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MUSE (microscopy with UV surface excitation) image of fixed unsectioned kidney, showing a renal artery with elastic lamina surrounded by collagen with renal tubules on either side. Cover image supplied by Richard Levenson, Department of Pathology and Laboratory Medicine, University of California Davis Medical Center at Sacramento, California, USA.
Pre-eclampsia is a common disorder of pregnancy for which the underlying mechanism is poorly understood. A genome-wide association study has now identified a pre-eclampsia susceptibility locus located near the FLT1 gene. This study brings us a step closer to dissecting the underlying causes of pre-eclampsia.
Management of mineral and bone disorders in patients with chronic kidney disease (CKD–MBD) requires an understanding of the complex interactions among ions, hormones and their target organs. Since publication of the KDIGO CKD–MBD guideline in 2009, our understanding of disease pathophysiology has improved; however, a paucity of high-quality clinical evidence to support specific interventions remains. Using available data, KDIGO has now updated diagnostic and therapeutic recommendations for patients with CKD–MBD.
Aspirin therapy for the prevention of pre-eclampsia in unselected women is minimally effective. New data suggest that use of a screening strategy based on clinical, biochemical and biophysical factors to identify those at high risk of pre-term pre-eclampsia could improve the efficacy of preventive aspirin therapy.
The incretin hormone glucagon-like peptide 1 (GLP-1) has been implicated in the gut–renal axis and incretin-based therapies might reduce the burden of diabetic kidney disease. Here, the authors review the physiological roles of GLP-1, the potential renoprotective mechanisms of incretin-based therapies and the available renal outcome data from clinical trials.
Mitochondria provide the kidney with energy to remove waste from the blood and regulate fluid and electrolyte balance. This Review discusses how mitochondrial homeostasis is maintained, the changes in mitochondrial energetics that occur in acute kidney injury and diabetic nephropathy, and how targeting mitochondrial energetics might aid the treatment of renal disease.
A growing body of evidence supports a key role for T helper type 17 (TH17) cells in the development of renal damage. This Review discusses the identification, regulation, and function of TH17 cells and their associated pathways in immune-mediated kidney diseases, with particular focus on the mechanisms underlying renal tissue injury.