9 research outputs found
The Real Exchange Rate and Growth in Zimbabwe: Does the Currency Regime Matter?
- Author
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2014
- Field of study
Full text linkZimbabwe faces growth and external competitiveness challenges, as indicated by its low trend growth and investment, declining share in the world exports, high current account deficits, and external debt. The stock-flow approach to the equilibrium exchange rate reveals that the real exchange rate experienced periods of sizeable overvaluation, both prior to the 2008 economic collapse and under the current multicurrency regime. While overvaluation hampers GDP growth, as well as growth and employment in export sectors, we have not found that undervaluation would raise it. Replacing the multicurrency regime anchored in the US$ by the South African rand as the sole transaction currency would help reduce overvaluation and stimulate exports and growth. Under any currency regime, Zimbabwe needs to adhere to sound macroeconomic policies, avoid overspending on public wages, and create environment conducive for investment.http://deepblue.lib.umich.edu/bitstream/2027.42/132981/1/wp1081.pd
Whole-genome sequencing reveals host factors underlying critical COVID-19
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- Woodyatt W.
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- Worsley L.
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- Wren L.
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- Wright J.
- Wright M.
- Wrobel N.
- Wu Y.
- Wulandari R.
- Wyllie D. H.
- Wynter I.
- Xavier K.
- Xue X.
- Yadav A.
- Yang J.
- Yassen A. M.
- Yates B.
- Ye C.
- Yun N.
- Zainy T.
- Zak A.
- Zaki A.
- Zamikula J.
- Zanella I.
- Zborowski A. C.
- Zeberg H.
- Zechner M.
- Zguro K.
- Zhang M.
- Zhao J. H.
- Zheng C.
- Zhou W.
- Zitter L.
- Zlatopolsky M.
- Zollner S.
- Zongo O.
- Zucchi P.
- Zyndorf M.
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Get PDFCritical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Genetic mechanisms of critical illness in COVID-19.
- Author
- A A Roger Thompson
- A Abraheem
- A Agasou
- A Ahmed
- A Ali
- A Allan
- A Altabaibeh
- A Alvaro
- A Aspinwall
- A Ayers
- A Bamford
- A Barron
- A Bashyal
- A Bellini
- A Bociek
- A Botello
- A Bowes
- A Brady
- A Brayne
- A Brown
- A Brown
- A Butler
- A Campbell
- A Carter
- A Collins
- A Cowley
- A Cowton
- A Cowton
- A Cox
- A Crew
- A Dance
- A Daniel
- A Daniels
- A Dela Rosa
- A Drummond
- A Durie
- A E Heron
- A Easthope
- A Easthope
- A Evans
- A Fofano
- A Gales
- A Ganesan
- A Gardner
- A Garg
- A Gherman
- A Gordon
- A Gratrix
- A Gulati
- A Gupta
- A Haigh
- A Haldeos
- A Harrison
- A Harvey
- A Hayes
- A Higham
- A Higham
- A Hilldrith
- A Holden
- A Hormis
- A Hutcheon
- A Javaid
- A Joseph
- A Kaliappan
- A Katary
- A Kay
- A Kayani
- A Kent
- A Kirkby
- A Knight
- A Kubisz-Pudelko
- A Kuravi
- A Lewis
- A Loveridge
- A Lyle
- A Mayer
- A McAlpine
- A McCarthy
- A McGregor
- A McGregor
- A Meikle
- A Mitchell
- A Mitra
- A Morris
- A Morrison
- A Naranjo
- A Nicholson
- A Nicholson
- A Nilsson
- A Noakes
- A Patel
- A Pickard
- A Poole
- A Price
- A Puxty
- A Quinn
- A Quinn
- A Raithatha
- A Rattray
- A Reddy
- A Reed
- A Reyes
- A Rose
- A Rose
- A Rostron
- A Roy
- A Roynon-Reed
- A S Raj
- A Salberg
- A Sanderson
- A Serrano-Ruiz
- A Solesbury
- A Sukha
- A Swain
- A Tariq
- A Thomas
- A Thomas
- A Todd
- A Tomas
- A Tridente
- A Tucci
- A Turnbull
- A Uriel
- A Ustianowski
- A Vochin
- A Vuylsteke
- A Waite
- A Walden
- A Whileman
- A Wilkinson
- A Williams
- A Williams
- A Wilson
- A Zak
- A Zaki
- Achille Iolascon
- Adam Auton
- Adam Brown
- Agnese Verzuri
- Agostino Ognibene
- Agostino Riva
- Ailsa Golightly
- Alan Maclean
- Alessandra
- Alessandra Stella
- Alessandra Vergori
- Alessia Giorli
- Alexander J Mentzer
- Alice Donati
- Alison M Meynert
