However, our population was similar to larger studies in the UK primary care setting, suggesting that this was broadly representative of people with CKD in this context.[34] Further limitations were that we had no specific measures of tubular dysfunction or Bence Jones protein to relate to NAP, and that prevalence of NAP may have been increased by the high proportion of people taking RAAS inhibitors. This evidence concerns the gene CTNNBL1 and chronic kidney disease.