How do nonsteroidal anti-inflammatory drugs (NSAIDs) affect renal function?

Nonsteroidal anti-inflammatory drugs (NSAIDs) can have a significant impact on renal function primarily by reducing glomerular filtration rate (GFR), which can in turn lead to acute kidney injury (AKI). NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes that are responsible for the production of prostaglandins. Prostaglandins play a crucial role in maintaining renal perfusion, especially in situations where renal blood flow may be compromised.

In instances of reduced blood flow, such as dehydration, heart failure, or renal artery stenosis, prostaglandins help dilate the afferent arterioles in the kidney, ensuring adequate blood supply to maintain GFR. When NSAIDs inhibit prostaglandin synthesis, this vasodilation is impaired, leading to constriction of the afferent arterioles. Consequently, the reduction in blood flow can decrease the GFR, ultimately increasing the risk of acute kidney injury.

Other options present alternative effects, but they do not accurately characterize the primary renal risks associated with NSAIDs. For example, NSAIDs do not increase renal blood flow; rather, they can compromise it. Additionally, while some diuretics induce enhanced sodium excretion, NSA