Volume 13 Issue 9, September 2017

Inhibitors of renal sodium/glucose cotransporter 2 (SGLT2) are new anti-hyperglycaemic drugs that reduce proximal tubular glucose and sodium reabsorption. The Canagliflozin Cardiovascular Assessment Study (CANVAS) Program is the second major trial to demonstrate beneficial effects of SGLT2 inhibitors on the kidney and cardiovascular system in patients with type 2 diabetes mellitus.

New findings demonstrate a link between mutations in DZIP1L and an autosomal recessive polycystic kidney disease (ARPKD)-like phenotype. Rather than focus on DZIP1L as a second genetic locus for ARPKD, we suggest these data identify the ciliary transition zone as a functional domain central to the pathogenesis of ARPKD.

Debate exists regarding the safety of metformin and the risk of metformin-associated lactic acidosis, particularly in the setting of kidney dysfunction. Data from two studies examining the interplay between metformin, acute kidney injury, and complications including lactic acidosis suggest that metformin should be used conservatively in patients with kidney dysfunction.

During injury, mitogenic signals from apoptotic cells may compensate for cell loss by promoting organ homeostasis and regeneration. A distinct type of early apoptotic extracellular vesicle with specific mitogenic activity has been identified. The detection of these vesicles in damaged mouse glomeruli highlights their possible role in response to renal injury.

Uromodulin is the most abundant urinary protein. Here, the authors discuss the physiological roles of uromodulin, the mechanisms by which mutations in theUMOD gene, which encodes uromodulin, cause autosomal dominant tubulointerstitial kidney disease and the association of common UMODvariants with complex disorders in the general population.

Extracellular vesicles, exosomes and microvesicles are host cell-derived packages of information that are involved in cell–cell communication. This Review discusses how the release and uptake of these vesicles has important physiological functions in renal processes and can contribute to the development of kidney diseases, and how extracellular vesicles might be targeted and used for the treatment of patients with renal diseases.

Membranous nephropathy is an immune-mediated disease and is the leading cause of nephrotic syndrome in adults. Here, the authors discuss the role of B cell-depleting regimens in the treatment of this disease and the potential use of rescue therapy with agents that target plasma cells, which might prevent antigen–antibody interactions and immune complex-mediated complement activation.

Patients with chronic kidney disease have elevated levels of carbamoylated proteins. Here the authors review the mechanisms of carbamoylation, the effects of this post-translational modification on renal function and strategies to reduce the carbamoylation load.