News & Views in 2017

Encouraging preliminary data from the NEFIGAN trial suggest that a novel oral formulation of budesonide might reduce disease progression in IgA nephropathy. This formulation releases corticosteroid in the distal small intestine and colon, so is thought to directly target the mucosal element of the pathogenesis of the disease.

The Oxford Classification of IgA nephropathy (IgAN) is the most widely accepted system for assessing histologic findings in IgAN. A new publication refines this classification by adding a crescent score, reassessing the segmental sclerosis score, and contextualizing the clinical relevance of the histologic lesions.

Mechanistic studies have implicated the alternative complement pathway, specifically C5a receptor activation, in the pathogenesis of anti-neutrophil cytoplasmic antibody-associated vasculitis. Results from a phase 2 trial suggest that C5a receptor blockade could enable the reduced use or complete withdrawal of steroids from induction protocols.

A recent study reports that coronary artery calcification (CAC) predicts the risk of heart failure, myocardial infarction and stroke in patients with moderate chronic kidney disease (CKD). This finding suggests that even in CKD, CAC is a marker of cardiovascular risk rather than a benign indicator of vessel healing and stability.

New findings challenge the dogma that high salt intake leads to increased thirst, water intake and diuresis. Titze and colleagues show that salt loading activates an adaptive regulatory network in the kidney, muscle and liver, which enables the reprioritization of energy metabolism to conserve plasma water in the setting of high salt intake.

Hypertension in pregnancy is a known risk factor for increased cardiovascular risk for both the mother and her offspring. New findings suggest the offspring of normotensive pregnancies should also be considered at risk of high blood pressure if their mother has had hypertension in other pregnancies.

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.

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.

T cells mediate injury in glomerulonephritis but mice devoid of T cells and B cells can also develop this disease. A new study shows that expression of the cytokine receptor common subunit γ and IL-15 in podocytes protects against crescentic glomerulonephritis, independent of B cells, T cells and natural killer cells.

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.

Elimination of donor-specific antibodies against HLA has been used to enable transplantation of HLA-incompatible kidneys from living donors. In contrast to two previous US studies, a UK study now reports that desensitization does not offer a survival benefit over remaining on the waitlist for a compatible organ.

Several recent studies have provided insights into the genetic regulation of blood pressure. A new study extends these findings by coupling genome-wide association study data with functional validation approaches to identify and explore loci associated with blood pressure, and by generating a genetic risk score model to predict future cardiovascular risk.

Acute kidney injury continues to challenge physicians, researchers and patients. To date, there is no efficient treatment for acute kidney injury and its occurrence in many critically ill patients seems inevitable. However, a new study might just change the way we approach this seemingly intractable problem.

New research supports the notion that pre-renal and intrinsic acute kidney injury are distinct molecular entities and hence different disease states despite similar increases in serum creatinine level. Pre-renal AKI induces protective molecular mechanisms whereas intrinsic AKI requires a 'second hit' that upregulates injury genes, and results in a persistent elevation of serum creatinine and kidney injury biomarkers.