- Alistair Nichol
- Ana da Silva Filipe
- Andrea Antinori
- Andrea Cossarizza
- Andrea Ganna
- Andrea Tommasi
- Andrew Rambaut
- Andrew Stenhouse
- Andy Law
- Anjali J Shastri
- Anna Canaccini
- Anna Maria Pinto
- Annarita Giliberti
- Annemarie B Docherty
- Antonella D'Arminio Monforte
- Antonia Ying Wai Ho
- Antonio Di Biagio
- Antony Symons
- Arianna Emiliozzi
- Arianna Gabrieli
- Audrey Coutts
- B Anwar
- B Attwood
- B Baines
- B Blackledge
- B Borislavova
- B Chandler
- B Charles
- B Creagh-Brown
- B David
- B Deacon
- B Deacon
- B Digby
- B Faulkner
- B Fuller
- B Gumbrill
- B Gurung
- B Hadebe
- B Hairsine
- B Hopkins
- B Johnston
- B Lenagh
- B Masunda
- B Ogg
- B Patel
- B Player
- B Purewal
- B Scholefield
- B Shelley
- B Sloan
- B Thomas
- B Wadams
- B Welsh
- B Wilkinson
- B Winter-Goodwin
- B Yates
- Baillie J Kenneth
- Barbara Rossetti
- Beale Rupert
- Beatrice Alex
- Benjamin Bach
- Bretherick Andrew D
- Bruno Frediani
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- C Ahmed
- C Almaden-Boyle
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- C Basikolo
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- C Beazley
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- C Lynch
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- C Stuart
- C Summers
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- Carmen Marciano
- Caroline Abernathy
- Carrol Gamble
- Caterina Lo Rizzo
- Catherine A Shaw
- Catherine H Weldon
- Caulfield Mark
- Ceilia Boz
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- Chiara Fallerini
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- Chloe Donohue
- Chris Ponting
- Christoper A Green
- Cinthia E Jannes
- Clare Jackson
- Clohisey Sara
- Cristina Mussini
- D Antcliffe
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- D Walker
- D Warren
- D Williams
- D Wood
- D Wright
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- Daniella Coker
- Danilo Tacconi
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- David Bennet
- David L Robertson
- David Stuart
- Dawn Law
- Debby Bogaert
- Derek Murphy
- Domenico A Coviello
- E Abaleke
- E Allan
- E Anastasescu
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- E Beech
- E Beranova
- E Bevan
- E Black
- E Brinkworth
- E Collins
- E Combes
- E Davies
- E Dobson
- E Dooks
- E Fisher
- E Gendall
- E Goff
- E Goodwin
- E Gordon
- E Heeney
- E Horsley
- E Hughes
- E Johnson
- E Knights
- E Lee
- E London
- E Maccacari
- E Massey
- E McKenna
- E Meadows
- E Moncur
- E Morino
- E Mwaura
- E Peasgood
- E Perkins
- E Radford
- E Raith
- E Raith
- E Salciute
- E Smith
- E Smithson
- E Stoddard
- E Stones
- E Thomas
- E Tilney
- E Timlick
- E Treus Gude
- E Virgilio
- E Watson
- E Wilby
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- Egle Saviciute
- Elena Bargagli
- Elena Desanctis
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- Elisabetta Schiaroli
- Ellie Mcmaster
- Emma C Thomson
- Emmanuelle Marques
- Enrico Martinelli
- Esther Duncan
- Esther Merlini
- Ewen M Harrison
- F Anderson
- F Auld
- F Bibi
- F Davies
- F Farquhar
- F Fisher
- F Hurford
- F Kibutu
- F McNeela
- F Moore
- F Nasir
- F Trim
- F Wakinshaw
- F Williams
- Fabio Lena
- Fawkes Angie
- Federico Anedda
- Federico Franchi
- Ferdinando Giannattasio
- Filip Taneski
- Filippo Aucella
- Filippo Biscarini
- Floriana Valentino
- Fourman Max Head
- Francesca Andretta
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- Francesco Castelli
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- Furniss James
- G Andrew
- G Arbane
- G Bell
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- G Croston
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- G Mills
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- G Sera Howe
- G Sloane
- G Subramanian
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- G Turner
- G Watson
- G Wray
