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Prog Transplant. 2017 Dec;27(4):386-391. doi: 10.1177/1526924817732020. Epub 2017 Sep 22.

Haptoglobin 2-2 Genotype, Patient, and Graft Survival in Renal Transplant Recipients.

Author information

1
1 Department of Nephrology, Aarhus University Hospital, Aarhus, Denmark.
2
2 Section of Nephrology, Department of Transplant Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
3
3 Department of Nephrology, Oslo University Hospital Ullevål, Oslo, Norway.
4
4 Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
5
5 Department of Nephrology, Aalborg University Hospital, Aalborg, Denmark.
6
6 Centre for Cardiovascular Research, Aalborg University Hospital, Aalborg, Denmark.
7
7 The Norwegian Renal Registry, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
8
8 Department of Pharmaceutical Biosciences, School of Pharmacy, University of Oslo, Oslo, Norway.
9
9 Metabolic and Renal Research Group, UiT The Arctic University of Norway, Tromsø, Norway.
10
10 Section of Molecular Diagnostics, Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark.
11
11 Department of Nephrology, Oslo University Hospital, Akershus University Hospital, Lørenskog, Norway.

Abstract

BACKGROUND:

Cardiovascular disease is the leading cause of death in renal transplant recipients. An association between haptoglobin genotype 2-2 and cardiovascular disease has been found in patients with diabetes mellitus and liver transplant recipients. To date, the role of haptoglobin genotype after renal transplantation has not been studied.

METHODS:

In this single-center retrospective cohort study of 1975 adult Norwegian transplant recipients, who underwent transplantation between 1999 and 2011, we estimated the risk of all-cause and cardiovascular mortality and overall and death-censored graft loss for patients with haptoglobin genotype 2-2 compared to genotype 2-1 or 1-1, after adjustment for confounders and competing risks.

RESULTS:

We found no associations between haptoglobin genotype 2-2 and cardiovascular mortality (subdistributional hazard ratio 1.08, 95% confidence interval 0.78-1.49; P = .63). We also failed to detect any association between haptoglobin 2-2 genotype and all-cause mortality, overall graft loss, and death-censored graft loss. Similar results were found in the subpopulation of transplant recipients with diabetes.

CONCLUSION:

In this large cohort of kidney transplant recipients, we could not demonstrate any association between haptoglobin 2-2 genotype and patient or graft survival after renal transplantation.

KEYWORDS:

cardiovascular disease; cardiovascular system; haptoglobin genotype; kidney transplantation recipients; mortality; oxidative stress; renal graft loss

PMID:
29187131
DOI:
10.1177/1526924817732020

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