Volume 10 Issue 7, July 2014

A reduction of salt intake to <5 g sodium chloride per day is generally advised for patients with chronic kidney disease. However, hard evidence to support this recommendation is lacking. New data from Fan et al. suggest that very strict sodium limits might be harmful in patients with renal disease.

Kidney transplant recipients who also receive a partial liver allograft have better long-term outcomes than those who receive a kidney alone, despite the more-complex surgery. Understanding how the liver exerts these beneficial effects might enable their exploitation in the future.

Secondary analysis of the FAVORIT data in kidney transplant recipients showed that systolic blood pressure ≥140 mmHg and diastolic blood pressure <70 mmHg at trial entry were associated with increased risks of cardiovascular disease over a mean of 4 years. Whether these blood pressure values are associated with mortality is unclear.

In the endoplasmic reticulum (ER), networks of protein homeostasis—proteostasis—regulate protein synthesis, folding and degradation via the unfolded protein response (UPR) pathway. A defective UPR is deleterious to renal cell function and viability and is implicated in the pathophysiology of various kidney pathologies. Here, the authors discuss the role of oxidative, glycative and hypoxic stress and how optimizing ER proteostasis might prevent and treat kidney diseases.

Fornoni et al. discuss the role of lipid biology in podocytes in the pathogenesis of glomerulopathies focusing on diabetic kidney disease and focal segmental glomerulosclerosis. They outline recent findings from genetic disorders that highlight the function of apolipoproteins in the podocyte and discuss the therapeutic implications.

Data from studies in humans and rodents suggest that B cells have the capacity to control or regulate the immune response to a transplanted organ. Here, the authors describe the phenotypes and mechanisms that have been associated with regulatory B cell function and discuss the evidence for a role of these cells in transplant tolerance.

In this Review, the authors discuss the pathological mechanisms related to Toll-like receptors, nucleotide-binding oligomerization domain receptors and the NACHT, LRR and PYD domains-containing protein 3 inflammasome in various kidney diseases. Although these receptors are protective in the host defence against urinary tract infection, they can perpetuate tissue damage in sterile inflammatory and immune-mediated kidney diseases—making them promising drug targets.

Recurrent dehydration and salt loss might be a mechanism that causes chronic kidney disease, whereby increased plasma osmolarity activates both intrarenal (polyol-fructokinase) and extrarenal (vasopressin) pathways to drive injury. The authors propose that water and salt influence blood pressure through the timing and combination of their intake, affecting plasma osmolarity and intrarenal and extrarenal mechanisms of renal injury.