• Kai-Uwe Eckardt, Josef Coresh, Olivier Devuyst, Richard J Johnson, Anna Köttgen, Andrew S Levey, and Adeera Levin.
• Department of Nephrology and Hypertension, University of Erlangen-Nürnberg, Erlangen, Germany. kai-uwe.eckardt@uk-erlangen.de
• Lancet. 2013 Jul 13;382(9887):158-69.

AbstractIn the past decade, kidney disease diagnosed with objective measures of kidney damage and function has been recognised as a major public health burden. The population prevalence of chronic kidney disease exceeds 10%, and is more than 50% in high-risk subpopulations. Independent of age, sex, ethnic group, and comorbidity, strong, graded, and consistent associations exist between clinical prognosis and two hallmarks of chronic kidney disease: reduced glomerular filtration rate and increased urinary albumin excretion. Furthermore, an acute reduction in glomerular filtration rate is a risk factor for adverse clinical outcomes and the development and progression of chronic kidney disease. An increasing amount of evidence suggests that the kidneys are not only target organs of many diseases but also can strikingly aggravate or start systemic pathophysiological processes through their complex functions and effects on body homoeostasis. Risk of kidney disease has a notable genetic component, and identified genes have provided new insights into relevant abnormalities in renal structure and function and essential homoeostatic processes. Collaboration across general and specialised health-care professionals is needed to fully address the challenge of prevention of acute and chronic kidney disease and improve outcomes.Copyright © 2013 Elsevier Ltd. All rights reserved.

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