- Gabriella Coiro
- Gabriella Doddato
- Gail Carson
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- Gary Leeming
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- Graham S Cooke
- Griffiths Fiona
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- H Tench
- H Tiveran
- H Turner
- H Whittle
- H Willis
- H Wood
- Haley Chris
- Hanning Mal
- Harrison David
- Hayley Hardwick
- Hayward Caroline
- Helen Szoor-McElhinney
- Hinds Charles
- Ho Antonia
- Horby Peter
- I Ali Mohamed Ali
- I Balagosa
- I Birkinshaw
- I Burn
- I Chadbourn
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- I Edmond
- I Frost
- I Hass
- I Hussain
- I Lancoma-Malcolm
- I Leadbitter
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- Ilaria Meloni
- Immacolata Andolfo
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- J Allan
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- J Cebrian Suarez
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- J Cole
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- J Cooper
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- J Finn
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- Maaike Swets
- Mahdad Noursadeghi
- Manu Shankar-Hari
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- Margherita Baldassarri
- Mari E K Niemi
- Mari Ward
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- Mario Capasso
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- Massimiliano Fabbiani
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- Summers Charlotte
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- Susanna Guerrini
- T Anderson
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- Tony Wackett
- Trevor Paterson
- Tullio Trotta
- Turtle Lance
- U Poultney
- V Amin
- V Anumakonda
- V Bastion
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- V Waugh
- Valentina Anemoli
- Vanessa Sancho-Shimizu
- Victoria Shaw
- Vitart Veronique
- W Harrison
- W Khaliq
- W Khaliq
- W McCormick
- W Woodyatt
- Walker Susan
- Walsh Timothy
- Wang Bo
- Wei Shen Lim
- Wendy S Barclay
- William A Paxton
- William Greenhalf
- Wilson James F
- Wrobel Nicola
- Wu Yang
- X Qiu
- Y Baird
- Y Choudhury
- Y Hussain
- Y Jackson
- Y Thirlwall
- Yang Jian
- Yang Zhijian
- Z Alldis
- Z Belagodu
- Z Bradshaw
- Z Coton
- Z Daly
- Z Farzad
- Z Fernandez
- Z Garland
- Z Maqsood
- Z Omar
- Z Prime
- Z Scott
- Zechner Marie
- Zhai Ranran
- Zheng Chenqing
- Publication venue
- Nature
- Publication date
- 01/01/2020
- Field of study
Get PDFHost-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice
Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity
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- Abaleke E.
- Abdelrazik M.
- Abedalthagafi M.
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
No full textThe combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management
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GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19
- Author
- Abdelrazik M
- Abedalthagafi M
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- Barrett F
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- Candalija AC
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- Cardwell A
- Carioca AAF
- Carmody M
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- Carpintero MS
- Carracedo A
- Carracedo A
- Carratto TMT
- Carrera LG
- Carrillo-Avila JA
- Carson G
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- Carter J
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- Castaño CF
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- Castelao JE
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- Choudhury Y
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- Chávez MEQ
- Cid-Lopez MA
- Cienfuegos-Jimenez O
- Cinquina Z
- Clamp S
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- Cordero-Lorenzana ML
- Corella D
- Corin C
