Why might the half-life of Digoxin be extended in patients with diabetic kidney disease?

The half-life of Digoxin is significantly extended in patients with diabetic kidney disease primarily due to decreased renal excretion. Digoxin is primarily eliminated from the body through the kidneys; therefore, any impairment in kidney function can lead to an accumulation of the drug in the system. In diabetic kidney disease, the kidneys may not filter waste products and drugs efficiently, which results in a longer duration for Digoxin to be cleared from the body. This is critical for clinicians to consider when prescribing this medication, as prolonged exposure can increase the risk of toxicity in patients with renal impairment.

Other options presented do not accurately explain why the half-life would be extended in this context. For instance, increased muscle mass would not significantly affect Digoxin clearance, while accelerated drug metabolism is not typically associated with Digoxin, as it is not extensively metabolized by the liver. Lastly, increased drug affinity would relate more to the drug’s effect rather than its elimination process. Therefore, the primary reason for the extended half-life in this scenario centers around the decreased ability of the kidneys to excrete the drug effectively.