Abstract
Chronic kidney disease (CKD) encompasses a group of diverse diseases that are associated with accumulating kidney damage and a decline in glomerular filtration rate (GFR). These conditions can be of an acquired or genetic nature and, in many cases, interactions between genetics and the environment also play a role in disease manifestation and severity. In this review, we focus on genetically inherited chronic kidney diseases and dissect the links between canonical and non-canonical Wnt signalling, and this umbrella of conditions that result in kidney damage. Most of the current evidence on the role of Wnt signalling in CKD is gathered from studies in polycystic kidney disease (PKD) and nephronophthisis (NPHP) and reveals the involvement of β-catenin. Nevertheless, recent findings have also linked planar cell polarity (PCP) signalling to CKD, with further studies being required to fully understand the links and molecular mechanisms.
Highlights
Chronic kidney disease (CKD) encompasses a group of diverse diseases that are associated with accumulating kidney damage and a decline in glomerular filtration rate (GFR)
Chronic kidney disease (CKD) is a term that denotes the presence of kidney damage, presenting with abnormalities or a decline in kidney function
In order to distinguish between chronic and acute kidney disease as well as assess the rate of decline in kidney function, kidney damage is measured over the course of three months via the glomerular filtration rate (GFR) and it can be split across five stages, depending on kidney function efficiency [1]
Summary
Inherited kidney diseases are an umbrella of various conditions that result from mutations in genes that regulate kidney function (Table 1). These can be of dominant or recessive inheritance and can manifest in individuals from a relatively young age. Genes 2020, 11, 496 conditions is autosomal dominant polycystic kidney disease (ADPKD). The disease itself is one of the most common causes of end-stage renal disease (ESRD), with statistics showing that ADPKD accounts for around 10% of all ESRD cases [2]. Evidence has suggested that PKD1 mutations account for the majority of ADPKD cases, patients with mutations in PKD2 are believed to have a better prognosis [4,5]. No pharmacological cure currently exists for ADPKD a recent drug, Tolvaptan, has been shown to slow down the progression of cysts [2]
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