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- Corrales A
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- Corton M
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- Coton Z
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- García-García I
- García-Ibarbia C
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- García-Soidán A
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- Álvarez BG
- Álvarez-Benítez Y
- Álvarez-Navia F
- Íñiguez M
- Publication venue
- Springer Nature
- Publication date
- 17/05/2023
- Field of study
Get PDFData availability: Downloadable summary data are available through the GenOMICC data site (https://genomicc.org/data). Summary statistics are available, but without the 23andMe summary statistics, except for the 10,000 most significant hits, for which full summary statistics are available. The full GWAS summary statistics for the 23andMe discovery dataset will be made available through 23andMe to qualified researchers under an agreement with 23andMe that protects the privacy of the 23andMe participants. For further information and to apply for access to the data, see the 23andMe website (https://research.23andMe.com/dataset-access/). All individual-level genotype and whole-genome sequencing data (for both academic and commercial uses) can be accessed through the UKRI/HDR UK Outbreak Data Analysis Platform (https://odap.ac.uk). A restricted dataset for a subset of GenOMICC participants is also available through the Genomics England data service. Monocyte RNA-seq data are available under the title ‘Monocyte gene expression data’ within the Oxford University Research Archives (https://doi.org/10.5287/ora-ko7q2nq66). Sequencing data will be made freely available to organizations and researchers to conduct research in accordance with the UK Policy Framework for Health and Social Care Research through a data access agreement. Sequencing data have been deposited at the European Genome–Phenome Archive (EGA), which is hosted by the EBI and the CRG, under accession number EGAS00001007111.Extended data figures and tables are available online at https://www.nature.com/articles/s41586-023-06034-3#Sec21 .Supplementary information is available online at https://www.nature.com/articles/s41586-023-06034-3#Sec22 .Code availability:
Code to calculate the imputation of P values on the basis of SNPs in linkage disequilibrium is available at GitHub (https://github.com/baillielab/GenOMICC_GWAS).Acknowledgements: We thank the members of the Banco Nacional de ADN and the GRA@CE cohort group; and the research participants and employees of 23andMe for making this work possible. A full list of contributors who have provided data that were collated in the HGI project, including previous iterations, is available online (https://www.covid19hg.org/acknowledgements).Change history: 11 July 2023: A Correction to this paper has been published at: https://doi.org/10.1038/s41586-023-06383-z. -- In the version of this article initially published, the name of Ana Margarita Baldión-Elorza, of the SCOURGE Consortium, appeared incorrectly (as Ana María Baldion) and has now been amended in the HTML and PDF versions of the article.Copyright © The Author(s) 2023, Critical illness in COVID-19 is an extreme and clinically homogeneous disease phenotype that we have previously shown1 to be highly efficient for discovery of genetic associations2. Despite the advanced stage of illness at presentation, we have shown that host genetics in patients who are critically ill with COVID-19 can identify immunomodulatory therapies with strong beneficial effects in this group3. Here we analyse 24,202 cases of COVID-19 with critical illness comprising a combination of microarray genotype and whole-genome sequencing data from cases of critical illness in the international GenOMICC (11,440 cases) study, combined with other studies recruiting hospitalized patients