Results
Seven SNPs were used as instrumental variables to represent genetically proxied inhibition of IL-6 signalling (table 1). The F-statistic for these genetic exposure associations ranged between 73.16 and 694.37, indicating strong associations between the IL6-R variant and CRP level (table 1). Outcome summary data was accessed from the CKDGen Consortium and details about the data source, population ancestry and beta coefficient units are described in table 2.
There was no strong evidence for an association of genetically proxied inhibition of IL-6 inhibition with log eGFR (0.002, 95% confidence interval -0.004 – 0.008), BUN (0.088, 95% confidence interval -0.003 – 0.019) and CKD (odds ratio 1.018, 95% confidence interval 0.899 – 1.153). The results were consistent across all measurements of kidney function (Figure 1, appendix I). MR-Egger estimates were also consistent across all metrics of kidney function. The intercept did not show evidence of pleiotropy for the eGFR, BUN or CKD (p = 0.645, p = 0.486 and p = 0.387 respectively).