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New findings implicate sodium transport in α-cell secretory dysfunction, leading to impaired counter-regulatory responses in diabetes. However, these findings also raise important questions about the tissue-specific roles of sodium transport and suggest that inhibitors of sodium transport may have potentially divergent roles in the pancreas, kidney and heart.
Discoveries in 2018 using single-cell sequencing and gene-editing technologies have revealed their transformative potential for the investigation of kidney physiology and disease. Their promise is matched by the speed of their evolution.
Numerous exciting studies that advanced our understanding of immune-mediated kidney disease were published in 2018. Whereas most of these studies analysed the role of pro-inflammatory mediators, several novel anti-inflammatory mechanisms were discovered that involve immune cells and mediators with previously unrecognized protective roles in renal disease.
With many failures, a sense of helplessness has overshadowed the field of acute kidney injury (AKI). Publications in 2018 offer new hope: better drug targets, better end points and improved understanding of conditions that cause AKI and its complications bring promise that a drug will soon be available.
In 2018, consolidating evidence for renoprotective benefits was seen with respect to sodium–glucose cotransporter 2 inhibitors and glucagon-like peptide 1 agonists, which are currently being incorporated into clinical practice. The focus now turns to novel therapeutic targets to optimize renoprotection as diabetic kidney disease grows to epidemic proportions worldwide.
In this Perspectives article, Porrini and colleagues appraise the results of studies that have compared the performance of formulae developed to estimate glomerular filtration rate (GFR) against measured GFR reference methods. They contend that the persistence of errors in GFR estimation formulae indicates an inadequacy of serum creatinine and cystatin C levels as markers of actual renal function.
A new study discovered thousands of expression quantitative trait loci (eQTLs) in the renal glomerular and tubulointerstitial compartments and integrated these data with other omics data sets to identify genes with roles in the pathogenesis of chronic kidney disease. This report reinforces the necessity of using compartment-derived eQTLs to advance kidney genomic discovery.
Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis by modulating renal phosphate absorption, vitamin D metabolism and parathyroid hormone secretion. In this Review, Marc Vervloet discusses the role of FGF23 on phosphate regulation as well as its additional effects in the cardiovascular and immune systems.
The IDEAL-ICU study reports no mortality benefit of early versus delayed initiation of renal replacement therapy (RRT) in patients with early septic shock and acute kidney injury. In the delayed initiation group, 17% of patients required emergency RRT but more than one-third spontaneously recovered renal function and did not require RRT.
This Expert Consensus Document from the International Kidney and Monoclonal Gammopathy Research Group includes an updated definition of monoclonal gammopathy of renal significance (MGRS) and recommendations for the use of kidney biopsy and other modalities for evaluating suspected MGRS
Klotho proteins are crucial elements of the receptor complex for the endocrine fibroblast growth factors FGF19, FGF21 and FGF23. In this Review, Makoto Kuro-o discusses the functions of the FGF–Klotho endocrine systems in health and disease, including their role in ageing-related disorders.