with a strong focus on severe and critical disease: ISARIC4C (676 cases) and the SCOURGE consortium (5,934 cases). To put these results in the context of existing work, we conduct a meta-analysis of the new GenOMICC genome-wide association study (GWAS) results with previously published data. We find 49 genome-wide significant associations, of which 16 have not been reported previously. To investigate the therapeutic implications of these findings, we infer the structural consequences of protein-coding variants, and combine our GWAS results with gene expression data using a monocyte transcriptome-wide association study (TWAS) model, as well as gene and protein expression using Mendelian randomization. We identify potentially druggable targets in multiple systems, including inflammatory signalling (JAK1), monocyte–macrophage activation and endothelial permeability (PDE4A), immunometabolism (SLC2A5 and AK5), and host factors required for viral entry and replication (TMPRSS2 and RAB2A).GenOMICC was funded by Sepsis Research (the Fiona Elizabeth Agnew Trust), the Intensive Care Society, a Wellcome Trust Senior Research Fellowship (to J.K.B., 223164/Z/21/Z), the Department of Health and Social Care (DHSC), Illumina, LifeArc, the Medical Research Council, UKRI, a BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070 and BBS/E/D/30002275) and UKRI grants MC_PC_20004, MC_PC_19025, MC_PC_1905 and MRNO2995X/1. A.D.B. acknowledges funding from the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z), the Edinburgh Clinical Academic Track (ECAT) programme. This research is supported in part by the Data and Connectivity National Core Study, led by Health Data Research UK in partnership with the Office for National Statistics and funded by UK Research and Innovation (grant MC_PC_20029). Laboratory work was funded by a Wellcome Intermediate Clinical Fellowship to B.F. (201488/Z/16/Z). We acknowledge the staff at NHS Digital, Public Health England and the Intensive Care National Audit and Research Centre who provided clinical data on the participants; and the National Institute for Healthcare Research Clinical Research Network (NIHR CRN) and the Chief Scientist’s Office (Scotland), who facilitate recruitment into research studies in NHS hospitals, and to the global ISARIC and InFACT consortia. GenOMICC genotype controls were obtained using UK Biobank Resource under project 788 funded by Roslin Institute Strategic Programme Grants from the BBSRC (BBS/E/D/10002070 and BBS/E/D/30002275) and Health Data Research UK (HDR-9004 and HDR-9003). UK Biobank data were used in the GSMR analyses presented here under project 66982. The UK Biobank was established by the Wellcome Trust medical charity, Medical Research Council, Department of Health, Scottish Government and the Northwest Regional Development Agency. It has also had funding from the Welsh Assembly Government, British Heart Foundation and Diabetes UK. The work of L.K. was supported by an RCUK Innovation Fellowship from the National Productivity Investment Fund (MR/R026408/1). J.Y. is supported by the Westlake Education Foundation. SCOURGE is funded by the Instituto de Salud Carlos III (COV20_00622 to A.C., PI20/00876 to C.F.), European Union (ERDF) ‘A way of making Europe’, Fundación Amancio Ortega, Banco de Santander (to A.C.), Cabildo Insular de Tenerife (CGIEU0000219140 ‘Apuestas científicas del ITER para colaborar en la lucha contra la COVID-19’ to C.F.) and Fundación Canaria Instituto de Investigación Sanitaria de Canarias (PIFIISC20/57 to C.F.). We also acknowledge the contribution of the Centro National de Genotipado (CEGEN) and Centro de Supercomputación de Galicia (CESGA) for funding this project by providing supercomputing infrastructures. A.D.L. is a recipient of fellowships from the National Council for Scientific and Technological Development (CNPq)-Brazil (309173/2019-1 and 201527/2020-0)
