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A mouse renal tubule expressing the mTmG reporter, which was grown ex vivo from primary cell organoids using a new 3D culture system for modelling pathogenesis in autosomal dominant polycystic kidney disease.
Cover image provided by Eryn E. Dixon of the Woodward Laboratory in the Department of Physiology and the Baltimore PKD Research and Clinical Core Center at the University of Maryland School of Medicine, Baltimore, MD, USA.
The AWARD-7 trial shows that the glucagon-like peptide 1 (GLP1) receptor agonist dulaglutide, which is not cleared by the kidney, seems to be renoprotective, ameliorates albuminuria and slows estimated glomerular filtration rate decline in patients with type 2 diabetes mellitus and chronic kidney disease, without increasing the risk of hypoglycaemia.
A recent observational study reports that after cardiac surgery, clinical outcomes differ significantly between patients with the same stage of acute kidney injury (AKI) depending on the diagnosis criteria used: urine output, serum creatinine or both. This finding emphasizes the limitations of current criteria for AKI risk stratification and diagnosis.
The application of precision gene editing has great potential to accelerate basic research and advance clinical practice in nephrology. Here, the authors discuss this technology and the challenges and potential of genome editing in the kidney.
In this Review, Caplan and colleagues describe the metabolic alterations in autosomal dominant polycystic kidney disease and how these might be novel therapeutic targets in the treatment of polycystic kidney disease.
Acute kidney injury (AKI) is a life-threatening complication in critically-ill neonates. This Review explores the evidence that intrauterine growth restriction, premature birth and low birth weight contribute to neonatal AKI, and discusses perinatal and postnatal risk factors that enhance the risk of AKI among neonates.
Here, Lam and colleagues review advances in understanding the pathogenesis of tuberous sclerosis complex (TSC). Although rapalogues are effective cytostatic treatments for TSC, the unique metabolic vulnerabilities of cells lacking hamartin and/or tuberin might represent opportunities for developing cytocidal treatments.