SEC61A1 and autosomal dominant medullary cystic kidney disease with or without hyperuricemia: Taken together, our data provide novel insights into the pathogenic mechanisms in the kidney that may very well contribute to the tissue-specific symptomatic of ADTKD–SEC61A1 patients, which seem to originate in a substrate-specific malfunction of protein transport that further spawn a dysregulation of Ca2+ homeostasis.