Teachable moment in classrooms:

  1. urinary system chapter – parts of the nephron and their functions
  2. endocrine system chapter – location and action of receptors for lipid-soluble hormones
  3. heart chapter within cardiovascular system – location of myocardium in the heart wall

The news item:  Recently the following article appeared online:

Utilization of Finerenone by Patients With T2D, CKD | Docwire News

Two years after its approval, researchers studied the use of finerenone in adults with type 2 diabetes and chronic kidney disease (CKD).

The report states that finerenone – a mineralocorticoid receptor antagonist – is approved for several medical conditions (type 2 diabetes, chronic kidney disease, end-stage renal disease, heart failure) where glomerular filtration rate was declining. The author states that utilization rate is still low for this drug.

So, Why Do I Care??  In the USA alone the combined number of people suffering from type II diabetes, chronic kidney disorder (CKD), end-stage renal disease (ESRD) and heart failure is over 100 million. Those disorders cause the death of over 500,000 people every year, and force many patients into hospitalizations, and into major changes in the quality of life. Therefore, it is worth finding and using new pharmaceutical treatments that may lower those disease and death numbers.

Plain English, Please!!! First, let’s talk about what is the shared, common, physiological malfunction in CKD, ESRD, and heart failure. In all three disorders damaged cells start inflammation, and the tissue is repaired by formation of scar tissue. In the case of CKD and ESRD the kidney accumulates unusually large amount of connective tissue (develops fibrosis) made by overstimulated fibroblast. In heart failure the myocardium portion of the heart wall accumulates unusually large amount of connective tissue. In the kidneys the filtration by the nephrons is slowed down by fibrosis, while in the heart the contraction of the ventricles is made difficult by the fibrosis.

Second, let’s talk about why fibrosis appears in the kidneys and in the heart. During early stage kidney disease and early-stage heart disease the cells of the nephron in the kidneys, and the cardiac muscle cells in the heart send out local stimulators of tissue repair. When those stimulators are released for years, the fibroblasts in the kidney and in the heart make unusually large amount of connective tissue. One recently identified stimulator of connective tissue production is the hormone aldosterone.

Third, let’s talk about how finerenone slow sdown the progression of CKD, ESRD, and heart failure. Knowing that fibrosis enhances damage to kidneys and the heart, it is intuitive that if we could slow the action of those stimulators, then less connective tissue would be made. Finerenone slows the action of the stimulator aldosterone. Finerenone goes to the aldosterone receptors in the nucleus and sticks to them. Picture the aldosterone receptor as a baseball mitt, and the aldosterone hormone as a baseball.  In fibrosis the ball hits the mitt, and the fibroblast is told to make connective tissue. Finerenone is like an apple, it fits into the mitt and stops the baseball from hitting the mitt. In more scientific words, finerenone inhibits the action of aldosterone. When fibroblasts receive less stimulation, they make less connective tissue, and that lowers the fibrosis, and improves functioning of the kidneys and the heart.

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