Volume 13 Issue 5, May 2017

A population of immature myeloid cells in the bone marrow can transfer proteinuric kidney disease from affected to unaffected mice. This new finding highlights a possible central role of bone marrow as the source of the circulating factor(s) that lead to recurrent focal segmental glomerulosclerosis and potentially other kidney diseases.

Iodinated contrast media are essential for diagnostic and interventional radiological and cardiological procedures, but may cause kidney damage. Intravenous hydration is the current cornerstone for prevention of contrast-induced acute kidney injury; however, new data from the AMACING trial suggest that this approach might not be beneficial in low-risk patients.

Achieving optimal blood pressure with antihypertensive agents in hypertensive patients can be particularly challenging. A major factor in this challenge is poor implementation of and compliance with multidrug regimens. However, a recent study shows encouraging results with a new single pill product that contains ultra-low doses of four antihypertensive agents.

Metabolomics has been instrumental for the identification of new biomarkers of chronic kidney disease (CKD). Here, the authors discuss metabolomics technologies and their application in renal disease, including the specificity and functional relevance of CKD-associated metabolic biomarkers.

Haemodialysis is associated with a high risk of cardiovascular events. Here, the authors discuss the mechanisms by which biomaterial-induced activation of the complement, contact and coagulation systems might contribute to the generation of arteriosclerosis and cardiovascular disease in patients on haemodialysis.

Non-alcoholic fatty liver disease (NAFLD) not only affects the liver, but can also increase the risk of developing extra-hepatic diseases, including type 2 diabetes mellitus, cardiovascular disease and chronic kidney disease (CKD). Here, Targher and Byrne discuss the epidemiologic and mechanistic evidence of a pathogenic link between NAFLD and CKD.

An increasing body of evidence points toward a role for the complement system in the pathogenesis of diabetic nephropathy. Here, Allan Flyvbjerg describes the underlying experimental and clinical evidence and discusses how the association between complement activation and diabetic nephropathy might facilitate the identification of new biomarkers of disease progression and targets for therapeutic intervention.