How do NSAIDs affect renal perfusion and prostaglandin synthesis?

• A. NSAIDs inhibit COX enzymes, reducing renal prostaglandins, decreasing renal blood flow and GFR, especially in volume-depleted states.
• B. NSAIDs increase prostaglandin synthesis
• C. NSAIDs cause dilation of efferent arterioles
• D. NSAIDs increase renin release

Answer: (A)

NSAIDs block cyclooxygenase enzymes, which reduces the kidney’s production of prostaglandins like PGE2 and PGI2. These prostaglandins normally dilate the afferent arteriole, helping to preserve renal blood flow and the glomerular filtration rate, especially when volume is low or there’s stress on the kidneys. By inhibiting prostaglandin synthesis, NSAIDs remove this vasodilatory support, causing afferent arteriolar constriction, decreased renal blood flow, and a lower GFR—an effect that can precipitate acute kidney injury in volume-depleted or compromised kidneys. The other statements don’t fit the primary mechanism: NSAIDs don’t increase prostaglandin synthesis, they don’t cause dilation of the efferent arteriole as their main action, and while reduced perfusion can affect renin release, the key concept here is the COX inhibition leading to lowered prostaglandins and renal perfusion.