Abstract
Chronic kidney disease (CKD) is one of the fastest growing global causes of death, estimated to rank among the top five by 2040 (Foreman et al, 2018). This illustrates current pitfalls in diagnosis and management of CKD. Advanced CKD requires renal function replacement by dialysis or transplantation. However, earlier CKD stages, even when renal function is still normal, are already associated with an increased risk of premature death (Perez‐Gomez et al, 2019). Thus, novel approaches to diagnose and treat CKD are needed. The histopathological hallmark of CKD is kidney fibrosis, which is closely associated with local inflammation and loss of kidney parenchymal cells. Thus, kidney fibrosis is an attractive process to develop tests allowing an earlier diagnosis of CKD and represents a potential therapeutic target to slow CKD progression or promote regression.
Highlights
Chronic kidney disease (CKD) is one of the fastest growing global causes of death, estimated to rank among the top five by 2040 (Foreman et al, 2018)
CKD risk categories are well defined and internationally accepted, they are based on estimated glomerular filtration rate (GFR) and assessment of albuminuria
From the therapeutic point of view, there is an ongoing discussion on the active contribution of fibrosis to CKD progression, and on whether targeting fibrosis may effectively slow or even reverse CKD; or on the contrary, if fibrosis represents a common end-stage of any CKD, its targeting would not alter the natural history of CKD
Summary
Chronic kidney disease (CKD) is one of the fastest growing global causes of death, estimated to rank among the top five by 2040 (Foreman et al, 2018). From the diagnostic point of view, tools for accurately staging CKD and for differentiating ongoing active kidney injury potentially responding to current therapies from therapy-resistant residual fibrosis are suboptimal. In the present issue of EMBO Molecular Medicine, Buhl et al (2020) conclusively demonstrate that deregulated hyperactivity of the platelet-derived growth factor receptor-b (PDGFR-b) in mouse renal mesenchymal cells leads to pathological proliferation of mesangial cells and interstitial fibroblasts.
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