Mapping the human genetic architecture of COVID-19
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- Publication venue
- Publication date
- 01/01/2021
- Field of study
Get PDFThe genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease
A second update on mapping the human genetic architecture of COVID-19
- Author
- Abd Elghafar MS
- Abdel-Aziz M
- Abdelrazik M
- Abdullah MS
- Abe R
- Abe S
- Abel L
- Abel L
- Abernathy C
- Abraham R
- Abraheem A
- Abu Alragheb BO
- Abulail JA
- Acklery A
- Acosta-Herrera M
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- Afrasiabi Z
- Afset JE
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- Aghemo A
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- Wignall A
- Wilby L
- Wilcox L
- Wild H
- Wild L
- Wilding L
- Wiles M
- Wilfling S
- Wiliams A
- Wilkin F
- Wilkins J
- Wilkinson A
- Wilkinson B
- Williams A
- Williams A
- Williams C
- Williams D
- Williams E
- Williams E
- Williams G
- Williams H
- Williams J
- Williams K
- Williams M
- Williams P
- Williams S
- Williams T
- Willis C
- Willis H
- Wills M
- Willson J
- Wilson A
- Wilson DJ
- Wilson J
- Wilson JF
- Wiltfang J
- Winchester J
- Winkler TW
- Winmill H
- Winnard S
- Winter C
- Winter K
- Winter-Goodwin B
- Wittig M
- Witzke O
- Wolf-Roberts R
- Wolford BN
- Wong I
- Wong J
- Wong J
- Wood D
- Wood H
- Wood S
- Wood S
- Wood T
- Woodford C
- Woodruff M
- Woods L
- Woodward E
- Woodward J
- Woolcock M
- Woolley AE
- Worner R
- Worsley L
- Wray G
- Wren L
- Wreybrown C
- Wright C
- Wright DJ
- Wright J
- Wright M
- Wright S
- Wrobel N
- Wu Y
- Wulandari R
- Wylie K
- Wyllie DH
- Wynter I
- Xavier K
- Xue X
- Yagi K
- Yamada M
- Yamada Y
- Yamagata K
- Yamasaki M
- Yang J
- Yaspan B
- Yassen AM
- Yasui Y
- Yates B
- Yatomi M
- Ye C
- Yermakovich D
- Yeung RSM
- Yi X
- Yonekawa A
- Yoo S
- Yoon K
- Yoshida K
- Yoshida S
- Yoshida S
- Yoshida T
- Yoshihara T
- Yoshiya K
- Yoshiyama T
- Young M
- Yue F
- Yun N
- Yáñez CE
- Yáñez Z
- Zainulabid UA
- Zainy T
- Zak A
- Zaki A
- Zamikula J
- Zamudio IPM
- Zanella A
- Zapata-Contreras D
- Zapatamartinez M
- Zarate R
- Zarei N
- Zavaleta DAF
- Zawadzki P
- Zawati MH
- Zborowski AC
- Zeberg H
- Zechner M
- Zhang Q
- Zhao X
- Zheng C
- Zheng T
- Zhlawi HJ
- Zhlawi MWJ
- Zholdybayeva E
- Zhou W
- Zhu W
- Zitter L
- Zoller H
- Zongo O
- Zorloni C
- Zuñiga-Pacheco P
- Zárate RN
- Zúñiga-Ramos J
- Álvarez BG
- Ávila-Arcos MA
- Ávila-Arcos MC
- Özer O
- Überla K
- Þorsteinsdóttir U
- Publication venue
- Nature Research
- Publication date
- 21/06/2023
- Field of study
Get PDFEffects of rare kidney diseases on kidney failure: a longitudinal analysis of the UK National Registry of Rare Kidney Diseases (RaDaR) cohort
- Author
- A Neil Turner (18271030)
- Abdulfattah Alejmi (18270697)
- Abhijit Dixit (7813040)
- Adam P Levine (18270916)
- Adam Rumjon (18270994)
- Adrian Woolf (18271069)
- Ajay Dhaygude (10682946)
- Alan Salama (790050)
- Albert CM Ong (11908934)
- Albert Power (12968087)
- Alexandra Howson (5005121)
- Alexandre Persu (396983)
- Alison Barratt (18270715)
- Alison Jenkins (13270838)
- Alison Turnbull (4920079)
- Alister Humphries (18270874)
- Alycon Walker (18271039)
- Alys Capell (18270751)
- Amanda Ayers (18270709)
- Amanda Davies (4495156)
- Amanda Jones (238766)
- Amrit Kaur (729306)
- Andrea Goodlife (8616183)
- Andrew Neil Turner (18270679)
- Angela Branson (18270736)
- Angela Watt (13747165)
- Angharad Williams (18271054)
- Anjali Date (18270805)
- Ann Morgan (10287162)
- Aoife Waters (110398)
- Arif Khwaja (800868)
- Asheesh Sharma (17200041)
- Ashutosh Wechalekar (8888570)
- Barry Gray (18270844)
- Brian Camilleri (18270745)
- Bridgett Masunda (18270928)
- Bruce Hendry (18270856)
- Candice Roufosse (8401275)
- Caroline A Jones (18270892)
- Carsten Bergmann (468004)
- Chadd Javier (18270991)
- Charles Pusey (790048)
- Chee Kay Cheung (7741436)
