The serum uric acid concentration is not causally linked to diabetic nephropathy in type 1 diabetes

Previous studies have shown a relationship between uric acid concentration and progression of renal disease. Here we studied causality between the serum uric acid concentration and progression of diabetic nephropathy in 3895 individuals with type 1 diabetes in the FinnDiane Study. The renal status w...

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Bibliographic Details
Published in:Kidney international 2017-05, Vol.91 (5), p.1178-1185
Main Authors: Ahola, Aila J, Sandholm, Niina, Forsblom, Carol, Harjutsalo, Valma, Dahlström, Emma, Groop, Per-Henrik
Format: Article
Language:English
Subjects:
Adult
Albuminuria - urine
Biomarkers - blood
Cross-Sectional Studies
Diabetes Mellitus, Type 1 - blood
Diabetes Mellitus, Type 1 - complications
Diabetes Mellitus, Type 1 - epidemiology
Diabetic Nephropathies - blood
Diabetic Nephropathies - epidemiology
Disease Progression
Female
Follow-Up Studies
Glomerular Filtration Rate
Glucose Transport Proteins, Facilitative - genetics
Humans
Male
Mendelian Randomization Analysis
Middle Aged
Polymorphism, Single Nucleotide
Risk Factors
Uric Acid - blood
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Summary:Previous studies have shown a relationship between uric acid concentration and progression of renal disease. Here we studied causality between the serum uric acid concentration and progression of diabetic nephropathy in 3895 individuals with type 1 diabetes in the FinnDiane Study. The renal status was assessed with the urinary albumin excretion rate and estimated glomerular filtration rate (eGFR) at baseline and at the end of the follow-up. Based on previous genomewide association studies on serum uric acid concentration, 23 single nucleotide polymorphisms (SNPs) with good imputation quality were selected for the SNP score. This score was used to assess the causality between serum uric acid and renal complications using a Mendelian randomization approach. At baseline, the serum uric acid concentration was higher with worsening renal status. In multivariable Cox regression analyses, baseline serum uric acid concentration was not independently associated with progression of diabetic nephropathy over a mean follow-up of 7 years. However, over the same period, baseline serum uric acid was independently associated with the decline in eGFR. In the cross-sectional logistic regression analyses, the SNP score was associated with the serum uric acid concentration. Nevertheless, the Mendelian randomization showed no causality between uric acid and diabetic nephropathy, eGFR categories, or eGFR as a continuous variable. Thus, our results suggest that the serum uric acid concentration is not causally related to diabetic nephropathy but is a downstream marker of kidney damage.
ISSN:0085-2538
1523-1755
DOI:10.1016/j.kint.2016.11.025