have identified >50 genomic regions in which common genetic variants associate with estimated glomerular filtration rate or urinary albumin-to-creatinine ratio. Case-control studies, used to study specific CKD aetiologies, have yielded risk loci for specific kidney diseases such as IgA nephropathy and membranous nephropathy. In this Review, we summarize important findings from GWAS and clinical and experimental follow-up studies. We also compare risk allele frequency, effect sizes, and specificity in GWAS of CKD-defining traits and GWAS of specific CKD aetiologies and the implications for study design. Genomic regions identified in GWAS of CKD-defining traits can contain causal genes for monogenic kidney diseases. Population-based research on kidney function traits can therefore generate insights into more severe forms of kidney diseases. Experimental follow-up studies have begun to identify causal genes and variants, which are potential therapeutic targets, and suggest mechanisms underlying the high allele frequency of causal variants. GWAS are thus a useful approach to advance knowledge in nephrology.
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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.