Chronic kidney disease (CKD) represents a global public health problem and is associated with substantial morbidity, reduced life expectancy and high healthcare resource utilization. Around 800 million people or as many as 15% of the population worldwide are affected by CKD, and the proportion of CKD patients in the total population increases significantly with age. Dickkopf-3 (DKK3) belongs to a family of glycoproteins (DKK1–4) that modulate the Wnt signalling pathway. They are encoded by DKK genes, which comprise an evolutionary conserved small gene family of four members (Dkk1–4) and the Dkk3-related gene, Dkkl1 (soggy). DKK proteins play an important role in vertebrate development, where they locally inhibit Wnt-regulated processes such as limb development and eye formation. Besides, several studies have shown significant effects of DKK proteins on Wnt/β-catenin signalling in experimental CKD models. In a study using high-throughput single-nucleotide polymorphism (SNP) genotyping of 173 candidate genes in 794 white patients from 227 families with autosomal dominant polycystic kidney disease (ADPKD), a genetic variation within the DKK3 locus was associated with more severe disease progression. It has been shown that urinary concentrations of DKK3 significantly increase in mice fed with an adenine-rich diet, whereas DKK3 was not detectable in the urine of healthy mice. To determine the DKK3-producing renal cell type, reporter mice have been generated expressing luciferase and mCherry under the regulatory sequences of the Dkk3 gene