- Christine Catley (18270763)
- Christopher Clayton (4594042)
- Christopher Goldsmith (17386327)
- Christopher Mark Taylor (18270685)
- Colin Geddes (8401272)
- Colin Jones (5560598)
- Conor Byrne (3909244)
- Constantina Chrysochou (4096549)
- Coralie Bingham (5534639)
- Daniel P Gale (10571691)
- David Game (17487015)
- David Jayne (714346)
- David Kavanagh (354267)
- David Pitcher (9557765)
- David PJ Hunt (18270877)
- David Wheeler (393528)
- David Wright (116911)
- Dawn Evans (10703476)
- Deborah H Wilson (18271057)
- Detlef Bockenhauer (209475)
- Dorothea Nitsch (232367)
- Durga Kanigicherla (14675650)
- Eamonn Maher (3421634)
- Eamonn R Maher (13562335)
- Edward J Sharples (18271003)
- Edwin Wong (9541083)
- Edyta Klata (18270907)
- Eileen Conway (18270790)
- Elizabeth Colby (18270784)
- Ellie Asgari (18270706)
- Emma Williams (2558197)
- Emma Woodward (18271063)
- Eunice Doctolero (18270811)
- Eva Garcia (238479)
- Ewa Kislowska (11359341)
- Fawad Muhammad (18270946)
- Felix Kpodo (18270712)
- Fiona Braddon (16471727)
- Fiona Karet Frankl (18270667)
- Frances Flinter (3120102)
- Frank Post (462543)
- Fred Tam (76983)
- Frederick WK Tam (18270676)
- Gabor Cserep (16666593)
- Garry King (18270904)
- Gary Campbell (18270748)
- Gavin Dreyer (595326)
- Gavin I Welsh (18271048)
- Gbemisola Jenfa (18270889)
- Gopalakrishnan Venkat-Raman (18271036)
- Gowrie Balasubramaniam (16661643)
- Graham Lipkin (55504)
- Graham Lovitt (18270922)
- Grahame Wood (4847932)
- Grant King (7848650)
- Guy Pratt (1725397)
- H Terence Cook (18270793)
- Haresh Selvaskandan (7669754)
- Harish Shetty (18271006)
- Helen Cockerill (18270778)
- Holly Mabillard (16026686)
- Houda Chea (17331277)
- Hugh Cairns (11268504)
- Hugh Gallagher (456790)
- Ian SD Roberts (17950019)
- Ian Stott (3767746)
- Jake Mayfair (18270934)
- James Chess (2818003)
- James Fotheringham (520715)
- James Pattison (14028465)
- Janet Bendle (18270724)
- Jean Patrick (18270961)
- Jennifer Pinney (18270979)
- Jenny Finch (18270826)
- Jenny Pinney (18270670)
- Joanna Mckinnell (18270937)
- John A Sayer (11908949)
- Jonathan Barratt (3387179)
- Joshua Coelho (18270781)
- Joy Agbonmwandolor (18270691)
- Joyce Popoola (367948)
- Justyna Szklarzewicz (18271024)
- Jyoti Baharani (3584696)
- Kanwaljit S Sandu (18270997)
- Karen Williams (771874)
- Karine Cesar (18270766)
- Karl Hunter (18270880)
- Kate Bramham (524805)
- Kate Hillman (18270862)
- Kate Osmaston (18270958)
- Kate Wiles (14576131)
- Katerina Stroud (18271018)
- Katherine Clark (267755)
- Katherine Davidson (12338542)
- Katherine Mackintosh (12339112)
- Katie Wong (12160978)
- Katy-Jane Chick (18270772)
- Kay Tan (18271027)
- Kay Thomas (4351738)
- Kay Tyerman (8412846)
- Kelly Kearley (18270901)
- Kerry Smith (8189019)
- Kevin J Marchbank (8896391)
- Khalid Mahdi (13204656)
- Kristina Novobritskaya (18270952)
- Kufreabasi Etuk (18270823)
- Lara Smith (18271015)
- Larissa Kerecuk (5486615)
- Laura Lawless (18270910)
- Lavanya Kamesh (435224)
- Len Woodward (18271066)
- Lewis Downard (18270817)
- Lewis Downward (18270658)
- Ling Wai Maggie Lai (18270919)
- Lisa Willcocks (16663344)
- Lorraine Harper (140622)
- Louise Haskell (18270850)
- Louise Oni (18270955)
- Lucy Francis (18270829)
- Lucy Plumb (9557777)
- Lynn Diskin (18270808)
- Madita Gavrila (18270832)
- Mahzuz Karim (18270898)
- Manish Sinha (18271012)
- Marc Tischkowitz (395208)
- Margaret Carmody (18270754)
- Maria Kokocinska (12092044)
- Marilyn Ijeomah-Orji (18270886)
- Marion Carson (18270757)
- Mark Drayson (4920754)
- Mark Gilchrist (42643)
- Mark Lambie (623652)
- Martin Christian (4799046)
- Matt Gittus (17720545)
- Matt Hall (5666026)
- Matthew C Pickering (18270976)
- May Rabuya (18270985)
- Megan Bates (18270718)
- Megan Griffith (9178151)
- Melanie Chan (18270769)
- Miranda Usher (18271033)
- Moin Saleem (11137830)
- Mrityunjay Hiremath (18270865)
- Nabil Melhem (8432529)
