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The development of new biomarkers that enable the early diagnosis of acute kidney injury (AKI) should facilitate early intervention and reduce the mortality associated with this disease. In this Perspectives article, Robert Schrier discusses the need to develop interventions to attenuate or prevent AKI and the requirement for such interventions to selectively improve renal hemodynamics, increase tubular flow rates, and decrease inflammation without causing systemic vasodilation.

Hyponatraemia—the most common serum electrolyte disorder—is an important marker of the severity and prognosis of a number of diseases. In this Review, Schrier et al. discuss the effect of hyponatraemia in different patient groups, including those with pneumonia, heart failure, cirrhosis, and the elderly population. The authors discuss the need for prospective studies to examine whether correcting hyponatraemia can improve outcomes or whether hyponatraemia is just a marker of severe disease.

Attempts to achieve pharmacological suppression of the renin–angiotensin–aldosterone system (RAAS) fall short of complete success, owing to the existence of accessory enzyme pathways. In this article, the therapeutic targets and limitations of RAAS inhibition are discussed, and the use of combination therapy and the direct renin inhibitor, aliskiren, are described.

Multifactorial approaches to the treatment of type 2 diabetes mellitus have proven more effective than any individual intervention alone in reducing the risk of cardiovascular complications. As the spread of diabetes and obesity accelerates worldwide, unhindered by lifestyle modification approaches, the authors of this Viewpoint propose an aggressive multifactorial strategy for treating patients who have one or more risk factors for the metabolic syndrome in an effort to prevent or delay the onset of diabetes.

Autosomal dominant polycystic kidney disease is a challenging disorder to diagnose and treat effectively. Promising research over the past decade has, however, provided novel interventions, modifications to clinical practice and new areas to investigate with the aim of identifying approaches to slow disease progression.

This Review describes the cardiovascular manifestations of autosomal-dominant polycystic kidney disease (ADPKD), including hypertension, left ventricular hypertrophy, aneurysms and cardiac valvular disorders. The authors focus particularly on hypertension, with a detailed discussion of the pathogenesis of this condition in ADPKD and a comprehensive review of the renal and cardiovascular effects of antihypertensive treatment in the ADPKD setting. Recommendations for the optimal cardiovascular management of ADPKD are provided.

The Appropriate Blood Pressure Control in Diabetes (ABCD) study remains one of the most relevant sources of data on the vexed issue of optimum management of blood pressure in diabetic patients. This Review by trial investigators provides a more-comprehensive description of data that have emerged from this 5-year, randomized study of moderate versus intensive control of blood pressure using either a calcium channel blocker or an ACE inhibitor.

Glomerular hyperfiltration occurs as a physiological response during pregnancy and after consumption of high-protein meals, but an elevation in glomerular filtration rate is also associated with various disease states. In this Review, the authors discuss the definitions of glomerular hyperfiltration as well as the underlying mechanisms and hemodynamic changes that can adversely affect kidney function. They also describe potential approaches to treat glomerular hyperfiltration.

The discovery of a gene associated with autosomal dominant polycystic kidney disease (ADPKD) was only the first step toward understanding the disease. Now researchers are determining what the gene' product normally does (pages 359–364).

Authors from the University of Colorado describe a 31-year-old white female with tuberous sclerosis complex who was diagnosed with very large bilateral angiomyolipoma of the kidneys after developing symptoms of urinary tract infection and septic shock. The lack of surveillance throughout the course of the patient's disease prevented early intervention before the development of end-stage renal disease and the need for bilateral nephrectomy. This case illustrates the importance of regular follow-up in patients with tuberous sclerosis complex.

A study that tracked mammal populations before, during and after a severe storm in Mozambique’s Gorongosa National Park finds that behavioural responses and survival are linked to body size, with increased mortality of small species owing to limited mobility and changes in food availability.

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.

New research indicates that intact soluble urokinase plasminogen activator receptor (suPAR) does not induce albuminuria in mice. These data corroborate the most recent clinical findings, showing that intact suPAR is not the plasma permeability factor responsible for recurrence of focal segmental glomerulosclerosis after renal transplantation.

Studies published in 2016 provide insights that bring us closer to achieving the goal of personalized therapy for primary glomerular diseases. Moreover, promising renal outcome data with new classes of glucose-lowering agents — SGLT2 inhibitors and GLP-1 agonists — offer new hope for patients with diabetic nephropathy.

Maintaining steroid-free remission in children with idiopathic nephrotic syndrome is an important goal of therapy. A new trial provides evidence that mycophenolate mofetil can be added to the list of effective steroid-sparing agents. The majority of participants relapsed, however, highlighting an unmet need for more effective treatment modalities.

Thiazide diuretics lower blood pressure and cardiovascular risk but can cause severe hyponatraemia. Researchers now demonstrate that thiazide-induced hyponatraemia is associated with a genetic variant in a distal nephron prostaglandin transporter. They propose that reduced prostaglandin reabsorption through this transporter facilitates activation of the prostaglandin EP4 receptor to increase water reabsorption.