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For GLUT9, marker rs10516195 located in intron 3 near to and in LD with our SNPs (7.6 kb upstream from rs6449213) showed high significance with gout (p = 3.7*10−8).
The log-rank test showed no survival difference between ESRD patients with gout and those without gout (P = 0.21).
Four loci reached genome-wide significant association when evaluating association with serum uric acid levels: the same ALDH16A1 SNP found with gout (P = 4.5 × 10−21), a novel association with the chromosome 1 centromere (P = 4.5 × 10−16), as well as previously reported signals at SLE2A9 (P = 1.0 × 10−80) and ABCG2 (P = 2.3 × 10−20).
Compared with their non-albuminuric counterparts, participants with albuminuria had higher prevalence of existing hypertension (p < 0.0001), diabetes (p < 0.003), gout (p = 0.0002) and longstanding use of herbal medicine (p = 0.0001), higher SBP (p = 0.019), and higher prevalence of any hypertension (p = 0.0001) and diabetes (p = 0.008).
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The proximate marker rs734553 also showed nominal deviation from HWE in gout cases (p = 0.05), whereas the other markers exhibited p-values>0.18.
Among patients with moderate renal impairment (figure 2C), however, febuxostat 40 mg showed lower efficacy in diabetic than in non-diabetic gout patients (p < 0.05), while febuxostat 80 mg showed higher efficacy (p < 0.05).
The Q141K variant hastened the gout onset (P = 0.0027), but significantly associated with later Parkinson's disease onset (P = 0.025).
The Q141K mutation of ABCG2 hastened the onset of gout significantly (P = 0.0027; see Fig. 1A); on the contrary, this variant significantly delayed the PD onset (P = 0.025; see Fig. 1B).
However, as previously reported [3], rs6855911 in SLC2A9 gene showed deviation from HWE in gout cases (p = 0.01).
In addition, febuxostat 40 mg was superior to allopurinol in this elderly gout population (p = 0.029).
The prevalence of moderate to severe LV diastolic dysfunction was higher in patients with gout (23%%, p = 0.02).
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