- Nadia Sarween (18271000)
- Natalie Bayne (18270721)
- Neal Padmanabhan (283793)
- Neeraj Dhaun (3456026)
- Neil Sebire (11219)
- Neil Sheerin (6004601)
- Nicholas Annear (18270661)
- Nick Inston (18187609)
- Nicol West (18271051)
- Nicola Hewitson (18270859)
- Nihil Chitalia (539263)
- Paraskevi Goggolidou (267854)
- Patricia D Wilson (18271060)
- Patricia Gooden (18270838)
- Patricia Wilson (2697652)
- Patrick B Mark (8425311)
- Patrick Hamilton (3556673)
- Paul Lyons (18632)
- Paul Winyard (11712458)
- Pauline Swift (18271021)
- Phil Webster (18271045)
- Preetham Boddana (18270730)
- Priyanka Goodwin (18270841)
- Putnam Morgan (18270943)
- Rachel Jones (66702)
- Rachel Lennon (3393728)
- Rachel Percival (18270967)
- Rashid Almasarwah (18270700)
- Retha Steenkamp (288231)
- Rhian Clissold (5534642)
- Ria Rabara (18270982)
- Richard Hull (4470196)
- Richard J Coward (18270664)
- Richard Sandford (2097682)
- Riny Paul (18270964)
- Robert Taylor (226235)
- Roslyn Simms (18270673)
- Rukshana Shroff (689740)
- Sally Bond (18270733)
- Sally Johnson (12392509)
- Samantha Hayward (9658676)
- Samantha Hunter (18270883)
- Sanjana Gupta (8551296)
- Sarah Benyon (18270727)
- Sarah Crosbie (18270802)
- Shabbir Moochhala (404267)
- Shalabh Srivastava (6889016)
- Sharanjit Budwal (18270742)
- Sharirose Abat (18270688)
- Sharon Huish (18270871)
- Sharon Parkes (2906510)
- Shazia Adalat (209470)
- Sherry Masoud (18270925)
- Shivaram Hegde (18270853)
- Shona Murray (18270949)
- Sian Griffin (8401269)
- Simon Meyrick (18270940)
- Smeeta Sinha (4847929)
- Steph Gumus (18270847)
- Stephen B Walsh (18270682)
- Stephen Brearey (18270739)
- Stephen J Perkins (18270970)
- Stephen McAdoo (11272254)
- Sue Hewins (5504585)
- Sunil Bhandari (3185595)
- Susie Gear (18270835)
- Suzannah Dorey (18270814)
- Tarun Bansal (13154308)
- Tassos Grammatikopoulos (11505256)
- Tess Harris (480258)
- Theresa Cooper (18270796)
- Thomas Ledson (18270913)
- Tina Chrysochou (18270775)
- Tina Dutt (18270820)
- Tina Raju (18270988)
- Tracy Cathcart (18270760)
- Vicky Brocklebank (9983960)
- Viv Colclough (18270787)
- Wendy Cook (9940355)
- William G Petchey (18270973)
- Yincent Tse (14803469)
- Zainab Mavani (18270931)
- Zay Htet (18270868)
- Zoe Plummer (8411850)
- Zubaidah Ahmad (18270694)
- Publication venue
- Publication date
- 28/03/2024
- Field of study
No full textIndividuals with rare kidney diseases account for 5-10% of people with chronic kidney disease, but constitute more than 25% of patients receiving kidney replacement therapy. The National Registry of Rare Kidney Diseases (RaDaR) gathers longitudinal data from patients with these conditions, which we used to study disease progression and outcomes of death and kidney failure.People aged 0-96 years living with 28 types of rare kidney diseases were recruited from 108 UK renal care facilities. The primary outcomes were cumulative incidence of mortality and kidney failure in individuals with rare kidney diseases, which were calculated and compared with that of unselected patients with chronic kidney disease. Cumulative incidence and Kaplan-Meier survival estimates were calculated for the following outcomes: median age at kidney failure; median age at death; time from start of dialysis to death; and time from diagnosis to estimated glomerular filtration rate (eGFR) thresholds, allowing calculation of time from last eGFR of 75 mL/min per 1·73 m2 or more to first eGFR of less than 30 mL/min per 1·73 m2 (the therapeutic trial window).Between Jan 18, 2010, and July 25, 2022, 27 285 participants were recruited to RaDaR. Median follow-up time from diagnosis was 9·6 years (IQR 5·9-16·7). RaDaR participants had significantly higher 5-year cumulative incidence of kidney failure than 2·81 million UK patients with all-cause chronic kidney disease (28% vs 1%; p
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