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Medtech Impact on Wellness

This episode offers listeners an expert view on diabetes and kidney damage treatments. Richard interviews researcher David J.

Leehey, who has focused on diabetic kidney disease for the last 30 years.

Listeners will learn:

  • What types of cells make up the kidney and how diabetic kidney disease stages progresses through these cells,
  • How hemodynamic factors, like blood pressure, also contribute to kidney stress, and
  • What drugs are making headway as effective treatment and what advances are needed.  

Diabetes’ prevalence has made it the most common cause of kidney disease. How does diabetes affect the kidneys? Professor David Leehey has the answers and catches listeners up with the latest in effective medications and discusses the lagging technology of dialysis.

He’s a nephrologist, professor, and Medical Director of Acute Dialysis at Loyola University. He’s also the Associate Chief of Staff of Clinical Affairs of Hines VA in Illinois. Dr. Leehey presents various pathways to kidney disease that necessitate dialysis and kidney transplantation with an emphasis on the primary cause of diabetes.

He explains exactly how high blood sugar creates the complications that lead to disease. He tells listeners to think of it like caramel formation—glucose molecules becomes large glycated molecules that get incorporated into base membranes of glomeruli, which are important to the filtering process. A characteristic pathology is therefore thickening of these membranes from the glycated proteins that accumulate.

He discusses some other causes and then heads into effective medications and dialysis treatment, which he notes begs for sorely needed innovation.

While dialysis treatment proved revolutionary when it first emerged, the technology has shown no improvement over the years and the profitability of the process may be one inhibitor.

For more about Dr. Leehey, see his information on Loyola’s web page: loyolamedicine.org/doctor/david-leehey.

Available on Apple Podcasts: apple.co/2Os0myK

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