INFLAMMATION + FIBROSIS IN CKD

KIDNEY FILTRATION FURTHER DETERIORATES AS INFLAMMATION AND FIBROSIS PROGRESS1

MR OVERACTIVATION SIGNIFICANTLY TRIGGERS INFLAMMATION AND FIBROSIS, CONTRIBUTING TO A DECLINE IN KIDNEY FUNCTION1

For patients with chronic kidney disease (CKD) and type 2 diabetes (T2D), unaddressed inflammation and fibrosis can lead to a variety of cellular changes that permanently alter the structure of the kidney.2

MR: mineralocorticoid receptor.

In the kidney, inflammation and fibrosis can lead to tissue expansion, increased pressure within the vasculature and internal structure, and eventually, to scarring that makes effective filtration increasingly difficult.2

INFLAMMATORY AND FIBROTIC DAMAGE IS A MAJOR CONSEQUENCE OF MR OVERACTIVATION IN THE KIDNEY1

Under normal conditions, MR signaling regulates electrolyte and fluid balance within the kidneys.1

However, under certain conditions, like T2D, the MR within the kidney can become pathologically overactivated. As MR activators proliferate and the cell begins producing:

  • Proinflammatory proteins
  • Profibrotic proteins

These factors eventually lead to inflammation and fibrosis in the kidneys, causing damage. Kidney damage, as shown by increased albuminuria, raises the risk of a cardiovascular (CV) event and declining kidney function.1,4

Normal MR Function
Normal MR
MR Overactivation
MR Overactivation

MR OVERACTIVATION CONTRIBUTES TO THE RISK OF A CV EVENT1

Though CV risk is a reality from the beginning of CKD in T2D, as CKD progresses, there is an increased chance a patient might experience a CV event like myocardial infarction or stroke. There is evidence in both preclinical and clinical trials to support the connection of MR overactivation with CV dysfunction.1,4,5

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References: