Key result
NTRK2 rs1036915 minor G allele linked to ~6% higher eGFR vs major A allele.
Why the study?
Do genetic variants in NTRK2 contribute to variation in eGFR in Mexican American subjects?
Observational (n=848)
No
Do genetic variants in NTRK2 contribute to variation in eGFR in Mexican American subjects?
Genetic variants in NTRK2, specifically rs1036915 and rs1187274, are associated with variations in eGFR in Mexican Americans, suggesting a novel genetic regulatory mechanism for kidney function.
Should not change clinical practice; hypothesis-generating for NTRK2 variants in eGFR among Mexican Americans.
BACKGROUND: The estimated glomerular filtration rate (eGFR) is a well-known measure of kidney function and is commonly used for the diagnosis and management of patients with chronic kidney disease. The inter-individual variation in eGFR has significant genetic component. However, the identification of underlying genetic susceptibility variants has been challenging. In an attempt to identify and characterize susceptibility genetic variant(s) we previously identified the strongest evidence for linkage of eGFR occurring on chromosome 9q21 in the Mexican American participants of San Antonio Family Heart Study (SAFHS). The objective of the present study was to examine whether the common genetic variants in Neurotrophic Tyrosine Receptor Kinase 2 (NTRK2), a positional candidate gene on 9q21, contribute to variation in eGFR. RESULTS: Twelve tagging single nucleotide polymorphisms (SNPs) across the NTRK2 gene region were selected (r2 ≥ 0.80, minor allele frequency of ≥ 0.05) from the Hapmap database. SNPs were genotyped by TaqMan assay in the 848 Mexican American subjects participated in the SAFHS. Association analysis between the genotypes and eGFR (estimated by the Modification of Diet in Renal Disease equation) were performed by measured genotype approach as implemented in the program SOLAR. Of the 12 common genetic variants examined, the rs1036915 (located in 3'UTR) and rs1187274 (located in intron-14), present in perfect linkage disequilibrium, exhibited an association (P = 0.017) with eGFR after accounting for the effects of age, sex, diabetes, diabetes duration, systolic blood pressure and blood pressure medication. The carriers of minor allele of rs1036915 (G; 38%) had increased eGFR (104 ± 25 ml/min/1.73 m(2)) in comparison to the carriers of major allele A (98 ± 25 ml/min/1.73 m(2)). CONCLUSION: Together, our results suggest for the first time that the genetic variants in NTRK2 may regulate eGFR.
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Thameem et al. (2015) conducted an observational in Variation in estimated Glomerular Filtration Rate (eGFR) (n=848). NTRK2 genetic variant rs1036915 (minor allele G) vs. Major allele A carriers was evaluated on Estimated Glomerular Filtration Rate (eGFR) (p=0.017). Carriers of the minor G allele of the NTRK2 genetic variant rs1036915 had a significantly higher estimated glomerular filtration rate (104 ml/min/1.73 m2) compared to major A allele carriers (98 ml/min/1.73 m2).
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