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Introduction {#sec1} ============ At normal levels, glucose is not detectable in urine. Glycosuria, the presence of glucose in urine above normal levels, may be caused by either an increase in blood glucose such that the renal tubules are overwhelmed and complete reabsorption of presented glucose is not possible, a lowering of the renal threshold, or inhibition of renal tubule reabsorption ([@ref1]). Although prevalence estimates for glycosuria vary, it seems likely that the condition effects around 50% of women at some stage of their pregnancy ([@ref2]) and is thought to occur primarily as a result of pregnancy-related increases in renal blood flow resulting in a lower threshold for excreting glucose in urine. It also reflects pregnancy-related increases in circulating blood glucose. While, outside of pregnancy, glycosuria is considered a diabetes indicator, glycosuria in pregnancy is not specific or sensitive for gestational diabetes risk and is not recommended as a screening tool for it ([@ref2],[@ref3]). There is evidence that glycosuria is associated with adverse cardio-metabolic outcomes, including non-alcoholic fatty liver disease, in offspring ([@ref4]) and with later life outcomes, such as cardiovascular disease death, in mothers ([@ref7]). Therefore, the presence of glycosuria may potentially indicate future adverse outcomes in pregnancy and the life course. Both glucose regulation and renal function are heritable, with reliable evidence for several genetic variants being associated with a range of relevant traits, including fasting glucose ([@ref8],[@ref9]), insulin sensitivity ([@ref8],[@ref9]), type 2 diabetes ([@ref10]) and glomerular filtration rate in general non-pregnant populations ([@ref11]). While these studies have yielded valuable new insights into glucose metabolism, still outstanding is an investigation of the genetic contribution to glycosuria during pregnancy. To investigate whether common genetic variants are associated with glucose in urine during pregnancy and to explore potential links to other glycaemic and renal-function-related traits, we set out to conduct a genome-wide association study (GWAS) of glycosuria during pregnancy in the Avon Longitudinal Study of Parents and Children (ALSPAC) and looked for confirmatory evidence in the Northern Finland Birth Cohort 1986 (NFBC1986). We further investigated the genetic overlap between identified loci and multiple diabetes-related traits. Results {#sec2} ======= A genome-wide association study (GWAS) of self-reported glycosuria during pregnancy performed in ALSPAC represents our primary analysis. Additional work exploring associations further was conducted in the same cohort. Due to lack of available data, a replication GWAS was not possible. We instead sought supporting evidence from a secondary GWAS analysis performed in NFBC1986 and combined GWAS results from ALSPAC and NFBC1986 to identify persistent associations. An overview of the study and its components is presented in [Figure 1](#f1){ref-type="fig"} and Supplementary Material, [Figure S1](#sup1){ref-type="supplementary-material"}. ![Analysis overview. The flowchart provides an overview of GWAS follow-up analysis.](ddaa054f1){#f1} Primary Analysis {#sec3} ================ ALSPAC GWAS {#sec4} ----------- Assuming an additive genetic model, the estimated variance explained by genotype across all variants in ALSPAC was estimated to be 1.6% (standard error (SE) = 0.08), corresponding to an estimated narrow-sense heritability of 10% (SE = 0.05, [@ref12]). There was evidence for association at genome-wide significance (*P*-value = 5 × 10^−8^)