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).