Association between cause of kidney failure and fracture incidence in a national US dialysis population cohort study.

dialysis end-stage kidney disease fracture

Journal

Clinical kidney journal
ISSN: 2048-8505
Titre abrégé: Clin Kidney J
Pays: England
ID NLM: 101579321

Informations de publication

Date de publication:
Dec 2022
Historique:
received: 23 03 2022
entrez: 16 11 2022
pubmed: 17 11 2022
medline: 17 11 2022
Statut: epublish

Résumé

Whether fracture rates, overall and by fracture site, vary by cause of kidney failure in patients receiving dialysis is unknown. Using the US Renal Data System, we compared fracture rates across seven causes of kidney failure in patients who started dialysis between 1997 and 2014. We computed unadjusted and multivariable adjusted proportional sub-distribution hazard models, with fracture events (overall, and by site) as the outcome and immunoglobulin A nephropathy as the reference group. Kidney transplantation and death were competing events. Among 491 496 individuals, with a median follow-up of 2.0 (25%, 75% range 0.9-3.9) years, 62 954 (12.8%) experienced at least one fracture. Patients with diabetic nephropathy, vasculitis or autosomal polycystic kidney disease (ADPKD) had the highest (50, 46 and 40 per 1000 person-years, respectively), and patient with lupus nephritis had the lowest (20 per 1000 person-years) fracture rates. After multivariable adjustment, diabetic nephropathy [hazard ratio (HR) 1.43, 95% confidence interval 1.33-1.53], ADPKD (HR 1.37, 1.26-1.48), vasculitis (HR 1.22, 1.09-1.34), membranous nephropathy (HR 1.16, 1.02-1.30) and focal segmental glomerulosclerosis (FSGS) (HR 1.13, 1.02-1.24) were associated with a significantly higher, and lupus nephritis with a significantly lower (HR 0.85, 0.71-0.98) fracture hazard. The hazards for upper extremity and lower leg fractures were significantly higher in diabetic nephropathy, ADPKD, FSGS and membranous nephropathy, while the hazard for vertebral fracture was significantly higher in vasculitis. Our findings were limited by the lack of data on medication use and whether fractures were traumatic or non-traumatic, among other factors. Fracture risk, overall and by fracture site, varies by cause of end-stage kidney disease. Future work to determine underlying pathogenic mechanisms contributing to differential risks might inform more tailored treatment strategies. Our study was limited by lack of data regarding numerous potential confounders or mediators including medications and measures or bone biomarkers.

Sections du résumé

Background UNASSIGNED
Whether fracture rates, overall and by fracture site, vary by cause of kidney failure in patients receiving dialysis is unknown.
Methods UNASSIGNED
Using the US Renal Data System, we compared fracture rates across seven causes of kidney failure in patients who started dialysis between 1997 and 2014. We computed unadjusted and multivariable adjusted proportional sub-distribution hazard models, with fracture events (overall, and by site) as the outcome and immunoglobulin A nephropathy as the reference group. Kidney transplantation and death were competing events.
Results UNASSIGNED
Among 491 496 individuals, with a median follow-up of 2.0 (25%, 75% range 0.9-3.9) years, 62 954 (12.8%) experienced at least one fracture. Patients with diabetic nephropathy, vasculitis or autosomal polycystic kidney disease (ADPKD) had the highest (50, 46 and 40 per 1000 person-years, respectively), and patient with lupus nephritis had the lowest (20 per 1000 person-years) fracture rates. After multivariable adjustment, diabetic nephropathy [hazard ratio (HR) 1.43, 95% confidence interval 1.33-1.53], ADPKD (HR 1.37, 1.26-1.48), vasculitis (HR 1.22, 1.09-1.34), membranous nephropathy (HR 1.16, 1.02-1.30) and focal segmental glomerulosclerosis (FSGS) (HR 1.13, 1.02-1.24) were associated with a significantly higher, and lupus nephritis with a significantly lower (HR 0.85, 0.71-0.98) fracture hazard. The hazards for upper extremity and lower leg fractures were significantly higher in diabetic nephropathy, ADPKD, FSGS and membranous nephropathy, while the hazard for vertebral fracture was significantly higher in vasculitis. Our findings were limited by the lack of data on medication use and whether fractures were traumatic or non-traumatic, among other factors.
Conclusions UNASSIGNED
Fracture risk, overall and by fracture site, varies by cause of end-stage kidney disease. Future work to determine underlying pathogenic mechanisms contributing to differential risks might inform more tailored treatment strategies. Our study was limited by lack of data regarding numerous potential confounders or mediators including medications and measures or bone biomarkers.

Identifiants

pubmed: 36381373
doi: 10.1093/ckj/sfac193
pii: sfac193
pmc: PMC9664571
doi:

Types de publication

Journal Article

Langues

eng

Pagination

2245-2257

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.

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Auteurs

Susan Ziolkowski (S)

Department of Medicine, Division of Nephrology, Stanford University School of Medicine, Stanford, CA, USA.

Sai Liu (S)

Department of Medicine, Division of Nephrology, Stanford University School of Medicine, Stanford, CA, USA.

Maria E Montez-Rath (ME)

Department of Medicine, Division of Nephrology, Stanford University School of Medicine, Stanford, CA, USA.

Michelle Denburg (M)

Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Division of Nephrology, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Wolfgang C Winkelmayer (WC)

Department of Medicine, Selzman Institute for Kidney Health, Section of Nephrology, Baylor College of Medicine, Houston, TX, USA.

Glenn M Chertow (GM)

Department of Medicine, Division of Nephrology, Stanford University School of Medicine, Stanford, CA, USA.

Michelle M O'Shaughnessy (MM)

Department of Medicine, Division of Renal Medicine, Cork University Hospital, Cork, Ireland.

Classifications MeSH