Search Results

You are looking at 1 - 3 of 3 items for

  • Author or Editor: Ian H. de Boer x
  • Refine by Content Type: Articles x
Clear All Modify Search
Ian H. de Boer

Diabetes treatment has advanced rapidly over the past decade, with new drugs and technologies developed and translated into clinical care. Many of these treatments affect the kidney, are affected by chronic kidney disease (CKD), or carry both effects. In addition, new data have been published on foundational elements of care for people with diabetes and CKD, including lifestyle, ascertainment of glycemia, glycemic targets, and use of renin-angiotensin system (RAS) inhibitors. Providers and patients rightly ask how to apply the new treatments and integrate them into tailored existing care paradigms.

KDIGO has initiated a new clinical practice guideline to help guide

Ian H. de Boer, Grant Olan, and Uptal D. Patel

In 2012, the Agency for Healthcare Research and Quality (AHRQ) comprehensively summarized the available evidence evaluating the risks and benefits of screening for chronic kidney disease (CKD) in the general population. Utilizing these data, the U.S. Preventive Services Task Force (USPSTF) determined that existing evidence was insufficient to balance the benefits and harms of routine screening for CKD in asymptomatic adults. Subsequently, the USPSTF identified screening for CKD as its top priority in a report to Congress on high-priority evidence gaps for clinical preventive services. USPSTF also identified screening for CKD in African Americans as the most important evidence gap

Steven Menez, Ashveena L. Dighe, Ian H. de Boer, and for the Kidney Precision Medicine Project

The Kidney Precision Medicine Project (KPMP) is a National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)-funded, multi-year collaboration of leading research institutions across the United States that aims to better understand the mechanisms of acute kidney injury (AKI) and chronic kidney disease (CKD) (1).

Our understanding of the pathophysiology of certain kidney diseases has improved dramatically in recent years, with discovery of the genetic mechanisms behind phenotypes, such as non-diabetic focal segmental glomerular sclerosis in patients with high-risk APOL1 genotypes (2). However, CKD and, in particular, AKI are defined broadly using serum creatinine and