Acute kidney injury articles from across Nature Portfolio

This Review describes parallels in the injury mechanisms that underlie acute kidney injury, chronic kidney disease and allograft injury, and explains how our understanding of the molecular changes that occur in epithelia in the context of kidney disease may contribute to the therapeutic targeting of specific epithelial cell phenotypes for the treatment of transplantation complications.

Addressing the burden of non-communicable diseases is a global public health priority. In this joint Consensus Statement, the American Society of Nephrology, the European Renal Association and the International Society of Nephrology highlight the need to recognize kidney disease as a key driver of premature mortality, in addition to other non-communicable diseases already prioritized by the World Health Organization.

Clonal hematopoiesis, which increases with age and is implicated in a variety of age-related diseases, is shown here to be associated with a greater risk of acute kidney injury and worse outcome following injury, as demonstrated using multiple patient cohorts, Mendelian randomization analysis and mechanistic studies in mouse disease models.

Acute kidney injury affects one in five hospitalized patients and can lead to lasting kidney damage or death. We show that clonal hematopoiesis of indeterminate potential — a common age-related condition caused by blood cell mutations — increases the risk of acute kidney injury in multiple cohorts of human patients and in mouse models.

Acute kidney injury (AKI) is a global concern that affects patient outcomes and resource utilization. An effective educational programme aimed at improving early AKI identification, triaging and treatment, using risk scores and care bundles coupled with access to point-of-care diagnostics, can help to prevent AKI-related deaths in regions with limited resources.